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null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/986", "Drug": "Cyclophosphamide (CTX)", "Drug_category": "Alkylating agents", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": "D07760", "Pubchem_ID": "2907", "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Single Drug", "PMID": "21156650", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma", "System": "MAFO-treated EG7 (MAFO-EG7) cells", "Dose": "CTX derivative MAFO at 10 μmol/L", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "sCRT, HMGB1", "Controlled_Terms_Function_enhanced_Number_increased": "HMGB1", "Immune_System-Function_inhibited/numbers_decreased": "CD31", "Controlled_Terms_Function_inhibited_Number_decreased": "CD31 / PECAM-1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, 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and granzyme B (GZMB), T-BET (Tbx21),TRAIL (TNFSF10) and Fas ligand (FASLG), lymphotactin (XCL1), Phospho-STAT4 levels , increased NK-cell cytotoxicity, higher levels of IFN-γ, TNF-α and granzyme B", "Immune_System-Function_enhanced/numbers_increased": "TRAIL; Granzyme B / GZMB; IFN-γ; TNF-α / TNF; Cytotoxicity / cytolysis; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "AN", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "trabectedin has a direct stimulatory effect on NK cells and can be combined with IL-12 to activate NK cells in the presence of TNBC", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "NK cells; IL-12", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": 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Cell proliferation", "Immune_System-Function_inhibited/numbers_decreased": "NF-κB pathway", "Controlled_Terms_Function_inhibited_Number_decreased": "NF-κB", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1009", "Drug": "Valproic acid", "Drug_category": "Fatty acid derivatives", "Drugbank_ID": "DB00313", "Target/s_or_mechanism_of_action": "Valproic acid exhibits its pharmacologic effects in a couple of ways, such as by acting on GABA (γ aminobutyric acid) levels in the CNS, blocking voltage-gated ion channels, and inhibiting histone deacetylase", "KEGG_Drug__ID": "D00399", "Pubchem_ID": "3121", "STR_LINK_(SMILES)": "CCCC(CCC)C(O)=O", "Single/Combination": "Single Drug", "PMID": "30387821", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "RPMI8226", "Dose": "0-4mM", "Technique": "Cell Counting kit-8 assay,Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "antiproliferation activity,apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis; Cell proliferation", "Immune_System-Function_inhibited/numbers_decreased": "NF-κB pathway", "Controlled_Terms_Function_inhibited_Number_decreased": "NF-κB", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1608", "Drug": "Valproic acid", "Drug_category": "Fatty acid derivatives", "Drugbank_ID": "DB00313", "Target/s_or_mechanism_of_action": "Valproic acid exhibits its pharmacologic effects in a couple of ways, such as by acting on GABA (γ aminobutyric acid) levels in the CNS, blocking voltage-gated ion channels, and inhibiting histone deacetylase", "KEGG_Drug__ID": "D00399", "Pubchem_ID": "3121", "STR_LINK_(SMILES)": "CCCC(CCC)C(O)=O", "Single/Combination": "Single Drug", "PMID": "29371976", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "Triple-negative MDA-MB231", "Dose": "1-5 µM", "Technique": "western blot, qReal-Time PCR", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in tumor cells.", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1400", "Drug": "ACY-241 (citarinostat)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB15449", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": "53340426", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1Cl", "Single/Combination": "Single Drug", "PMID": "30728070", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin -Metastatic Melanoma Patients", "System": "T-cells isolated from melanoma patient PBMC samples(activated via αCD3/CD28)", "Dose": "500nM", "Technique": "Luminex", "Controlled_Technique": "Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Th2 cytokine production (e.g. IL-4, IL-5, IL-6,IL-10, IL-13)", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-4; 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Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD86 expression cancer testis antigen- PRAME", "Controlled_Terms_Function_enhanced_Number_increased": "CD86; Cancer-testis antigens; PRAME antigen; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/28", "Drug": "Chidamide (CS055/HBI-8000/Tucidinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06334", "Target/s_or_mechanism_of_action": "Histone deacetylase inhibitor", "KEGG_Drug__ID": "D10993", "Pubchem_ID": "12136798", "STR_LINK_(SMILES)": "NC1=CC(F)=CC=C1NC(=O)C1=CC=C(CNC(=O)\\C=C\\C2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "23940586", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "NB4", "Dose": "1 µM for 24 h", "Technique": "real-time quantitative RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD86 expression cancer testis antigen- PRAME", "Controlled_Terms_Function_enhanced_Number_increased": "CD86; Cancer-testis antigens; PRAME antigen; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/29", "Drug": "Chidamide (CS055/HBI-8000/Tucidinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06334", "Target/s_or_mechanism_of_action": "Histone deacetylase inhibitor", "KEGG_Drug__ID": "D10993", "Pubchem_ID": "12136798", "STR_LINK_(SMILES)": "NC1=CC(F)=CC=C1NC(=O)C1=CC=C(CNC(=O)\\C=C\\C2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "23940586", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "U937", "Dose": "1 µM for 24 h", "Technique": "real-time quantitative RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD86 expression cancer testis antigen- PRAME", "Controlled_Terms_Function_enhanced_Number_increased": "CD86; Cancer-testis antigens; PRAME antigen; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/675", "Drug": "Domatinostat (4SC-202)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB17521", "Target/s_or_mechanism_of_action": "Inhibits HDAC1, HDAC2, HDAC3; also inhibits LSD1/REST at μM concentrations; induces G2/M arrest, apoptosis and increases APM/MHC-I expression", "KEGG_Drug__ID": null, "Pubchem_ID": "15985904", "STR_LINK_(SMILES)": "CN1C=C(C=N1)C2=CC=C(C=C2)S(=O)(=O)N3C=CC(=C3)/C=C/C(=O)NC4=CC=CC=C4N", "Single/Combination": "Single", "PMID": "33002502", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Aggressive neuroendocrine skin cancer", "System": "MKL-2 (MCPyV+)", "Dose": "2.5 μM; 24–48 h", "Technique": "Cell-cycle analysis; apoptosis; RT-qPCR; flow cytometry", "Controlled_Technique": "MHC-I or HLA class I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/557", "Drug": "Depsipeptide (FK228) or Romidepsin", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "57515973", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Single Drug", "PMID": "18185535", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "C57BL/6 mice were immunized by s.c. injection of irradiated IL-12/IL-18 cDNA-transduced B16/F10 cells. Spleen cells were isolated and used as effectors against luc-B16/F10 cells", "Dose": "depsipeptide (5 nM) and recombinant FLAG-tagged FasL (10 ng/ ml ) and multimerized with anti-FLAG M2 antibodies (1 mg/ ml ) for 16 hours.", "Technique": "Luciferase activity (photon counts) n evaluated in the presence of D-luciferin", "Controlled_Technique": "Bioluminescence/luciferase assay", "Immune_System-Function_enhanced/numbers_increased": "cytotoxicity IFNγ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; Cytotoxicity / cytolysis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1416", "Drug": "Depsipeptide (FK228) or Romidepsin", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "57515973", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Single Drug", "PMID": "18185535", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "B16/F10", "Dose": "depsipeptide (10 nM) for 16 hours", "Technique": "RT-PCR, Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "major histocompatibility complex (MHC) class I (H2-Db ) and Fas (CD95) death receptor expression in B16/F10 cells gp100/ pmel17 melanoma antigen", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; CD95 / Fas / FAS; Melanoma differentiation antigens; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1417", "Drug": "Depsipeptide (FK228) or Romidepsin", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "57515973", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Single Drug", "PMID": "18185535", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "MC (RPM-MC)", "Dose": "depsipeptide (10 nM) for 16 hours", "Technique": "RT-PCR, Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "MHC class I gp100/ pmel17 melanoma antigen", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Melanoma differentiation antigens;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1418", "Drug": "Depsipeptide (FK228) or Romidepsin", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "57515973", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Single Drug", "PMID": "18185535", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "BP (MM-BP)", "Dose": "depsipeptide (10 nM) for 16 hours", "Technique": "RT-PCR, Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "MHC class I gp100/ pmel17 melanoma antigen", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Melanoma differentiation antigens;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1419", "Drug": "Depsipeptide (FK228) or Romidepsin", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "57515973", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Single Drug", "PMID": "18185535", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "LH (MM-LH)", "Dose": "depsipeptide (10 nM) for 16 hours", "Technique": "RT-PCR, Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "MHC class I gp100/ pmel17 melanoma antigen", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Melanoma differentiation antigens;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1420", "Drug": "Depsipeptide (FK228) or Romidepsin", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "57515973", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Single Drug", "PMID": "18185535", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "RU (MM-RU)", "Dose": "depsipeptide (10 nM) for 16 hours", "Technique": "RT-PCR, Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "MHC class I gp100/ pmel17 melanoma antigen", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Melanoma differentiation antigens;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/320", "Drug": "Depsipeptide (FK228) or Romidepsin", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "57515973", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Single Drug", "PMID": "18185535", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Luc-B16/F10 cells", "Dose": "1–10 nM", "Technique": "Luciferase activity (photon counts) n evaluated in the presence of D-luciferin, Caspase-Glo 3/7 Assay system (Promega), Western blot", "Controlled_Technique": "Western blot/immunoblot analysis; Apoptosis/cell viability assay; Bioluminescence/luciferase assay; Caspase-Glo3/7 Assay", "Immune_System-Function_enhanced/numbers_increased": "caspase-3/7 activity,cell cycle regulator p21Waf/Cip1-induce apoptosis and cell cycle arrest", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase activation; Apoptosis; Cell-cycle arrest; p21 / CDKN1A", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/673", "Drug": "Domatinostat (4SC-202)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB17521", "Target/s_or_mechanism_of_action": "Inhibits HDAC1, HDAC2, HDAC3; also inhibits LSD1/REST at μM concentrations; induces G2/M arrest, apoptosis and increases APM/MHC-I expression", "KEGG_Drug__ID": null, "Pubchem_ID": "15985904", "STR_LINK_(SMILES)": "CN1C=C(C=N1)C2=CC=C(C=C2)S(=O)(=O)N3C=CC(=C3)/C=C/C(=O)NC4=CC=CC=C4N", "Single/Combination": "Single", "PMID": "33002502", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Aggressive neuroendocrine skin cancer", "System": "WaGa (MCPyV+)", "Dose": "2.5 μM; 24 h for scRNA-seq; 2.5 μM; 24–72 h for other assays", "Technique": "scRNA-seq; cell-cycle analysis; apoptosis; RT-qPCR; immunoblot; flow cytometry", "Controlled_Technique": "APM genes increased: large multifunctional protease 2 and 7 (LMP2 and LMP7), transporter associated with antigen processing 1 and 2 (TAP1 and TAP2); HLA-A, β2-Microglobulin and MHC-I surface expression increased", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; HLA-A; TAP1; TAP2; LMP2 / PSMB9; LMP7 / PSMB8; β2-microglobulin / B2M; Antigen presentation; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/674", "Drug": "Domatinostat (4SC-202)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB17521", "Target/s_or_mechanism_of_action": "Inhibits HDAC1, HDAC2, HDAC3; 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Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CIITA and CD74, MHCII and CD74, PD-L1 expression , costimulatory molecules, 41BB, CD40, and ICOSL, the inhibitory ligand, PD-L1, and the T-cell chemoattractant, CXCL10 impairs tumor cell proliferation", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; MHC class II; CIITA; CD40; ICOS ligand / ICOSL / CD275; 4-1BB / CD137; CD74; CXCL10 / IP-10; Cell proliferation; CD80/CD86 costimulation; T cells; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1364", "Drug": "Entinostat (MS-275)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": "D09338", "Pubchem_ID": "4261", "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "31720815", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "TS/A", "Dose": "5 μM", "Technique": "RT-PCR, Flow cytometry, propidium iodide staining", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CIITA and CD74, MHCII and CD74, PD-L1 expression , costimulatory molecules, 41BB, CD40, and ICOSL, the inhibitory ligand, PD-L1, and the T-cell chemoattractant, CXCL10 impairs tumor cell proliferation", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; MHC class II; CIITA; CD40; ICOS ligand / ICOSL / CD275; 4-1BB / CD137; CD74; CXCL10 / IP-10; Cell proliferation; CD80/CD86 costimulation; T cells; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1403", "Drug": "Entinostat (MS-275)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": "D09338", "Pubchem_ID": "4261", "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "23789844", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Diffuse Large B Cell Lymphoma (DLBCL)", "System": "NCI-H929", "Dose": "100 nm MS-275", "Technique": "RT-PCR, Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CIITA,MHCI", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; CIITA;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1404", "Drug": "Entinostat (MS-275)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": "D09338", "Pubchem_ID": "4261", "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "23789844", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Diffuse Large B Cell Lymphoma (DLBCL)", "System": "DB cells", "Dose": "250 nM", "Technique": "Flow cytometry and quantitative RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "HLA-DR, CIITA and HLA-DRα,HLA-ABC", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; MHC class II; HLA-DR; CIITA", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1407", "Drug": "Entinostat (MS-275)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": "D09338", "Pubchem_ID": "4261", "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "KMS-11", "Dose": "0.25 μM or 1 μM", "Technique": "Flow cytometry,RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "NKG2D ligands, MICA/B and ULBP2/5/6,IFN-γR1", "Controlled_Terms_Function_enhanced_Number_increased": "NKG2D / KLRK1; ULBP2; ULBP2/5/6 family; MICA; NKG2D ligand; MICA/MICB", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1408", "Drug": "Entinostat (MS-275)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": "D09338", "Pubchem_ID": "4261", "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "MM.1S cells", "Dose": "0.25 μM or 1 μM", "Technique": "Flow cytometry,RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "NKG2D ligands, MICA/B and ULBP2/5/6,IFN-γR1", "Controlled_Terms_Function_enhanced_Number_increased": "NKG2D / KLRK1; ULBP2; ULBP2/5/6 family; MICA; NKG2D ligand; MICA/MICB", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1409", "Drug": "Entinostat (MS-275)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": "D09338", "Pubchem_ID": "4261", "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "OPM-2", "Dose": "0.25 μM or 1 μM", "Technique": "Flow cytometry,RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "NKG2D ligands, MICA/B and ULBP2/5/6,IFN-γR1", "Controlled_Terms_Function_enhanced_Number_increased": "NKG2D / KLRK1; ULBP2; ULBP2/5/6 family; MICA; NKG2D ligand; MICA/MICB", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/51", "Drug": "Entinostat (MS-275)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": "D09338", "Pubchem_ID": "4261", "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "26964571", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "A549 cells", "Dose": "500nM", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "T cell attracting chemokine genes - Cxcl10", "Controlled_Terms_Function_enhanced_Number_increased": "CXCL10 / IP-10; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/75", "Drug": "Entinostat (MS-275)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": "D09338", "Pubchem_ID": "4261", "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "23789844", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Diffuse Large B Cell Lymphoma (DLBCL)", "System": "SUDHL-6 GCB", "Dose": "25-250 nM", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CIITA and HLA-DRα", "Controlled_Terms_Function_enhanced_Number_increased": "HLA-DR; CIITA", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/536", "Drug": "FK228 (Romidepsin)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "HDAC inhibitor; reported to directly inhibit HDAC1, HDAC2, HDAC4 and HDAC6. In this study, FK228 induces ER-stress-associated necroptosis in tumor cells, producing immunogenic cell death and remodeling the tumor immune microenvironment.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "5352062", "STR_LINK_(SMILES)": "C/C=C\\1/C(=O)N[C@H](C(=O)O[C@H]\\2CC(=O)N[C@@H](C(=O)N[C@H](CSSCC/C=C2)C(=O)N1)C(C)C)C(C)C", "Single/Combination": "Single", "PMID": "40940553", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": null, "System": "In vitro: MC38 tumor cells", "Dose": "IC50 concentration 43.37 nM", "Technique": "7-AAD staining/flow cytometry, CCK-8 cell viability assay, colony-formation assay, Western blotting, Luminex cytokine/chemokine analysis, ATP-release assay, calreticulin immunofluorescence/flow cytometry", "Controlled_Technique": "FK228 increased acetylation of histones, including H3K9, H3K27, H4K8 and H4K16, consistent with HDAC inhibition. FK228 predominantly induces necroptosis in MC38 cells. FK228 resulted in immunogenic cell death by increasing inflammatory chemokines, including CX3CL1 and CXCL10.", "Immune_System-Function_enhanced/numbers_increased": "Immunogenic cell death; CXCL10 / IP-10", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/537", "Drug": "FK228 (Romidepsin)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "HDAC inhibitor; reported to directly inhibit HDAC1, HDAC2, HDAC4 and HDAC6. In this study, FK228 induces ER-stress-associated necroptosis in tumor cells, producing immunogenic cell death and remodeling the tumor immune microenvironment.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "5352062", "STR_LINK_(SMILES)": "C/C=C\\1/C(=O)N[C@H](C(=O)O[C@H]\\2CC(=O)N[C@@H](C(=O)N[C@H](CSSCC/C=C2)C(=O)N1)C(C)C)C(C)C", "Single/Combination": "Single", "PMID": "40940553", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": null, "System": "In vitro: CT26 tumor cells", "Dose": "IC50 concentration CT26 58.61 nM", "Technique": "7-AAD staining/flow cytometry, CCK-8 cell viability assay, colony-formation assay, Western blotting, Luminex cytokine/chemokine analysis, ATP-release assay, calreticulin immunofluorescence/flow cytometry", "Controlled_Technique": "FK228 increased acetylation of histones, including H3K9, H3K27, H4K8 and H4K16, consistent with HDAC inhibition. FK228 predominantly induces necroptosis in MC38 cells. FK228 resulted in immunogenic cell death by increasing inflammatory chemokines, including CX3CL1 and CXCL10.", "Immune_System-Function_enhanced/numbers_increased": "Immunogenic cell death; CXCL10 / IP-10", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/538", "Drug": "FK228 (Romidepsin)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "HDAC inhibitor; reported to directly inhibit HDAC1, HDAC2, HDAC4 and HDAC6. In this study, FK228 induces ER-stress-associated necroptosis in tumor cells, producing immunogenic cell death and remodeling the tumor immune microenvironment.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "5352062", "STR_LINK_(SMILES)": "C/C=C\\1/C(=O)N[C@H](C(=O)O[C@H]\\2CC(=O)N[C@@H](C(=O)N[C@H](CSSCC/C=C2)C(=O)N1)C(C)C)C(C)C", "Single/Combination": "Single", "PMID": "40940553", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": null, "System": "In vitro: 4T1 tumor cells", "Dose": "IC50 concentration 4T1 13.49 nM", "Technique": "7-AAD staining/flow cytometry, CCK-8 cell viability assay, colony-formation assay, Western blotting, Luminex cytokine/chemokine analysis, ATP-release assay, calreticulin immunofluorescence/flow cytometry", "Controlled_Technique": "FK228 increased acetylation of histones, including H3K9, H3K27, H4K8 and H4K16, consistent with HDAC inhibition. FK228 predominantly induces necroptosis in MC38 cells. FK228 resulted in immunogenic cell death by increasing inflammatory chemokines, including CX3CL1 and CXCL10.", "Immune_System-Function_enhanced/numbers_increased": "Immunogenic cell death; CXCL10 / IP-10", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/707", "Drug": "FOLFOX (5-FU + leucovorin + oxaliplatin)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "5-FU inhibits nucleotide synthesis; leucovorin enhances 5-FU activity; oxaliplatin causes DNA crosslinks", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "40380807", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "gastric cancer cell line", "System": "AGS", "Dose": "leucovorin: 14 μM; 5-Fu: 200 μM; oxaliplatin: 6 μM) for 48 h", "Technique": "Flow cytometry; Western blot", "Controlled_Technique": "Increased cell-surface PD-L1 and MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; PD-L1 / CD274", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "Increased PD-L1 may promote inhibitory immune-checkpoint signaling", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 immune checkpoint pathway; Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/708", "Drug": "FOLFOX (5-FU + leucovorin + oxaliplatin)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "5-FU inhibits nucleotide synthesis; leucovorin enhances 5-FU activity; oxaliplatin causes DNA crosslinks", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "40380807", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "gastric cancer cell line", "System": "SNU-1", "Dose": "leucovorin: 14 μM; 5-Fu: 200 μM; oxaliplatin: 6 μM) for 48 h", "Technique": "Flow cytometry; Western blot", "Controlled_Technique": "Increased cell-surface PD-L1 and MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; PD-L1 / CD274", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "Increased PD-L1 may promote inhibitory immune-checkpoint signaling", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 immune checkpoint pathway; Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1108", "Drug": "LBH589 (panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "WM983A", "Dose": "(10nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, 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"Cancer_Type_Description": "Skin - Melanoma", "System": "WM793", "Dose": "(10nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1110", "Drug": "LBH589 (panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "B78H1", "Dose": "(10nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1111", "Drug": "LBH589 (panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "SkMel21", "Dose": "(10nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1113", "Drug": "LBH589 (panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "WM35", "Dose": "(10nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1114", "Drug": "LBH589 (panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "WM1366", "Dose": "(10nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1115", "Drug": "LBH589 (panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "B16F10", "Dose": "(10nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1116", "Drug": "LBH589 (panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single 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"CANIMM/1117", "Drug": "LBH589 (panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Mel-888", "Dose": "(10nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", 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"CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "primary human melanomas", "Dose": "10-40nM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1, PD-L2 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L2 / PDCD1LG2; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1228", "Drug": "LBH589 (panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "25957812", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "B16–F10", "Dose": "25-nM", "Technique": "Flow cytometry to evaluate Annexin V and DAPI.", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1229", "Drug": "LBH589 (panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "25957812", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "WM164", "Dose": "25-nM", "Technique": "Flow cytometry to evaluate Annexin V and DAPI.", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/325", "Drug": "LBH589 (Panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "26176219", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Wilms Tumor ( Embryonic Kidney Cancer)", "System": "SK-NEP-1", "Dose": "50nM and 100nM for 24 hours", "Technique": "Annexin V, cell cycle, tunnel and Hochest33342 assays,western blotting", "Controlled_Technique": "Western blot/immunoblot analysis; Cell viability/proliferation assay; Apoptosis/cell viability assay; Cell-cycle analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Bcl-2", "Controlled_Terms_Function_inhibited_Number_decreased": "BCL-2", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/326", "Drug": "LBH589 (Panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone 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"Colorectal cancer", "System": "MC38 cells", "Dose": "10 nM", "Technique": "Flow cytometry; intracellular cytokine staining; Ac-H3K27 analysis", "Controlled_Technique": "TNFα-producing T cells", "Immune_System-Function_enhanced/numbers_increased": "T cells; TNF-α / TNF", "Controlled_Terms_Function_enhanced_Number_increased": "IL-2, IFNγ, IL-4 and IL-17 production", "Immune_System-Function_inhibited/numbers_decreased": "IFN-γ; IL-2; IL-4", "Controlled_Terms_Function_inhibited_Number_decreased": "NR", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "NR", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/767", "Drug": "Panobinostat (LBH589)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "23963286", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "B16 murine melanoma cells (H-2b) + naöve OVA-specific CD4+ T-cells (OT-II) with the presence of cognate OVA-peptide", "Dose": "25nM, 50nM", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IL-2 and IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IL-2; IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, 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{"study_type": "cell_line", "ID": "CANIMM/1152", "Drug": "Panobinostat (LBH589)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "23963286", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "WM983A", "Dose": "25nM, 50nM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC class I, CD40 and CD86 apoptosis and a G1 cell cycle arrest", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; CD40; CD86; Apoptosis; Cell-cycle arrest;", 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"CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "23963286", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "B16", "Dose": "25nM, 50nM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC class I, MHC class II CD40, CD80 and CD860 (modest upregulation) apoptosis and a G1 cell cycle arrest", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; MHC class II; CD40; CD80; Apoptosis; Cell-cycle arrest; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1365", "Drug": "Panobinostat (LBH589)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "31720815", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "4T1", "Dose": "10 nM", "Technique": "RT-PCR, Flow cytometry, propidium iodide staining", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain 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null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1366", "Drug": "Panobinostat (LBH589)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "31720815", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "TS/A", "Dose": "10 nM", "Technique": "RT-PCR, Flow cytometry, propidium iodide staining", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CIITA and CD74, MHCII and CD74, PD-L1 expression , costimulatory molecules, 41BB, CD40, and ICOSL, the inhibitory ligand, PD-L1, and the T-cell chemoattractant, CXCL10 impairs tumor cell proliferation", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; MHC class II; CIITA; CD40; ICOS ligand / ICOSL / CD275; 4-1BB / CD137; CD74; CXCL10 / IP-10; Cell proliferation; CD80/CD86 costimulation; T cells; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/53", "Drug": "Panobinostat (LBH589)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "26964571", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "A549 cells", "Dose": "100nM", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "T cell attracting chemokine genes - Cxcl10", "Controlled_Terms_Function_enhanced_Number_increased": "CXCL10 / IP-10; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/94", "Drug": "Panobinostat (LBH589)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "23963286", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "WM793", "Dose": "12.5 nM-50nM", "Technique": "qRT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "gp100, mart1, tyrp1 and tyrp2- melanoma antigens", "Controlled_Terms_Function_enhanced_Number_increased": "Melanoma differentiation antigens", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/95", "Drug": "Panobinostat (LBH589)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "23963286", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "B16", "Dose": "12.5 nM-50nM", "Technique": "qRT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "gp100, mart1, tyrp1 and tyrp2- melanoma antigens", "Controlled_Terms_Function_enhanced_Number_increased": "Melanoma differentiation antigens", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/448", "Drug": "Panobinostat (PAN/LBH589)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "HDAC inhibitors", "KEGG_Drug__ID": "D10319", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(C2=CC=CC=C2N1)CCNCC3=CC=C(C=C3)/C=C/C(=O)NO", "Single/Combination": "Single", "PMID": "31720815", 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"Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1141", "Drug": "PDX101 (belinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB05015", "Target/s_or_mechanism_of_action": "histone deacetylase inhibitor", "KEGG_Drug__ID": "D08870", "Pubchem_ID": "6918638", "STR_LINK_(SMILES)": "ONC(=O)\\C=C\\C1=CC=CC(=C1)S(=O)(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "primary human melanomas", "Dose": "0.5-2 μM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1, PD-L2 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L2 / PDCD1LG2; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", 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"Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1389", "Drug": "Ricolinostat (ACY-1215)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB12376", "Target/s_or_mechanism_of_action": "Ricolinostat (ACY-1215) is an orally available selective HDAC6 inhibitor", "KEGG_Drug__ID": "D10661", "Pubchem_ID": "53340666", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "30728070", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin -Metastatic Melanoma Patients", "System": "T-cells isolated from melanoma patient PBMC samples(activated via αCD3/CD28)", "Dose": "500nM", "Technique": "Luminex", "Controlled_Technique": "Cytokine/multiplex immunoassay", 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"Pubchem_ID": "53340666", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "30728070", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin -Metastatic Melanoma Patients", "System": "T-cells isolated from melanoma patient PBMC samples(activated via αCD3/CD28)", "Dose": "500nM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8 + TBET+PD1+ T-cells, a less terminally differentiated phenotype, CD4+ T-cells ( CD45RA-CD45RO + CD62L + CCR7+ central memory markers),CD45RA-CD62L+ (central memory phenotype) in CD8+ IFNγ and TNF T-BET expression in T cells, T-BET expression in CD8+ and CD4+ T-cells", "Controlled_Terms_Function_enhanced_Number_increased": "PD-1 / PDCD1; CD4; CD8; TNF-α / TNF; IFN-γ; T cells; CD4+ T cells; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": "GATA3 levels in CD 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"Ricolinostat (ACY-1215)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB12376", "Target/s_or_mechanism_of_action": "Ricolinostat (ACY-1215) is an orally available selective HDAC6 inhibitor", "KEGG_Drug__ID": "D10661", "Pubchem_ID": "53340666", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "30728070", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin -Metastatic Melanoma Patients", "System": "isolated nTregs (CD4 + CD127-/lowCD25+) co-cultured with autologous CD8+ T-cells (Tcons) and activated via αCD3/CD28", "Dose": "500nM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Ki67 expression in CD8+ Tcons", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1149", "Drug": "Ricolinostat (ACY-1215)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB12376", "Target/s_or_mechanism_of_action": "Ricolinostat (ACY-1215) is an orally available selective HDAC6 inhibitor", "KEGG_Drug__ID": "D10661", "Pubchem_ID": "53340666", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "30728070", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin -Metastatic Melanoma 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"Drugbank_ID": "DB17021", "Target/s_or_mechanism_of_action": "BRD4 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": "46907787", "STR_LINK_(SMILES)": "CC1=C(SC2=C1C(=N[C@H](C3=NN=C(N32)C)CC(=O)OC(C)(C)C)C4=CC=C(C=C4)Cl)C", "Single/Combination": "Single", "PMID": "35517410", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": "LS174T", "Dose": "0.1 μM", "Technique": "Flow cytometry", "Controlled_Technique": "HLA-ABC, MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I", "Controlled_Terms_Function_enhanced_Number_increased": "surface PD-L1", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 / CD274", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1465", "Drug": "Ricolinostat (ACY-1215)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB12376", "Target/s_or_mechanism_of_action": "Ricolinostat (ACY-1215) is an orally available selective HDAC6 inhibitor", "KEGG_Drug__ID": "D10661", "Pubchem_ID": "53340666", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "30788349", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": "HCT-116", "Dose": "1-10 µM", "Technique": "Flow cytometry, Immunoblot analysis", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "apoptosis, antiproliferation activity", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis; Cell proliferation", "Immune_System-Function_inhibited/numbers_decreased": "MARK/ERK pathway", "Controlled_Terms_Function_inhibited_Number_decreased": "ERK / MAPK", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/420", "Drug": "Ricolinostat (ACY-1215)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB12376", "Target/s_or_mechanism_of_action": "Ricolinostat (ACY-1215) is an orally available selective HDAC6 inhibitor", "KEGG_Drug__ID": "D10661", "Pubchem_ID": "53340666", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "30728070", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin -Metastatic Melanoma Patients", "System": "CD4+ naïve-derived iTregs from seven patient samples", "Dose": "500nM", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "inducible Tregs (iTregs)", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, 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Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "57515973", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Single Drug", "PMID": "28167529", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": "SKOV3", "Dose": "10 nm", "Technique": "real-time RT-PCR analysis", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "proangiogenic chemokine IL-8 (CXCL-8)", "Controlled_Terms_Negative_Regulation": "IL-8 / CXCL8; IL-8/CXCL8", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/110", "Drug": "Romidepsin", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "57515973", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Single Drug", "PMID": "26964571", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "A549", "Dose": "(30nM)", "Technique": "RT-PCR,ELISA", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "T cell attracting chemokine genes (Ccl5, Cxcl9 and Cxcl10)", "Controlled_Terms_Function_enhanced_Number_increased": "CCL5 / RANTES; CXCL10 / IP-10; CXCL9 / MIG; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/111", "Drug": "Romidepsin", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "57515973", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Single Drug", "PMID": "26964571", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "KRAS mutant LKR-13 (LKR)", "Dose": "(5nM–30nm)", "Technique": "RT-PCR, ELISA", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "T cell attracting chemokine genes (Ccl5, Cxcl9 and Cxcl10), CCL5 and CXCL10 secretion in LKR cells", "Controlled_Terms_Function_enhanced_Number_increased": "CCL5 / RANTES; CXCL10 / IP-10; CXCL9 / MIG; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/57", "Drug": "SAHA (Vorinostat)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "22419072", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "NCI-H292", "Dose": "SAHA (5 μM)", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD1d", "Controlled_Terms_Function_enhanced_Number_increased": "CD1d", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/59", "Drug": "SAHA (Vorinostat)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "22419072", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "TC-1", "Dose": "SAHA (5 μM)", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD1d", "Controlled_Terms_Function_enhanced_Number_increased": "CD1d", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/60", "Drug": "SAHA (Vorinostat)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "29872551", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "A549", "Dose": "5 μM", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD1d", "Controlled_Terms_Function_enhanced_Number_increased": "CD1d", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/61", "Drug": "SAHA (Vorinostat)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "29872551", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "SK-MES-1", "Dose": "5 μM", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD1d", "Controlled_Terms_Function_enhanced_Number_increased": "CD1d", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/62", "Drug": "SAHA (Vorinostat)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "22419072", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "A549 cells", "Dose": "SAHA (5 μM)", "Technique": "RT-PCR andwestern blot", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD1d", "Controlled_Terms_Function_enhanced_Number_increased": "CD1d", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/96", "Drug": "SAHA (Vorinostat)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "22419072", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "B16/F0 cells", "Dose": "SAHA (5 μM)", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD1d", "Controlled_Terms_Function_enhanced_Number_increased": "CD1d", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/856", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "25313353", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "HL60", "Dose": "0-100 nM", "Technique": "CCK-8 assay", "Controlled_Technique": "Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "antiproliferation activity", "Controlled_Terms_Function_enhanced_Number_increased": "Cell proliferation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/324", "Drug": "SAHA/Vorinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "26862729", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": "LNCaP +CD8+ T cells", "Dose": "3 μM", "Technique": "111In-release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells-mediated cytotoxicity", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Cytotoxicity / cytolysis; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1233", "Drug": "SAHA/Vorinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "26862729", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "MDA-MB-231+CD8+ T cells", "Dose": "3 μM", "Technique": "111In-release assay,Flow cytometry", "Controlled_Technique": "Flow cytometry; Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells-mediated cytotoxicity, Antigen Processing Machinery-immune proteosome subunits LMP2 and LMP7, the peptide transporter TAP1, the chaperone calnexin, and the HLA class I heavy chain-associated β2-microglobulin. HLA class I antigens and ICAM-1,TAAs CEA and MUC1", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; β2-microglobulin / B2M; CD8; ICAM-1 / CD54; Cytotoxicity / cytolysis; Antigen presentation; TAP1; LMP2 / PSMB9; LMP7 / PSMB8; Calnexin; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1486", "Drug": "SAHA/Vorinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "19759901", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "CLL cells", "Dose": "0.5 μM lenalidomide for 48 hours + IL21 (100 ng/ml)", "Technique": "immunoblot, AnnexinV-FITC/PI Flow cytometry", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "IL21-mediated cytotoxicity in CLL B cells STAT1 and STAT3 phosphorylation", "Controlled_Terms_Function_enhanced_Number_increased": "IL-21; IL-6/JAK/STAT3 signaling; STAT1; STAT3; Cytotoxicity / cytolysis; B cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1104", "Drug": "Sodium butyrate", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": "5222465", "STR_LINK_(SMILES)": "CCCC(=O)[O-].[Na+]", "Single/Combination": "Single Drug", "PMID": "29308322", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Ma-Mel-86f", "Dose": "5mM sodium butyrate", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NKG2D-L (MHC-1, MICA, UBLP2/5/6, CD112)", "Controlled_Terms_Function_enhanced_Number_increased": "CD112 / Nectin-2 / PVRL2; NKG2D / KLRK1; MICA; ; MICA/MICB", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD155", "Controlled_Terms_Unaffected": "CD155 / PVR", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1105", "Drug": "Sodium butyrate", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": "5222465", "STR_LINK_(SMILES)": "CCCC(=O)[O-].[Na+]", "Single/Combination": "Single Drug", "PMID": "29308322", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Ma-Mel-55", "Dose": "5mM sodium butyrate", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NKG2D-L (MHC-1, MICA, UBLP3, UBLP2/5/6, CD112)", "Controlled_Terms_Function_enhanced_Number_increased": "CD112 / Nectin-2 / PVRL2; NKG2D / KLRK1; ULBP3; MICA; ; MICA/MICB", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD155", "Controlled_Terms_Unaffected": "CD155 / PVR", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1106", "Drug": "Sodium butyrate", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": "5222465", "STR_LINK_(SMILES)": "CCCC(=O)[O-].[Na+]", "Single/Combination": "Single Drug", "PMID": "29308322", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Ma-Mel-86c", "Dose": "5mM sodium butyrate", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NKG2D-L (MHC-1, MICA, UBLP3, UBLP2/5/6, CD112)", "Controlled_Terms_Function_enhanced_Number_increased": "CD112 / Nectin-2 / PVRL2; NKG2D / KLRK1; ULBP3; MICA; ; MICA/MICB", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD155", "Controlled_Terms_Unaffected": 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"Controlled_Terms_Function_enhanced_Number_increased": "CD112 / Nectin-2 / PVRL2; NKG2D / KLRK1; ULBP3; MICA; ; MICA/MICB", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD155", "Controlled_Terms_Unaffected": "CD155 / PVR", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/987", "Drug": "Sodium butyrate", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": "5222465", "STR_LINK_(SMILES)": "CCCC(=O)[O-].[Na+]", "Single/Combination": "Single Drug", "PMID": "23789844", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Diffuse Large B Cell Lymphoma (DLBCL)", "System": "NCI-H929", "Dose": "2 mm sodium butyrate", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "(HLA-ABC)", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/994", "Drug": "Sodium butyrate", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": "5222465", "STR_LINK_(SMILES)": "CCCC(=O)[O-].[Na+]", "Single/Combination": "Single Drug", "PMID": "23789844", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Diffuse Large B Cell Lymphoma (DLBCL)", "System": "DB cells", "Dose": "2 mM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "HLA-DR expression,HLA-ABC", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; MHC class II; HLA-DR; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1637", "Drug": "Sodium butyrate (NaBu)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": "5222465", "STR_LINK_(SMILES)": "CCCC(=O)[O-].[Na+]", "Single/Combination": "Single Drug", "PMID": "11120829", "Cancer_Type": "Brain Cancer", "Cancer_Type_Description": "Neuroblastoma", "System": "SK-N-MC (MC)", "Dose": "1 mM NaBu", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "HLA-DR (DR), MHC class II", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class II; HLA-DR;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/359", "Drug": "Suberoylanilide hydroxamic acid (SAHA)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "30745455", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Breast Carcinoma", "System": "MDA-MB-231(mutp53 carrying cell line)", "Dose": "0-10 µM, 0-20 µM for autophagy studies", "Technique": "Western blot, immunofluorescence assays", "Controlled_Technique": "Western blot/immunoblot analysis; Immunofluorescence assay; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "p53 degradation", "Controlled_Terms_Function_enhanced_Number_increased": "p53 / TP53", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "impaired autophagy", "Controlled_Terms_Negative_Regulation": "Autophagy / macroautophagy", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/360", "Drug": "Suberoylanilide hydroxamic acid (SAHA)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "30745455", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "DLD1 cells (mutp53 carrying cell line)", "Dose": "0-2.5 µM", "Technique": "Western blot, immunofluorescence assays", "Controlled_Technique": "Western blot/immunoblot analysis; Immunofluorescence assay; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "p53 degradation", "Controlled_Terms_Function_enhanced_Number_increased": "p53 / TP53", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1622", "Drug": "Trichostatin A (TSA)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": "444732", "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Single Drug", "PMID": "17725605", "Cancer_Type": "Hpv16-Expressing Tumors", "Cancer_Type_Description": "Human Papilloma Virus 16-Associated Tumours", "System": "TC-1/A9 cells + spleen cells from animals immunized with TC-1 cells", "Dose": "10 ng/ml TSA", "Technique": "chromium-release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "cytotoxic T lymphocyte (CTL)-mediated lysis", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1633", "Drug": "Trichostatin A (TSA)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": "444732", "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Single Drug", "PMID": "19759901", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "lenalidomide-treated NK cells from a healthy donor + target CLL patient cells", "Dose": "10 μg/mL rituximab", "Technique": "standard 4-hour 51Cr-release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell cytotoxicity, ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/3", "Drug": "Trichostatin A (TSA)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": "444732", "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Single Drug", "PMID": "19759901", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "lenalidomide-treated NK cells from patientsr + target CLL patient cells", "Dose": "10 μg/mL rituximab", "Technique": "standard 4-hour 51Cr-release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell cytotoxicity, ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/732", "Drug": "Trichostatin A (TSA)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": "444732", "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Single Drug", "PMID": "19759901", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "PBMCs from healthy donors cocultured with purified leukemia cells obtained from CLL patients for 4 hours", "Dose": "1 μM lenalidomide + rituximab (20 μg/mL)", "Technique": "CD107a lysosome-associated membrane protein-1 (LAMP-1) was used to measure NK-, NKT-like-, and CD8-cell cytotoxic activity", "Controlled_Technique": "Degranulation assay", "Immune_System-Function_enhanced/numbers_increased": "NK Cell-Mediated Natural Cytotoxicity and ADCC CD20 expression on leukemia cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD20 / MS4A1; Cytotoxicity / cytolysis; ADCC; NK cells; Antibody-dependent cytotoxicity; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/739", "Drug": "Trichostatin A (TSA)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": "444732", "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Single Drug", "PMID": "18046553", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "CD8+ T cells, isolated from ova-primed OT-I mice + B16F10 cells(Splenocytes and B16F10 cells (TSA- or the treated and untreated) were pulsed with ova, ova–peptide257–266 control peptide mgp100 and irradiated before use in the assay)", "Dose": "(500 nM for 48 h)", "Technique": "ELISPOT assay", "Controlled_Technique": "ELISpot/FluoroSpot assay", "Immune_System-Function_enhanced/numbers_increased": "IFN-γ producing CD8+ T cells IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; IFN-γ; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/758", "Drug": "Trichostatin A (TSA)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": "444732", "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Single Drug", "PMID": "27614429", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Mantle Cell Lymphoma (MCL)", "System": "JeKo-1 + pulsed with α-GalCer (100 ng/mL) and co-cultured with primary human NKT cells derived from healthy donor blood", "Dose": "1 μM TSA for 4 hours", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "CD1D-mediated antigen presentation by MCL cells , CD1D-mediated NKT cell activation IFNγ", "Controlled_Terms_Function_enhanced_Number_increased": "CD1d; IFN-γ; Antigen presentation; NKT cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/759", "Drug": "Trichostatin A (TSA)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": "444732", "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Single Drug", "PMID": "27614429", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Mantle Cell Lymphoma (MCL)", "System": "SP53 +pulsed with α-GalCer (100 ng/mL) and co-cultured with primary human NKT cells derived from healthy donor blood", "Dose": "1 μM TSA for 4 hours", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent 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Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "cancer-testis antigens (CTAs)-MAGE-A1, MAGE-A3, and SP17", "Controlled_Terms_Function_enhanced_Number_increased": "Cancer-testis antigens; MAGE antigens", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/205", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "19965642", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "primary CLL cells", "Dose": "depsipeptide -10 nmol/L,TRAIL (100 ng/mL)", "Technique": "Western blotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "TRAIL-induced apoptosis-phosphatidylserine externalization, processing of caspase-3 to its catalytically active large subunits (p19/p17) and cleavage of PARP", "Controlled_Terms_Function_enhanced_Number_increased": "TRAIL; 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Caspase-3; Caspase activation; Apoptosis; PARP cleavage / PARP", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/406", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "22031859", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "primary MM cells+ Healthy NK cells", "Dose": "5μM", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "IFN-y", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/407", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "22031859", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "patient-derived NK cells+ autologous MM tumor cells", "Dose": "5μM", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "IFN-y", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/584", "Drug": "Lenalidomide (LEN)", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "Suppresses TNF-α production and modulates NF-κB-associated signaling", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "C1CC(=O)NC(=O)C1N2CC3=C(C2=O)C=CC=C3N", "Single/Combination": "Single", "PMID": "40528981", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "mouse HCC cell line", "System": "Hepa1–6", "Dose": "40 µmol/L in vitro", "Technique": "Western blot, RT-qPCR, ELISA, cGAS–STING signaling", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": "expression of TNF-α mRNA and protein", "Immune_System-Function_inhibited/numbers_decreased": "Expression / abundance phenotype; TNF-α / TNF", "Controlled_Terms_Function_inhibited_Number_decreased": "no significant impact on the expression of IFN-β mRNA and protein", "Immune_System_function_unaffected": "Expression / abundance phenotype; IFN-β", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/585", "Drug": "Lenalidomide (LEN)", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "Suppresses TNF-α production and modulates NF-κB-associated signaling+Suppresses TNF-α production and modulates NF-κB-associated signaling", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "C1CC(=O)NC(=O)C1N2CC3=C(C2=O)C=CC=C3N", "Single/Combination": "Single", "PMID": "40528981", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Human HCC cell line", "System": "HepG2", "Dose": "40 µmol/L in vitro", "Technique": "Western blot, RT-qPCR, ELISA, cGAS–STING signaling", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": "expression of TNF-α mRNA and protein", "Immune_System-Function_inhibited/numbers_decreased": "Expression / abundance phenotype; TNF-α / TNF", "Controlled_Terms_Function_inhibited_Number_decreased": "no significant impact on the expression of IFN-β mRNA and protein", "Immune_System_function_unaffected": "Expression / abundance phenotype; IFN-β", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1025", "Drug": "Lenalidomide (Lena)", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "26269456", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "CD138+ MM cells from the bone marrow of MM patients", "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MICA and/or PVR/CD155 on primary cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD155 / PVR; MICA;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/541", "Drug": "Cobimetinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB05239", "Target/s_or_mechanism_of_action": "Inhibits MEK1/2 → suppresses MAPK/ERK signaling", "KEGG_Drug__ID": "D10405", "Pubchem_ID": "16222096", "STR_LINK_(SMILES)": "CN1CCN(CC1)C(=O)C2=C(C=C(C=C2F)F)NC3=C(C=C(C=C3)F)I", "Single/Combination": "Single", "PMID": "34389557", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "CT26 murine colorectal carcinoma cells", "System": "MEK1 KO D12 CT26 cells", "Dose": "1 µM", "Technique": "Flow cytometry", "Controlled_Technique": "MHC-I, MHC-II", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; MHC class II", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1290", "Drug": "Lenalidomide (Lena)", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "26269456", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "NK cells, prepared from PBMCs of healthy donors, were incubated with SKO-007(J3) cells", "Dose": "(10 μM) for 72h", "Technique": "Flow cytometry, degranulation assay, blocking antibodies", "Controlled_Technique": "Flow cytometry; Immune suppression/blocking/depletion assay; Degranulation assay", "Immune_System-Function_enhanced/numbers_increased": "cytotoxic function of natural killer (NK) cells", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1291", "Drug": "Lenalidomide (Lena)", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "26269456", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "patient-derived NK cells against lenalidomide-treated autologous MM targets", "Dose": "(10 μM) for 72h", "Technique": "Flow cytometry, degranulation assay, blocking antibodies", "Controlled_Technique": "Flow cytometry; Immune suppression/blocking/depletion assay; Degranulation assay", "Immune_System-Function_enhanced/numbers_increased": "cytotoxic function of natural killer (NK) cells", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1294", "Drug": "Lenalidomide (Lena)", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "26269456", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "OPM-2", "Dose": "(10 μM) for 72h", "Technique": "immunofluorescence and Flow cytometry", "Controlled_Technique": "Flow cytometry; Immunofluorescence assay; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "PVR/CD155 on SKO-007(J3) cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD155 / PVR", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1295", "Drug": "Lenalidomide (Lena)", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "26269456", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "KMS27", "Dose": "(10 μM) for 72h", "Technique": "immunofluorescence and Flow cytometry", "Controlled_Technique": "Flow cytometry; Immunofluorescence assay; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "PVR/CD155 on SKO-007(J3) cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD155 / PVR", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1298", "Drug": "Lenalidomide (Lena)", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "26269456", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "ARP-1", "Dose": "(10 μM) for 72h", "Technique": "immunofluorescence and Flow cytometry", "Controlled_Technique": "Flow cytometry; 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Immunofluorescence assay; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "MICA on SKO-007(J3) cells", "Controlled_Terms_Function_enhanced_Number_increased": "MICA", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1413", "Drug": "Lenalidomide (Lena)", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "26269456", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "SKO-007(J3)", "Dose": "(10 μM) for 72h, 48 hr for Real-Time qPCR", "Technique": "Flow cytometry, Real-Time qRT-PCR", "Controlled_Technique": "Flow cytometry; 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It is shown to inhibit the proliferation and induce apoptosis of various tumour cells.", "KEGG_Drug__ID": "D08976", "Pubchem_ID": "134780", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1C(=O)N(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "26269456", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "SKO-007(J3)", "Dose": "(10 μM) for 72h, 48 hr for Real-Time qPCR", "Technique": "Flow cytometry, Real-Time qRT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "MICA and PVR/CD155 on SKO-007(J3) cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD155 / PVR; MICA;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/664", "Drug": "Pomalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB08910", "Target/s_or_mechanism_of_action": "Suppresses IFN-γ-induced PD-L1 and IFN-γ signaling-related transcription", "KEGG_Drug__ID": "D08976", "Pubchem_ID": "134780", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1C(=O)N(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single", "PMID": "30315115", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "SK-MEL-624 — human melanoma", "System": "SK-MEL-624 — human melanoma", "Dose": "IFN-γ stimulation with pomalidomide", "Technique": "Flow cytometry, RT-PCR/qPCR, RNA sequencing", "Controlled_Technique": "Potentially improved CTL activity through reduced tumor-cell PD-L1", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 / CD274", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 mRNA and surface expression; 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These 2 transcription factors are vital for the proliferation and survival of malignant myeloma cells", "KEGG_Drug__ID": "D00754", "Pubchem_ID": "5426", "STR_LINK_(SMILES)": "O=C1N(C2CCC(=O)NC2=O)C(=O)C2=CC=CC=C12", "Single/Combination": "Single Drug", "PMID": "11418482", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "Labeled K562 (NK sensitive/LAK sensitive) + Normal PBMCs were treated with IL-2 for 72 hour", "Dose": "5µg/ml", "Technique": "standard 51Cr release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK-cell", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/225", "Drug": "Thalidomide / Immunomodulatory Derivatives", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB01041", "Target/s_or_mechanism_of_action": "Previous research indicate that thalidomide binds to cerebron, a component of the E3 ubiquitin ligase complex, to selectively degrade the transcription factor IKZF3 and IKZF1. These 2 transcription factors are vital for the proliferation and survival of malignant myeloma cells", "KEGG_Drug__ID": "D00754", "Pubchem_ID": "5426", "STR_LINK_(SMILES)": "O=C1N(C2CCC(=O)NC2=O)C(=O)C2=CC=CC=C12", "Single/Combination": "Single Drug", "PMID": "11418482", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "MM.1S + Normal PBMCs treated with IL-2 for 72 hours and then by IMiD1 5 mg/mLdaily for 3 days. CD41, CD81, CD561, or CD141 cellswere depleted (more than 97% depletion by Flow cytometry analysis) using immunomagnetic beads", "Dose": "1-5µg/ml", "Technique": "standard 51Cr release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK-cell", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/782", "Drug": "Thalidomide / Immunomodulatory Derivatives", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB01041", "Target/s_or_mechanism_of_action": "Previous research indicate that thalidomide binds to cerebron, a component of the E3 ubiquitin ligase complex, to selectively degrade the transcription factor IKZF3 and IKZF1. These 2 transcription factors are vital for the proliferation and survival of malignant myeloma cells", "KEGG_Drug__ID": "D00754", "Pubchem_ID": "5426", "STR_LINK_(SMILES)": "O=C1N(C2CCC(=O)NC2=O)C(=O)C2=CC=CC=C12", "Single/Combination": "Single Drug", "PMID": "11418482", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "CD3 cells from 4 healthy donors and 4 patients with MM stimulated with anti-CD3 and treated with Thal/IMiDs daily for 5 days", "Dose": "1-5µg/ml", "Technique": "ELISA, . Proliferation was determined by measuring the uptake of tritiated thymidine (3[H]TdR", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Cell viability/proliferation assay; Cell proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "CD3 cells, CD 4, CD 8 IL-2 and IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "CD3; CD4; CD8; IL-2; IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/482", "Drug": "TPH104", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Induces immunogenic cell death and release of damage-associated molecular patterns", "KEGG_Drug__ID": null, "Pubchem_ID": "18326651", "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "33919653", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "MDA-MB-231 human TNBC cell line", "System": "MDA-MB-231", "Dose": "IC50: 140 nM at 72 h; 1–5 µM in selected assays", "Technique": "qPCR, ATP assay, immunofluorescence", "Controlled_Technique": "Extracellular ATP release increased; cell-surface calreticulin increased; TNF-α expression increased", "Immune_System-Function_enhanced/numbers_increased": "Calreticulin / CRT; TNF-α / TNF; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1311", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "23531921", "Cancer_Type": "Brain Cancer", "Cancer_Type_Description": "Neuroblastoma", "System": "KCNR", "Dose": "(0, 0.5, 1.0 and 2.5 μM) for 24 hours", "Technique": "Caspase-Glo3/7 Assay", "Controlled_Technique": "Apoptosis/cell viability assay; Caspase-Glo3/7 Assay", "Immune_System-Function_enhanced/numbers_increased": "caspase3/7-dependent apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase activation; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1422", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "23531921", "Cancer_Type": "Brain Cancer", "Cancer_Type_Description": "Neuroblastoma", "System": "SY5Y", "Dose": "(0, 0.5, 1.0 and 2.5 μM) for 24 hours", "Technique": "Caspase-Glo3/7 Assay", "Controlled_Technique": "Apoptosis/cell viability assay; Caspase-Glo3/7 Assay", "Immune_System-Function_enhanced/numbers_increased": "caspase3/7-dependent apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase activation; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1533", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "23531921", "Cancer_Type": "Rhabdomyosarcoma", "Cancer_Type_Description": "Rhabdomyosarcoma", "System": "Rh18", "Dose": "(0, 0.5, 1.0 and 2.5 μM) for 24 hours", "Technique": "Caspase-Glo3/7 Assay", "Controlled_Technique": "Apoptosis/cell viability assay; Caspase-Glo3/7 Assay", "Immune_System-Function_enhanced/numbers_increased": "caspase3/7-dependent apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase activation; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/2", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "23531921", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Ewing Sarcoma", "System": "TC32", "Dose": "(0, 0.5, 1.0 and 2.5 μM) for 24 hours", "Technique": "Caspase-Glo3/7 Assay", "Controlled_Technique": "Apoptosis/cell viability assay; Caspase-Glo3/7 Assay", "Immune_System-Function_enhanced/numbers_increased": "caspase3/7-dependent apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase activation; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1221", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "21164517", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Myeloma", "System": "U266", "Dose": "0.5 - 2 μM", "Technique": "Flow cytometry using Annexin V/Propidium Iodide staining", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1222", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "21164517", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Myeloma", "System": "Kms.11", "Dose": "0.5 - 2 μM", "Technique": "Flow cytometry using Annexin V/Propidium Iodide staining", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1466", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "25216185", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "HCT116", "Dose": "(0, 0.5, 1, 2, 5 and 10 µM)", "Technique": "Western blot,Flow cytometry", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "STAT3 and JAK2 phosphorylation, presence of cleaved PARP", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6/JAK/STAT3 signaling; STAT3; JAK2; PARP cleavage / PARP", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1468", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "25216185", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "HT29", "Dose": "(0, 0.5, 1, 2, 5 and 10 µM)", "Technique": "Western blot,Flow cytometry", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "STAT3 and JAK2 phosphorylation, presence of cleaved PARP", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6/JAK/STAT3 signaling; STAT3; JAK2; PARP cleavage / PARP", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1469", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "25216185", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "SW480", "Dose": "(0, 0.5, 1, 2, 5 and 10 µM)", "Technique": "Western blot,Flow cytometry", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "STAT3 and JAK2 phosphorylation, presence of cleaved PARP", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6/JAK/STAT3 signaling; STAT3; JAK2; PARP cleavage / PARP", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1524", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "25149535", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "MO4 cell line, which lacks constitutive expression of P-STAT3, was treated with IL-6,", "Dose": "(0.5 μM, 1 μM, 5 μM and 10 μM) and 48 hours", "Technique": "Flow cytometry using Annexin-V/7-AAD staining, western blotting", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "inhibits P-STAT3 expression but does not induce apoptosis", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6/JAK/STAT3 signaling; STAT3; Apoptosis; Expression / abundance phenotype; STAT3 phosphorylation", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1525", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "25149535", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "K1735-C4 cell line, characerized by constitutive expression of P-STAT3", "Dose": "(0.5 μM, 1 μM, 5 μM and 10 μM) and 48 hours", "Technique": "Flow cytometry using Annexin-V/7-AAD staining, western blotting", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "inhibits P-STAT3 expression but does not induce apoptosis", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6/JAK/STAT3 signaling; STAT3; Apoptosis; Expression / abundance phenotype; STAT3 phosphorylation", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1526", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. 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These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "26660519", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Carcinoma Cells", "System": "OVCAR-8", "Dose": "AZD1480 (0.05, 0.1, 1, 5, 10 μmol/L) for 24 h", "Technique": "Immunoblot analysis with antibodies recognizing pSTAT3Y705 and total STAT3, Annexin V staining and western blotting", "Controlled_Technique": "Western blot/immunoblot analysis; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "STAT3 activation, measured by evaluating pSTAT3Y705, apoptosis,cleaved PARP", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6/JAK/STAT3 signaling; STAT3; Apoptosis; PARP cleavage / PARP", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/421", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "25149535", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "co-culture of splenocytes derived from healthy animals with grMDSC or moMDSC sorted from spleens of AZD1480 treated MO4 tumor-bearing mice", "Dose": "MO4 tumor-bearing mice were treated with AZD1480 at 30 mg/kg", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "IFN-γ secretion", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "suppressive function of both grMDSCs and moMDSCs on the proliferation of T cells.", "Controlled_Terms_Negative_Regulation": "Cell proliferation; T cells; Myeloid-derived suppressor cells / MDSCs; T-cell suppressive function", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/769", "Drug": "AZD6244 (MEKi)/Selumetinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": "D09666", "Pubchem_ID": "10127622", "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Single Drug", "PMID": "25256614", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "A375 melanoma cells + M1 or M2 macrophages", "Dose": "2μM AZD6244 (MEKi)", "Technique": "Survival assay, ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "protected melanoma cells from MEKi exposure, MITF (microphthalmia transcription factor)", "Controlled_Terms_Function_enhanced_Number_increased": "Melanoma differentiation antigens", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "TNFα expression and secretion by the macrophages", "Controlled_Terms_Unaffected": "TNF-α / TNF; Macrophages; Expression / abundance phenotype", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/864", "Drug": "MEK inhibitor selumetinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": "D09666", "Pubchem_ID": "10127622", "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Single Drug", "PMID": "28807001", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "CT26 KRASG12D mutant mouse colorectal cancer cells", "Dose": "48 h treatment with selumetinib - (1-10 μM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "H2-Kd class-I MHC proteins", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I;", "Immune_System-Function_inhibited/numbers_decreased": "expression of PD-L1", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1437", "Drug": "MEK inhibitor trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "30546955", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "SCCVII mouse cells", "Dose": "trametinib (30 nM)", "Technique": "Flow cytometry,qRT-PCR, Western blotting", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "CXCL9 and CXCL10 MHC-encoded class I molecule H-2Kk", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; CXCL10 / IP-10; CXCL9 / MIG;", "Immune_System-Function_inhibited/numbers_decreased": "Erk1/2 activation", "Controlled_Terms_Function_inhibited_Number_decreased": "ERK / MAPK", "Immune_System_function_unaffected": "PD-L1", "Controlled_Terms_Unaffected": "PD-L1 / CD274; PD-L1 immune checkpoint pathway", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/219", "Drug": "Selumetinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": "D09666", "Pubchem_ID": "10127622", "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Single Drug", "PMID": "30995478", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": "CL25", "Dose": "selumetinib (0-1uM)", "Technique": "Western Blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "pERK in CD8+ T cells and CD4+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD8; ERK / MAPK; T cells; CD8+ T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1455", "Drug": "MEK inhibitor trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "30546955", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "SNU-1041", "Dose": "50 nM", "Technique": "Flow cytometry, Western blotting,siRNA transfections,qRT-PCR, ELISA", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "T cell chemoattractants CXCL9 and CXCL10 IFN-γ-induced MHC class I, p-STAT1 expression, and this effect was enhanced in the presence of exogenous IFN-γ, STAT3", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; IFN-γ; CXCL10 / IP-10; CXCL9 / MIG; IL-6/JAK/STAT3 signaling; STAT1; STAT3; T cells; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "IFN-γ-induced PD-L1", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; IFN-γ; PD-L1 immune checkpoint pathway", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1457", "Drug": "MEK inhibitor trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "30546955", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "SNU-1066", "Dose": "50 nM", "Technique": "Flow cytometry, Western blotting,qRT-PCR, ELISA", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "T cell chemoattractants CXCL9 and CXCL11 IFN-γ-induced MHC class I p-STAT1 expression, and this effect was enhanced in the presence of exogenous IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; IFN-γ; CXCL9 / MIG; STAT1; T cells; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": "IFN-γ-induced PD-L1", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; IFN-γ; PD-L1 immune checkpoint pathway", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1458", "Drug": "MEK inhibitor trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "30546955", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "SNU-1076 cells", "Dose": "50 nM", "Technique": "Flow cytometry, Western blotting,qRT-PCR, ELISA", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "T cell chemoattractants CXCL9 and CXCL12 IFN-γ-induced MHC class I, p-STAT1 expression, and this effect was enhanced in the presence of exogenous IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; IFN-γ; CXCL9 / MIG; STAT1; T cells; Expression / abundance phenotype; ; CXCL12 / SDF-1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "IFN-γ-induced PD-L1", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; IFN-γ; PD-L1 immune checkpoint pathway", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1459", "Drug": "MEK inhibitor trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "30546955", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "HN31 cells", "Dose": "Cells were treated with trametinib (50 nM), IFN-γ (1 ng/ml) or the combination of trametinib and IFN-γ (pretreated with DMSO or trametinib one hour prior to the addition of IFN-γ) for 72 hours", "Technique": "Flow cytometry, Western blotting,qRT-PCR, ELISA", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "T cell chemoattractants CXCL9 and CXCL13 p-STAT1 expression, and this effect was enhanced in the presence of exogenous IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CXCL9 / MIG; CXCL13; STAT1; T cells; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1460", "Drug": "MEK inhibitor trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "30546955", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "Detroit 562", "Dose": "Cells were treated with trametinib (50 nM), IFN-γ (1 ng/ml) or the combination of trametinib and IFN-γ (pretreated with DMSO or trametinib one hour prior to the addition of IFN-γ) for 72 hours", "Technique": "Flow cytometry, Western blotting,qRT-PCR, ELISA", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "T cell chemoattractants CXCL9 and CXCL14 p-STAT1 expression, and this effect was enhanced in the presence of exogenous IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CXCL9 / MIG; STAT1; T cells; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1461", "Drug": "MEK inhibitor trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "30546955", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "FaDu", "Dose": "Cells were treated with trametinib (50 nM), IFN-γ (1 ng/ml) or the combination of trametinib and IFN-γ (pretreated with DMSO or trametinib one hour prior to the addition of IFN-γ) for 72 hours", "Technique": "Flow cytometry, Western blotting,qRT-PCR, ELISA", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "T cell chemoattractants CXCL9 and CXCL15 p-STAT1 expression, and this effect was enhanced in the presence of exogenous IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CXCL9 / MIG; STAT1; T cells; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/950", "Drug": "Selumetinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": "D09666", "Pubchem_ID": "10127622", "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Single Drug", "PMID": "30995478", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": "Splenocytes from HKP1 lung tumor-bearing mice", "Dose": "Pulsative traetment , selumetinib (0-1uM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "Maintained Ki-67, 4–1BB, CTLA-4, and PD-1 better in CD8+ T cells and CD4+Foxp3– effector T cells", "Controlled_Terms_Unaffected": "PD-1 / PDCD1; CTLA-4; 4-1BB / CD137; CD4; CD8; T cells; CD8+ T cells; Regulatory T cells / Tregs", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/218", "Drug": "Selumetinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": "D09666", "Pubchem_ID": "10127622", "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Single Drug", "PMID": "30995478", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": "CL13", "Dose": "selumetinib (0-1uM)", "Technique": "Western Blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "pERK in CD8+ T cells and CD4+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD8; ERK / MAPK; T cells; CD8+ T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/484", "Drug": "Cobimetinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB05239", "Target/s_or_mechanism_of_action": "MEK1/MEK2 inhibition", "KEGG_Drug__ID": "D10405", "Pubchem_ID": "16222096", "STR_LINK_(SMILES)": "C1CCN[C@@H](C1)C2(CN(C2)C(=O)C3=C(C(=C(C=C3)F)F)NC4=C(C=C(C=C4)I)F)O", "Single/Combination": "Single", "PMID": "42183887", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "MDA-MB-231, human TNBC", "System": "In vitro human TNBC cells", "Dose": null, "Technique": "flow cytometry, Western blot", "Controlled_Technique": "Increased CRT expression", "Immune_System-Function_enhanced/numbers_increased": "Calreticulin / CRT; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/220", "Drug": "Selumetinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": "D09666", "Pubchem_ID": "10127622", "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Single Drug", "PMID": "30995478", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": "IO33", "Dose": "selumetinib (0-1uM)", "Technique": "Western Blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "pERK in CD8+ T cells and CD4+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD8; ERK / MAPK; T cells; CD8+ T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/221", "Drug": "Selumetinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": "D09666", "Pubchem_ID": "10127622", "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Single Drug", "PMID": "30995478", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": "HKP1", "Dose": "selumetinib (0-1uM)", "Technique": "Western Blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "pERK in CD8+ T cells and CD4+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD8; ERK / MAPK; T cells; CD8+ T cells; CD4+ 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Cancer (NSCLC))", "System": "LLC", "Dose": "selumetinib (0-1uM)", "Technique": "Western Blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "pERK in CD8+ T cells and CD4+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD8; ERK / MAPK; T cells; CD8+ T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/393", "Drug": "Selumetinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": "D09666", "Pubchem_ID": "10127622", "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Single Drug", "PMID": "30995478", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": "Splenocytes from Pmel-1 TCR transgenic mice were pulsed with gp100 (Pmel) peptide", "Dose": "Pulsative traetment , selumetinib (0-1uM)", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "CD44+CD62L effector memory CD8 T cells IFNγ", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD44; IFN-γ; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "differentiation of Pmel-1 CD8+ T cells, CD44+CD62L+ 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"CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Murine Melanoma", "System": "gp10025-33-activated pmel-1 mouse splenocytes", "Dose": "trametinib: L=0.005μM, M=0.25μM, H=1μM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "IFN-γ expressing CD3+ CD8+ cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD3; CD8; IFN-γ", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/821", "Drug": "Trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "28928458", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "ovalbumin-specific CD8+ OT-I T cells co-cultured with trametinib (MEKi) pre-treated AT3ova tumor cells", "Dose": "0–100 nM of trametinib for 12 h", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "IFNγ cytokine production by these CD8+ OT-I T cells MHC-I expression, 4-1BB and OX-40 on T cells", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; 4-1BB / CD137; CD8; IFN-γ; T cells; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/822", "Drug": "Trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "28928458", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "ovalbumin-specific CD8+ OT-I T cells co-cultured with AT3ova tumor cells in contuinuing presence of trametinib (MEKi)", "Dose": "0–100 nM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "IFNγ production", "Controlled_Terms_Function_inhibited_Number_decreased": "IFN-γ", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/824", "Drug": "Trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "28928458", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "AT3ova", "Dose": "trametinib treatment alone 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"Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "28928458", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "4T1Ch9", "Dose": "trametinib treatment alone (100 nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Fas, TRAIL, and NKG2D (RAE-1), MHC-I expression", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; CD95 / Fas / FAS; NKG2D / KLRK1; TRAIL; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, 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extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "29050218", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Mel-RM cells", "Dose": "trametinib (1 μM)", "Technique": "Western blot analysis,Flow cytometry, qPCR analysis", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "CD47 expression activation of ERK", "Controlled_Terms_Function_enhanced_Number_increased": "ERK / MAPK; Expression / abundance phenotype; CD47", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, 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Cobimetinib and vemurafenib target two different kinases in the RAS/RAF/MEK/ERK pathway.", "KEGG_Drug__ID": "D10405", "Pubchem_ID": "16222096", "STR_LINK_(SMILES)": "OC1(CN(C1)C(=O)C1=C(NC2=C(F)C=C(I)C=C2)C(F)=C(F)C=C1)[C@@H]1CCCCN1", "Single/Combination": "Single Drug", "PMID": "31671149", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "Activated CD8+ T cells+pooled B cells isolated from tumor draining lymph nodes of mice treated with cobimetinib", "Dose": "7.5 mg/kg of cobimetinib(MEKi) three times weekly via intraperitoneal injection", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Expansion of T cells interferon-gamma and granzyme B", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; Granzyme B / GZMB; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/770", "Drug": "MEK inhibitors U0126", "Drug_category": "MEK inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "MEK Inhibitor U0126 is a chemically synthesized organic compound that inhibits activation of MAPK (ERK 1/2) by inhibiting the kinase activity of MAP Kinase Kinase (MAPKK or MEK 1/2).", "KEGG_Drug__ID": null, "Pubchem_ID": "3006531", "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)SC(=C(C#N)C(=C(N)SC2=CC=CC=C2N)C#N)N", "Single/Combination": "Single Drug", "PMID": "20551059", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "UACC903 melanoma cells -cultured with CTL specific for either MART-1 (left) or gp100 (right)", "Dose": "(10 μmol/L", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "IFN-γ", "Controlled_Terms_Negative_Regulation": "IFN-γ", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/800", "Drug": "MEK inhibitors U0126", "Drug_category": "MEK inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "MEK Inhibitor U0126 is a chemically synthesized organic compound that inhibits activation of MAPK (ERK 1/2) by inhibiting the kinase activity of MAP Kinase Kinase (MAPKK or MEK 1/2).", "KEGG_Drug__ID": null, "Pubchem_ID": "3006531", "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)SC(=C(C#N)C(=C(N)SC2=CC=CC=C2N)C#N)N", "Single/Combination": "Single Drug", "PMID": "20551059", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "HLA-A2+ UACC903 melanoma cells- cultured with CTL specific for MART-1 or gp100 versus control lymphocytes\n (GFP-transduced) at various E:T ratios", "Dose": "(10 μmol/L)", "Technique": "ELISA,cytotoxicity assay", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); 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Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 protein expression and mRNA exxpression phospho ERK", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; ERK / MAPK; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1617", "Drug": "MEKi PD0325901", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB07101", "Target/s_or_mechanism_of_action": "PD0325901 is a selective, cell permeable inhibitor of the MEK/ERK pathway that inhibits the activation and downstream signaling of MEK.", "KEGG_Drug__ID": null, "Pubchem_ID": "9826528", "STR_LINK_(SMILES)": "[H][C@@](O)(CO)CONC(=O)C1=C(NC2=CC=C(I)C=C2F)C(F)=C(F)C=C1", "Single/Combination": "Single Drug", "PMID": "26943572", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer", "System": "BCPAP", "Dose": "MEKi PD0325901 10μM", "Technique": "Quantitative PCR, Western blot", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 protein expression and mRNA exxpression phospho ERK", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; ERK / MAPK; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1566", "Drug": "Blocking antibody against CD47 (B6H12.2)", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29050218", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Mel-RM cells + blocking antibody against CD47 = human peripheral blood mononuclear cells (PBMC)", "Dose": "CD47 (B6H12.2, 10 μg/ml)", "Technique": "con-focal microscopy, phagocytic assay", "Controlled_Technique": "Microscopy", "Immune_System-Function_enhanced/numbers_increased": "phagocytosis by macrophages higher levels of CRT", "Controlled_Terms_Function_enhanced_Number_increased": "Calreticulin / CRT; 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CD73 expression analysis; CD73 enzymatic assay; Western blot", "Controlled_Technique": "cyclin D1 expression", "Immune_System-Function_enhanced/numbers_increased": "Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "CD73 expression and enzymatic activity increased, promoting immunosuppressive adenosine signaling", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; Adenosine signaling", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/544", "Drug": "Trametinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "Selective MEK1/MEK2 inhibition → inhibition of RAS–RAF–MEK–ERK signaling; sustained compensatory p38 activation", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Single", "PMID": "34165921", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "CT26 mouse colon carcinoma cell line", "System": "CT26", "Dose": "100 nM", "Technique": "Flow cytometry; CD73 expression analysis; CD73 enzymatic assay; Western blot", "Controlled_Technique": "cyclin D1 expression", "Immune_System-Function_enhanced/numbers_increased": "Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "CD73 expression and enzymatic activity increased, resulting in enhanced immunosuppressive adenosine signaling", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; Adenosine signaling", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/545", "Drug": "Trametinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "Selective MEK1/MEK2 inhibition → inhibition of RAS–RAF–MEK–ERK signaling; sustained compensatory p38 activation", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Single", "PMID": "34165921", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "MC38 mouse colon adenocarcinoma cell line", "System": "MC38", "Dose": "100 nM", "Technique": "Flow cytometry; CD73 expression analysis; CD73 enzymatic assay; Western blot", "Controlled_Technique": "cyclin D1 expression", "Immune_System-Function_enhanced/numbers_increased": "Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "CD73 expression and enzymatic activity increased, enhancing the immunosuppressive adenosine pathway", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; Adenosine signaling", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/617", "Drug": "Trametinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "Selective MEK1/MEK2 inhibition → inhibition of RAS–RAF–MEK–ERK signaling; sustained compensatory p38 activation", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Single", "PMID": "34165921", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "PC9 human EGFR-mutant non-small-cell lung cancer cell line", "System": "PC9", "Dose": "100 nM", "Technique": "Flow cytometry; CD73 expression analysis; CD73 enzymatic assay; Western blot", "Controlled_Technique": "cyclin D1 expression", "Immune_System-Function_enhanced/numbers_increased": "Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": "CD73/adenosine pathway associated with suppression of T-cell activity", "Immune_System-Function_inhibited/numbers_decreased": "Adenosine signaling; T cells", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "CD73 expression and enzymatic activity increased after prolonged trametinib exposure, increasing immunosuppressive signaling", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/618", "Drug": "Trametinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "Selective MEK1/MEK2 inhibition → inhibition of RAS–RAF–MEK–ERK signaling; sustained compensatory p38 activation", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Single", "PMID": "34165921", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "A549 human non-small-cell lung cancer cell line", "System": "A549", "Dose": "100 nM", "Technique": "Flow cytometry; CD73 expression analysis; CD73 enzymatic assay; Western blot", "Controlled_Technique": "cyclin D1 expression", "Immune_System-Function_enhanced/numbers_increased": "Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": "CD73 expression decreased rather than increased", "Immune_System-Function_inhibited/numbers_decreased": "Expression / abundance phenotype", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "No enhancement of CD73-mediated negative immune regulation", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/619", "Drug": "Trametinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "Selective MEK1/MEK2 inhibition → inhibition of RAS–RAF–MEK–ERK signaling; sustained compensatory p38 activation", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Single", "PMID": "34165921", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "HCT116 human colon cancer cell line", "System": "HCT116", "Dose": "100 nM", "Technique": "Flow cytometry; CD73 expression analysis; CD73 enzymatic assay; Western blot", "Controlled_Technique": "cyclin D1 expression", "Immune_System-Function_enhanced/numbers_increased": "Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": "CD73 expression decreased rather than increased", "Immune_System-Function_inhibited/numbers_decreased": "Expression / abundance phenotype", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "No enhancement of CD73-mediated negative immune regulation", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/455", "Drug": "Trametinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "MEK1/2 inhibition; MAPK/ERK suppression", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Single", "PMID": "33062958", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "E0771-Ova, ovalbumin-expressing E0771 derivative", "System": "E0771-OVA", "Dose": "50 nM; 72 h", "Technique": null, "Controlled_Technique": "increased H2Kb-SIINFEKL, MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/449", "Drug": "Trametinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "Selective MEK1/MEK2 inhibition → inhibition of RAS–RAF–MEK–ERK signaling; sustained compensatory p38 activation", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Single", "PMID": "34165921", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "SKBr3 human breast cancer cell line", "System": "SKBR3", "Dose": "100 nM", "Technique": "Flow cytometry; CD73 expression analysis; CD73 enzymatic assay; Western blot", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "CD73 expression remained approximately unchanged", "Immune_System_function_unaffected": "Expression / abundance phenotype", "Controlled_Terms_Unaffected": "No significant increase in CD73-mediated negative immune regulation reported", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/451", "Drug": "Trametinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "MEK1/2 inhibition; MAPK/ERK suppression", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Single", "PMID": "33062958", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "MMTV-Neu murine mammary tumor", "System": "MMTV-Neu", "Dose": "50 nM; 24–72 h", "Technique": "Western blot; flow cytometry; STAT knockdown", "Controlled_Technique": "STAT1/3/5 activation; MHC-I increased; PD-L1 increased", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; PD-L1 / CD274; STAT1", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "PD-L1 increased", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/452", "Drug": "Trametinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "MEK1/2 inhibition; MAPK/ERK suppression", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Single", "PMID": "33062958", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "4T1 murine mammary carcinoma", "System": "4T1", "Dose": "50 nM; 24–72 h", "Technique": "Western blot; flow cytometry; STAT knockdown", "Controlled_Technique": "STAT3 activation; detectable STAT5 activation; MHC-I increased; PD-L1 increased", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; PD-L1 / CD274; STAT3", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "PD-L1 increased", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/454", "Drug": "Trametinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "MEK1/2 inhibition; MAPK/ERK suppression", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Single", "PMID": "33062958", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "E0771 murine mammary tumor", "System": "E0771", "Dose": "50 nM; 24–72 h", "Technique": "Western blot; flow cytometry; STAT knockdown", "Controlled_Technique": "STAT3 activation; MHC-I increased", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; STAT3", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "No significant PD-L1 increase", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/453", "Drug": "Trametinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "MEK1/2 inhibition; MAPK/ERK suppression", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Single", "PMID": "33062958", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "EMT6 murine mammary carcinoma", "System": "EMT6", "Dose": "50 nM; 24–72 h", "Technique": "Western blot; flow cytometry; STAT knockdown", "Controlled_Technique": "STAT3 activation; STAT5 activation detectable in responsive models", "Immune_System-Function_enhanced/numbers_increased": "STAT3", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "No significant PD-L1 increase", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1266", "Drug": "Anti PD-1 Nivolumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB09035", "Target/s_or_mechanism_of_action": "The ligands PD-L1 and PD-L2 bind to the PD-1 receptor on T-cells, inhibiting the action of these cells. Tumor cells express PD-L1 and PD-L2.Nivolumab binds to PD-1, preventing PD-L1 and PD-L2 from inhibiting the action of T-cells, restoring a patient's tumor-specific T-cell response", "KEGG_Drug__ID": "D10316", "Pubchem_ID": "348000000", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29100374", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma (RCC)", "System": "Teff: PB-Tregs pretreated with anti-PD 1(1:1)", "Dose": "20 μg/mL of anti PD-1", "Technique": "Flow cytometry, ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "peripheral CD4+CD25− T effector (Teff) cells proliferation IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD25 / IL2RA; IFN-γ; Cell proliferation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/926", "Drug": "Anti-CD3 5 ug/mL", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31648326", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "CD3+CD8+ cells from AML mice", "Dose": "anti-CD3 5 ug/mL", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD44+CD62L–, CD44+CD62L+, CD44–CD62L–", "Controlled_Terms_Function_enhanced_Number_increased": "CD44", "Immune_System-Function_inhibited/numbers_decreased": "CD44–CD62L+", "Controlled_Terms_Function_inhibited_Number_decreased": "CD44", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1050", "Drug": "Anti-PD1", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "30940657", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Ductal Adenocarcinoma (PDA)", "System": "PDA slice cultures", "Dose": "PD-1 blocking mAb", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "EpCAM+ cells, CD45+ immune cells, including both CD4+ and CD8+ cells, CD8+ T cell migration into the juxtatumoral compartment", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; T cells; CD8+ T cells; T-cell migration / chemotaxis; Cell migration and invasion", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", 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"Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1237", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "21308409", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast -Triple Negative Breast Cancer (TNBC))", "System": "IIB-BR-G + purified NK cells", "Dose": "1 μg/ml Cetuximab", "Technique": "Flow cytometry, Calcein release\n assay.", "Controlled_Technique": 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agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "21308409", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast -Triple Negative Breast Cancer (TNBC))", "System": "IIB-BR-G + purified NK cells", "Dose": "1 μg/ml Cetuximab", "Technique": "Flow cytometry, Calcein release\n assay.", "Controlled_Technique": "Flow cytometry; Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK-mediated ADCC antibody dependent cellular cytotoxicity (ADCC)", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; Antibody-dependent cytotoxicity", 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"CANIMM/197", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "26876213", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "UDSCC2", "Dose": "5.0μg/ml", "Technique": "SDS-PAGE and immunoblotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, 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"STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "26579227", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "JHU029 + PBMC or purified monocytes from HNSCC patients with new active diseases", "Dose": "10 μg/mL cetuximab", "Technique": "Flow cytometry, ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IL-12 p70 PD-L1,HLA-DR and CD86-on CD14+ monocytes within PBMC - M1-like phenotype", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; MHC class II; HLA-DR; CD86; IL-12; Macrophages; Monocytes; PD-L1 immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": "IL-10 CD163", "Controlled_Terms_Function_inhibited_Number_decreased": "CD163; IL-10", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1283", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "23444227", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head 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"Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1324", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "25972070", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Cancer (HNC)", "System": "JHU-029 HNC", "Dose": "cetuximab (10 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{"study_type": "cell_line", "ID": "CANIMM/1326", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29056908", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Adenocarcinoma", "System": "H125", "Dose": "10 μg/ml", "Technique": "Flow cytometry, real-time quantitative PCR (qPCR)", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "HLA-ABC membrane expression, HLA-A, HLA-B, and HLA-C β2-m, LMP 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"Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "26876213", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "SCC90", "Dose": "5.0μg/ml", "Technique": "SDS-PAGE and immunoblotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "autophagy- associated with poor response to cetuximab therapy.", "Controlled_Terms_Negative_Regulation": "Autophagy / macroautophagy", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/199", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural 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"Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/200", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "32195020", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "SCC4", "Dose": "100 μg/mL cetuximab for 2 h, and then stimulated with 1 μg/mL LPS for 0, 15, 30, 60 min", "Technique": "western blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "p-p65 and p-c-jun-increased signaling events downstream of TLR4", "Controlled_Terms_Negative_Regulation": "TLR4; c-Jun / JUN; p65 / RELA", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/332", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an 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"Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "TNF-α, PGE2 and NO-suggest TLR4 induced tumor-associated inflammation was increased after EGFR inhibition, COX2 (PGE2 synthetase) and iNOS (NO synthetase), MyD88 proteins", "Controlled_Terms_Negative_Regulation": "TNF-α / TNF; NOS2 / iNOS; COX-2 / PTGS2; PGE2; EGFR; TLR4", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1006", "Drug": "IPH2101", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB06049", "Target/s_or_mechanism_of_action": "The therapeutic principle of IPH 2101 (NN 1975) is based on the activation of Natural Killer (NK) cells by a monoclonal antibody which blocks the NK’s KIR 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"Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1007", "Drug": "IPH2101", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB06049", "Target/s_or_mechanism_of_action": "The therapeutic principle of IPH 2101 (NN 1975) is based on the activation of Natural Killer (NK) cells by a monoclonal antibody which blocks the NK’s KIR inhibitory receptors, thereby potentiating NK cells anti-cancer action.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "22031859", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "Primary MM cells", "Dose": "30 μg/mL", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "granzyme B", "Controlled_Terms_Function_enhanced_Number_increased": "Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": null, 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"Cancer_Type_Description": "Lung Adenocarcinoma", "System": "H125", "Dose": "10 μg/ml", "Technique": "Flow cytometry, real-time quantitative PCR (qPCR)", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "HLA-ABC membrane expression, HLA-A, HLA-B, and HLA-C β2-m, LMP subunits, TAPs, as well as tapasin", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; HLA-A; HLA-B; HLA-C; Tapasin; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/889", "Drug": "Panitumumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB01269", "Target/s_or_mechanism_of_action": "Panitumumab binds specifically to EGFR on both normal and tumor cells, and competitively inhibits the binding of ligands for EGFR. 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Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "ADCC 25%", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1234", "Drug": "Rituximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "30767211", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Follicular Lymphoma (FL)", "System": "DOHH2", "Dose": "1 μg/ml rituximab", "Technique": "Apoptosis analysis by Annexin V and TO-PRO-3 staining", "Controlled_Technique": "Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "ADCC 44%", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/551", "Drug": "Irinotecan", "Drug_category": "topoisomerase I inhibitor", "Drugbank_ID": "DB00762", "Target/s_or_mechanism_of_action": "Inhibits TOP1", "KEGG_Drug__ID": "D08086", "Pubchem_ID": "60838", "STR_LINK_(SMILES)": "CCC1=C2CN3C(=CC4=C(C3=O)COC(=O)[C@@]4(CC)O)C2=NC5=C1C=C(C=C5)OC(=O)N6CCC(CC6)N7CCCCC7", "Single/Combination": "Single", "PMID": "36589674", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": "HCT116", "Dose": "25 µg/mL", "Technique": "Flow cytometry", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "Increased PD-L1", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1356", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "20865050", "Cancer_Type": "Esophageal Cancer", "Cancer_Type_Description": "Esophageal - EAC (Esophageal Adenocarcinoma)", "System": "OE19 coculture with CTLs cytotoxic T lymphocytes+IFN-y", "Dose": "10 mg/ml trastuzumab for 48 hours", "Technique": "Cytometric Bead Array", "Controlled_Technique": "Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "IFN-y", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1051", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "30596643", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": "NK+ Panc-1 (HER2-low-expressing cell line), effector/target (E/T) ratio was set at 10:1", "Dose": "10 μg/ml of Tmab", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD137", "Controlled_Terms_Function_enhanced_Number_increased": "4-1BB / CD137; CD137", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "PD-1, NKG2D", "Controlled_Terms_Unaffected": "PD-1 / PDCD1; NKG2D / KLRK1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1052", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "30596643", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": "NK+Capan-1 (HER2-high-expressing cell line), effector/target (E/T) ratio was set at 10:1", "Dose": "10 μg/ml of Tmab", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD137", "Controlled_Terms_Function_enhanced_Number_increased": "4-1BB / CD137; CD137", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "PD-1, NKG2D", "Controlled_Terms_Unaffected": "PD-1 / PDCD1; NKG2D / KLRK1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/827", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29746929", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "BT474 -HER2-overexpressing breast cancer cell (The indicated HER2-overexpressing breast cancer cells were treated with trastuzumab (5 μg/ml, equivalent to ~30 nM) or a control IgG (rituximab) in monoculture or co-culture with PBMC (at a cancer cell: PBMC ratio of 1:5) for 48 h. After treatment, cell-free conditioned media from mono-cultures and co-cultures were collected and added into new cultures of the breast cancer cells by mixing the conditioned medium with fresh medium at a 1:1 ratio. After culture for another 48 h, the cells were harvested and stained with APC-conjugated anti-PD-L1 antibody and then subjected to Flow cytometry analysis)", "Dose": "trastuzumab (5 μg/ml, equivalent to ~30 nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "IFNγ in the conditioned media from trastuzumab-treated co-cultures than in the conditioned media from control antibody-treated co-cultures)", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; Antibody / IgG / IgM", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 in HER2-overexpressing breast cancer cells co-cultured with human PBMC", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; HER2 / ERBB2; PD-L1 immune checkpoint pathway", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/828", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29746929", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "SKBR3- HER2-overexpressing breast cancer cell (The indicated HER2-overexpressing breast cancer cells were treated with trastuzumab (5 μg/ml, equivalent to ~30 nM) or a control IgG (rituximab) in monoculture or co-culture with PBMC (at a cancer cell: PBMC ratio of 1:5) for 48 h. After treatment, cell-free conditioned media from mono-cultures and co-cultures were collected and added into new cultures of the breast cancer cells by mixing the conditioned medium with fresh medium at a 1:1 ratio. After culture for another 48 h, the cells were harvested and stained with APC-conjugated anti-PD-L1 antibody and then subjected to Flow cytometry analysis)", "Dose": "trastuzumab (5 μg/ml, equivalent to ~30 nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "IFNγ in the conditioned media from trastuzumab-treated co-cultures than in the conditioned media from control antibody-treated co-cultures)", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; Antibody / IgG / IgM", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 in HER2-overexpressing breast cancer cells co-cultured with human PBMC", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; HER2 / ERBB2; PD-L1 immune checkpoint pathway", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/829", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29746929", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "SUM190- HER2-overexpressing breast cancer cell(The indicated HER2-overexpressing breast cancer cells were treated with trastuzumab (5 μg/ml, equivalent to ~30 nM) or a control IgG (rituximab) in monoculture or co-culture with PBMC (at a cancer cell: PBMC ratio of 1:5) for 48 h. After treatment, cell-free conditioned media from mono-cultures and co-cultures were collected and added into new cultures of the breast cancer cells by mixing the conditioned medium with fresh medium at a 1:1 ratio. After culture for another 48 h, the cells were harvested and stained with APC-conjugated anti-PD-L1 antibody and then subjected to Flow cytometry analysis)", "Dose": "trastuzumab (5 μg/ml, equivalent to ~30 nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "IFNγ in the conditioned media from trastuzumab-treated co-cultures than in the conditioned media from control antibody-treated co-cultures)", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; Antibody / IgG / IgM", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 in HER2-overexpressing breast cancer cells co-cultured with human PBMC", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; HER2 / ERBB2; PD-L1 immune checkpoint pathway", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/830", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29746929", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "HCC1954- HER2-overexpressing breast cancer cell(The indicated HER2-overexpressing breast cancer cells were treated with trastuzumab (5 μg/ml, equivalent to ~30 nM) or a control IgG (rituximab) in monoculture or co-culture with PBMC (at a cancer cell: PBMC ratio of 1:5) for 48 h. After treatment, cell-free conditioned media from mono-cultures and co-cultures were collected and added into new cultures of the breast cancer cells by mixing the conditioned medium with fresh medium at a 1:1 ratio. After culture for another 48 h, the cells were harvested and stained with APC-conjugated anti-PD-L1 antibody and then subjected to Flow cytometry analysis)", "Dose": "trastuzumab (5 μg/ml, equivalent to ~30 nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "IFNγ in the conditioned media from trastuzumab-treated co-cultures than in the conditioned media from control antibody-treated co-cultures)", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; Antibody / IgG / IgM", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 in HER2-overexpressing breast cancer cells co-cultured with human PBMC", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; HER2 / ERBB2; PD-L1 immune checkpoint pathway", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/831", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "28819024", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "Cocultute of Mature DCs and SKBR3", "Dose": "Trastuzumab was then added to the media at various concentrations (0 – 80 µg/mL) and cells\n were cultured for up to 24 hours", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Significant increases in HER2 uptake by DCs were observed in presence of Trastuzumab", "Controlled_Terms_Function_enhanced_Number_increased": "HER2 / ERBB2; Dendritic cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/386", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": "D06402", "Pubchem_ID": "5329102", "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "18927310", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma (RCC)", "System": "PBMCs stimulated with anti-CD3/anti-CD28 antibodies for 72 h", "Dose": null, "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "IFNgamma-producing T cells IFNgamma", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/832", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "28819024", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "Cocultute of Mature DCs and BT474", "Dose": "Trastuzumab was then added to the media at various concentrations (0 – 80 µg/mL) and cells\n were cultured for up to 24 hours", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Significant increases in HER2 uptake by DCs were observed in presence of Trastuzumab", "Controlled_Terms_Function_enhanced_Number_increased": "HER2 / ERBB2; Dendritic cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/833", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "28735814", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "SKBR3", "Dose": "PBMC-induced trastuzumab-mediated ADCC", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "increase in trastuzumab-mediated ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/835", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "28735814", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "MCF-7", "Dose": "PBMC-induced trastuzumab-mediated ADCC", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "increase in trastuzumab-mediated ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1217", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "20865050", "Cancer_Type": "Esophageal Cancer", "Cancer_Type_Description": "Esophageal - EAC (Esophageal Adenocarcinoma)", "System": "OE19", "Dose": "2.5 mg of trastuzumab", "Technique": "Flow cytometry, Annexin V and\n 7aad (Cell viablity assay)", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "HER-2", "Controlled_Terms_Function_enhanced_Number_increased": "HER2 / ERBB2", "Immune_System-Function_inhibited/numbers_decreased": "HER-2", "Controlled_Terms_Function_inhibited_Number_decreased": "HER2 / ERBB2", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1218", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "20865050", "Cancer_Type": "Esophageal Cancer", "Cancer_Type_Description": "Esophageal - EAC (Esophageal Adenocarcinoma)", "System": "OE33", "Dose": "2.5 mg of trastuzumab", "Technique": "Flow cytometry, Annexin V and\n 7aad (Cell viablity assay)", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "HER-2", "Controlled_Terms_Function_enhanced_Number_increased": "HER2 / ERBB2", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1292", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "21387286", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "SKBR3", "Dose": "0.021 mg/ml or 0.105 mg/ml", "Technique": "immunocytochemical staining, FACS analysis", "Controlled_Technique": "Flow cytometry; Immunocytochemistry (ICC)", "Immune_System-Function_enhanced/numbers_increased": "HER2", "Controlled_Terms_Function_enhanced_Number_increased": "HER2 / ERBB2", "Immune_System-Function_inhibited/numbers_decreased": "E‐cadherin", "Controlled_Terms_Function_inhibited_Number_decreased": "E-cadherin / CDH1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1293", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "21387286", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "HCC1569", "Dose": "0.021 mg/ml or 0.105 mg/ml", "Technique": "immunocytochemical staining, FACS analysis", "Controlled_Technique": "Flow cytometry; Immunocytochemistry (ICC)", "Immune_System-Function_enhanced/numbers_increased": "E‐cadherin HER2", "Controlled_Terms_Function_enhanced_Number_increased": "E-cadherin / CDH1; HER2 / ERBB2", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1308", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "30290143", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "SKBR3 -Macrophages labeled by CMFDA were co-incubated with SKBR3", "Dose": "1-10 μg/ml", "Technique": "Flow cytometry, confocal microscopy", "Controlled_Technique": "Flow cytometry; Microscopy; Confocal microscopy", "Immune_System-Function_enhanced/numbers_increased": "phagocytosis of HER2+ cancer cells by human macrophages", "Controlled_Terms_Function_enhanced_Number_increased": "HER2 / ERBB2; Macrophages; Phagocytosis / trogocytosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1309", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "30290143", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "BT-474 Macrophages labeled by CMFDA were co-incubated with BT-474", "Dose": "1-10 μg/ml", "Technique": "Flow cytometry, confocal microscopy", "Controlled_Technique": "Flow cytometry; Microscopy; Confocal microscopy", "Immune_System-Function_enhanced/numbers_increased": "phagocytosis of HER2+ cancer cells by human macrophages", "Controlled_Terms_Function_enhanced_Number_increased": "HER2 / ERBB2; Macrophages; Phagocytosis / trogocytosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1560", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "30596643", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": "NK+Capan-1 (HER2-high-expressing cell line), effector/target (E/T) ratio was set at 10:1", "Dose": "10 μg/ml of Tmab", "Technique": "LDH-releasing assays", "Controlled_Technique": "LDH-releasing assays", "Immune_System-Function_enhanced/numbers_increased": "Tmab-mediated ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1561", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "30596643", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": "NK+ Panc-1 (HER2-low-expressing cell line), effector/target (E/T) ratio was set at 10:1", "Dose": "10 μg/ml of Tmab", "Technique": "LDH-releasing assays", "Controlled_Technique": "LDH-releasing assays", "Immune_System-Function_enhanced/numbers_increased": "Tmab-mediated ADCC against Panc-1 was elevated, the level was significantly weaker compared with that against Capan-1", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/121", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "20865050", "Cancer_Type": "Esophageal Cancer", "Cancer_Type_Description": "Esophageal - EAC (Esophageal Adenocarcinoma)", "System": "OE19", "Dose": "2.5 mg of trastuzumab", "Technique": "RT-PCR and IHC/ICC,", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunohistochemistry (IHC); Immunocytochemistry (ICC)", "Immune_System-Function_enhanced/numbers_increased": "TAP-1 and Tapasin", "Controlled_Terms_Function_enhanced_Number_increased": "TAP1; Tapasin", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/122", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "20865050", "Cancer_Type": "Esophageal Cancer", "Cancer_Type_Description": "Esophageal - EAC (Esophageal Adenocarcinoma)", "System": "OE33", "Dose": "2.5 mg of trastuzumab", "Technique": "RT-PCR and IHC/ICC,", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunohistochemistry (IHC); Immunocytochemistry (ICC)", "Immune_System-Function_enhanced/numbers_increased": "TAP-1, TAP-2 and Tapasin", "Controlled_Terms_Function_enhanced_Number_increased": "TAP1; TAP2; Tapasin", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/456", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Binds HER2/ERBB2 and blocks HER2 signaling; immune stimulation contributes to cytotoxicity", "KEGG_Drug__ID": "D03257", "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "33292267", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "HER2 + breast cancer", "System": "BT474 cancer cells + Jurkat CD4+ T cells", "Dose": "10, 25, 50, 100 µg/mL; 25 µg/mL used for subsequent experiments", "Technique": "western blot and ELISA", "Controlled_Technique": "TNF-α expression, CD4+ T-cells TNF-α increased. Trastuzumab + T cells: 81.4 ± 6.9% vs 100.2 ± 3% viability increase; p=0.01", "Immune_System-Function_enhanced/numbers_increased": "CD4; T cells; TNF-α / TNF; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/457", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Binds HER2/ERBB2 and blocks HER2 signaling; immune stimulation contributes to cytotoxicity", "KEGG_Drug__ID": "D03257", "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "33292267", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "HER2 + breast cancer", "System": "SKBR3 cancer cells + Jurkat CD4+ T cells", "Dose": "10, 25, 50, 100 µg/mL; 25 µg/mL used for subsequent experiments", "Technique": "western blot and ELISA", "Controlled_Technique": "TNF-α expression, CD4+ T-cells TNF-α increased. Trastuzumab + T cells: 81.4 ± 6.9% vs 100.2 ± 3% viability increase; p=0.01", "Immune_System-Function_enhanced/numbers_increased": "CD4; T cells; TNF-α / TNF; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/459", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Binds HER2/ERBB2 and blocks HER2 signaling; immune stimulation contributes to cytotoxicity", "KEGG_Drug__ID": "D03257", "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "33292267", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "HER2 + breast cancer", "System": "MDA-MB-453 cancer cells + Jurkat CD4+ T cells", "Dose": "10, 25, 50, 100 µg/mL; 25 µg/mL used for subsequent experiments", "Technique": "western blot and ELISA", "Controlled_Technique": "TNF-α expression, CD4+ T-cells TNF-α increased. 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The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "17725605", "Cancer_Type": "Hpv16-Expressing Tumors", "Cancer_Type_Description": "Human Papilloma Virus 16-Associated Tumours", "System": "TC-1/A9 (MHC class I-deficient)", "Dose": "50 µm 5-azaC", "Technique": "Flow cytometry, quantitative real-time RT-PCR,Western blot analysis", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "MHC class I molecules apoptosis,TAP-1, TAP-2 and LMP-7", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Apoptosis; TAP1; TAP2; LMP7 / PSMB8;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1470", "Drug": "5-azacytidine (5-AC)", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "32079180", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "SW480", "Dose": null, "Technique": "immunoblotting, Flow cytometry", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "tumor programmed cell death 1 ligand 1 (PD-L1) level", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/186", "Drug": "5-azacytidine (5-AC)", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "32079180", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "HCT116", "Dose": null, "Technique": "immunoblotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "tumor programmed cell death 1 ligand 1 (PD-L1) level", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/461", "Drug": "5-Azacytidine (Azacitidine; 5-Aza)", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "Inhibits DNMT activity at low doses; DNA/RNA incorporation at higher doses; hypomethylation can increase antigen-presentation gene expression", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "single", "PMID": "41019037", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast cancer", "System": "4T1", "Dose": "0–10 μM, 24 h in vitro", "Technique": "Flow cytometry", "Controlled_Technique": "MHC-I expression", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/665", "Drug": "5-Azacytidine (Azacitidine; 5-Aza)", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "Inhibits DNMT activity at low doses; DNA/RNA incorporation at higher doses; hypomethylation can increase antigen-presentation gene expression", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "single", "PMID": "41019037", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "melanoma", "System": "B16F10", "Dose": "0–10 μM, 24 h in vitro", "Technique": "Flow cytometry", "Controlled_Technique": "MHC-I expression", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1427", "Drug": "5-fluorouracil", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D00584", "Pubchem_ID": "3385", "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O", "Single/Combination": "Single Drug", "PMID": "16957513", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": "Colon cancer (SW480) cells", "Dose": "5-FU (5-fluorouracil) IC50 11.70 ug/ml", "Technique": "Immunocytochemistry\n and Flow cytometry, RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunocytochemistry (ICC)", "Immune_System-Function_enhanced/numbers_increased": "Fas", "Controlled_Terms_Function_enhanced_Number_increased": "CD95 / Fas / FAS", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1471", "Drug": "5-fluorouracil", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D00584", "Pubchem_ID": "3385", "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O", "Single/Combination": "Single Drug", "PMID": "32079180", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "SW480", "Dose": "10 mg/mL", "Technique": "immunoblotting, Flow cytometry", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "tumor programmed cell death 1 ligand 1 (PD-L1) level", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/187", "Drug": "5-fluorouracil", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D00584", "Pubchem_ID": "3385", "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O", "Single/Combination": "Single Drug", "PMID": "32079180", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "HCT116", "Dose": "10 mg/mL", "Technique": "immunoblotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "tumor programmed cell death 1 ligand 1 (PD-L1) level", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/188", "Drug": "5-fluorouracil", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D00584", "Pubchem_ID": "3385", "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O", "Single/Combination": "Single Drug", "PMID": "32079180", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "LoVo", "Dose": "10 mg/mL", "Technique": "immunoblotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "tumor programmed cell death 1 ligand 1 (PD-L1) level", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/696", "Drug": "5-Fluorouracil (5-FU)", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Thymidylate synthase inhibition; disruption of DNA/RNA synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "40380807", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "gastric cancer cell line", "System": "AGS", "Dose": "59.63 μM", "Technique": "Flow cytometry; Western blot", "Controlled_Technique": "Increased cell-surface PD-L1 and MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; PD-L1 / CD274", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "Increased PD-L1 may promote inhibitory immune-checkpoint signaling", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 immune checkpoint pathway; Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1584", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "18791715", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": "OV-90", "Dose": "1-10 µM", "Technique": "PCR", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "cancer-testis antigens (CTA) on ovarian cell line", "Controlled_Terms_Function_enhanced_Number_increased": "Cancer-testis antigens", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/697", "Drug": "5-Fluorouracil (5-FU)", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Thymidylate synthase inhibition; disruption of DNA/RNA synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "40380807", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "gastric cancer cell line", "System": "SNU-1", "Dose": "33.7 μM", "Technique": "Flow cytometry; Western blot", "Controlled_Technique": "Increased PD-L1 and MHC-I, predominantly in apoptotic cells", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; PD-L1 / CD274", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "Increased PD-L1 may promote inhibitory immune-checkpoint signaling", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 immune checkpoint pathway; Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/577", "Drug": "5-FU", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D00584", "Pubchem_ID": "3385", "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O", "Single/Combination": "Single", "PMID": "32078695", "Cancer_Type": "Esophageal Cancer", "Cancer_Type_Description": "esophageal cancer cells (OE33 cells", "System": "OE33", "Dose": "0, 10 and 100 μM cisplatin", "Technique": "Flow cytometry", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "No significant differences were observed in CD1d expression in OE33 cells", "Immune_System_function_unaffected": "Expression / abundance phenotype; CD1d", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/700", "Drug": "5-FU", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D00584", "Pubchem_ID": "3385", "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O", "Single/Combination": "Single", "PMID": "32078695", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "upper gastrointestinal cancer", "System": "Invariant natural killer T (iNKT) cells+CD1d-transfected HeLa cells", "Dose": "10 or 100 μM", "Technique": "Flow cytometry", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": "inhibited CD107a externalization", "Immune_System-Function_inhibited/numbers_decreased": "CD107a / LAMP1", "Controlled_Terms_Function_inhibited_Number_decreased": "No significant decrease in IFN-γ expression by viable iNKT cells, No significant difference in granzyme B or perforin production by activated iNKT cells", "Immune_System_function_unaffected": "Expression / abundance phenotype; Granzyme B / GZMB; IFN-γ", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1159", "Drug": "Azacitidine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Mel-624", "Dose": "5µM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1160", "Drug": "Azacitidine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Mel-888", "Dose": "5µM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/928", "Drug": "Azacitidine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "23242597", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Myelodysplastic Syndrome (MDS)", "System": "Treg from three patients-stimulation with CD3/CD28 beads", "Dose": "(2 μM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Treg", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Th1 cells", "Controlled_Terms_Negative_Regulation": "Th1 cells", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/361", "Drug": "Azacitidine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "24162015", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Fibrosarcoma", "System": "MCA205", "Dose": "7.5, 15, 30 µM", "Technique": "cytoplasmic GFP-HMGB1 fluorescence intensit, immunostaining, immunofluorescence,western blotting", "Controlled_Technique": "Western blot/immunoblot analysis; Immunofluorescence assay; Immunostaining/image analysis; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "HMGB1 release", "Controlled_Terms_Function_enhanced_Number_increased": "HMGB1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/362", "Drug": "Azacitidine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "24162015", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Osteosarcoma", "System": "U2OS", "Dose": "7.5, 15, 30 µM", "Technique": "cytoplasmic GFP-HMGB1 fluorescence intensit, immunostaining, immunofluorescence,western blotting", "Controlled_Technique": "Western blot/immunoblot analysis; Immunofluorescence assay; Immunostaining/image analysis; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "HMGB1 release", "Controlled_Terms_Function_enhanced_Number_increased": "HMGB1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1269", "Drug": "Azacytidine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "28404876", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "KG1a", "Dose": "(1 μM or 5 μM)", "Technique": "sandwich ELISA,Flow cytometry", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "NKG2DL (MICA, MICB, ULBPs1-3)-on the surface of AML cells", "Controlled_Terms_Function_enhanced_Number_increased": "MICA; MICB; NKG2D ligand; MICA/MICB", "Immune_System-Function_inhibited/numbers_decreased": "release of soluble sNKG2DL from AML cells", "Controlled_Terms_Function_inhibited_Number_decreased": "Soluble NKG2D ligand", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1270", "Drug": "Azacytidine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "28404876", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "NB4 cells", "Dose": "(1 μM or 5 μM)", "Technique": "sandwich ELISA,Flow cytometry", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "NKG2DL (MICA, MICB, ULBPs1-3)-on the surface of AML cells", "Controlled_Terms_Function_enhanced_Number_increased": "MICA; MICB; NKG2D ligand; MICA/MICB", "Immune_System-Function_inhibited/numbers_decreased": "release of soluble sNKG2DL from AML cells", "Controlled_Terms_Function_inhibited_Number_decreased": "Soluble NKG2D ligand", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1487", "Drug": "Azacytidine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "20126405", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "KG-1a cells", "Dose": "(0–3 µM)", "Technique": "Flow cytometry, western blot", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "apoptosis markers-Annexin V (early apoptosis) and 7-AAD (late apoptosis),PARP cleavage", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis; PARP cleavage / PARP; Annexin V; 7-AAD", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/929", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "28321548", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "PBMCs from 4 patients", "Dose": "(0.1 to 10 μM) for 7 days", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "ILT2 expression on the surface of both healthy and leukemic B cells,", "Controlled_Terms_Function_enhanced_Number_increased": "B cells; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": "ILT2 on NK cells from CLL patients", "Controlled_Terms_Function_inhibited_Number_decreased": "NK cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1310", "Drug": "Cetuximab + GILF chemotherapy", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441\n DB00762\n DB11596\n DB00544\n DB00002", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase,\n Irinotecan inhibits the action of topoisomerase I,\n As levoleucovorin and leucovorin are analogs of tetrahydrofolate (THF), they are able to bypass DHFR reduction and act as a cellular replacement for the co-factor THF, thereby preventing these toxic side effects,\n Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA,\n Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D02368,D08086, D04715, D00584, D03455", "Pubchem_ID": "60750, 60838, 149436, 3385, 46507042", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F, \n CCC1=C2CN3C(=CC4=C(COC(=O[C@]4(O)CC)C3=O)C2=NC2=CC=C(OC(=O)N3CCC(CC3)N3CCCCC3)C=C12, \n NC1=NC(=O)C2=C(NC[C@H](CNC3=CC=C(C=C3)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N2C=O)N1, \n FC1=CNC(=O)NC1=O", "Single/Combination": null, "PMID": "21618510", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer Cells", "System": "WiDr + DC,s", "Dose": null, "Technique": "Flow cytometry,Transmission electron microscopy", "Controlled_Technique": "Flow cytometry; Microscopy; Electron microscopy", "Immune_System-Function_enhanced/numbers_increased": "DC-mediated phagocytosis/trogocytosis of these tumor cells CD80, CD83, CD86 and HLA-DR on the surface of DCs", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class II; HLA-DR; CD80; CD83; CD86; CD80/CD86 costimulation; Dendritic cells; Phagocytosis / trogocytosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1313", "Drug": "Cetuximab + GILF chemotherapy", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441\n DB00762\n DB11596\n DB00544\n DB00002", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase,\n Irinotecan inhibits the action of topoisomerase I,\n As levoleucovorin and leucovorin are analogs of tetrahydrofolate (THF), they are able to bypass DHFR reduction and act as a cellular replacement for the co-factor THF, thereby preventing these toxic side effects,\n Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA,\n Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D02368,D08086, D04715, D00584, D03455", "Pubchem_ID": "60750, 60838, 149436, 3385, 46507042", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F, \n CCC1=C2CN3C(=CC4=C(COC(=O[C@]4(O)CC)C3=O)C2=NC2=CC=C(OC(=O)N3CCC(CC3)N3CCCCC3)C=C12, \n NC1=NC(=O)C2=C(NC[C@H](CNC3=CC=C(C=C3)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N2C=O)N1, \n FC1=CNC(=O)NC1=O", "Single/Combination": null, "PMID": null, "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer Cells", "System": "HT29 + DC,s", "Dose": null, "Technique": "Flow cytometry,Transmission electron microscopy", "Controlled_Technique": "Flow cytometry; Microscopy; Electron microscopy", "Immune_System-Function_enhanced/numbers_increased": "DC-mediated phagocytosis/trogocytosis of these tumor cells CD80, CD83, CD86 and HLA-DR on the surface of DCs", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class II; HLA-DR; CD80; CD83; CD86; CD80/CD86 costimulation; Dendritic cells; Phagocytosis / trogocytosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/768", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "28404876", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "NKL cells co-cultured with K562 cells", "Dose": "1 μM DAC", "Technique": "cell lysis assay", "Controlled_Technique": "Cell lysis assay", "Immune_System-Function_enhanced/numbers_increased": "NKL cells", "Controlled_Terms_Function_enhanced_Number_increased": "NKL cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/790", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "30210693", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "CD3+ T cells from CLL patients were stimulated with autologous irradiated CD19+ CLL cells", "Dose": "2 μM", "Technique": "CFSE assay", "Controlled_Technique": "Cell proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "CD4+ and CD8+ T cells IFNγ from both CD4+ and CD8+ cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; IFN-γ; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/733", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "30210693", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "PBMCs from healthy donors cocultured with purified leukemia cells obtained from CLL patients for 4 hours", "Dose": "1 μM lenalidomide", "Technique": "CD107a lysosome-associated membrane protein-1 (LAMP-1) was used to measure NK-, NKT-like-, and CD8-cell cytotoxic activity", "Controlled_Technique": "Degranulation assay", "Immune_System-Function_enhanced/numbers_increased": "NK Cell-Mediated Natural Cytotoxicity and ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, 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and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Mel-624", "Dose": "500nM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1162", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Mel-888", "Dose": "500nM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint 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"Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1213", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "26692933", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "Human NK92 cells used as effector cells, and HL-60 cells as target cells", "Dose": "DAC (0.2-1.0 μM)", "Technique": "CFSE 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cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "17545540", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Mel 275", "Dose": "1 µM /L", "Technique": "Flow cytometry,Cytotoxicity assay,IFN-g release assay", "Controlled_Technique": "Flow cytometry; Cytotoxicity/release assay; Cellular cytotoxicity/function assay", "Immune_System-Function_enhanced/numbers_increased": "CTL IFNγ HLA class I antigens and of ICAM-1", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; ICAM-1 / CD54; IFN-γ; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1271", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "28404876", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "KG1a", "Dose": "(1 μM or 5 μM)", "Technique": "sandwich ELISA,Flow cytometry", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", 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differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "28404876", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "NB4 cells", "Dose": "(1 μM or 5 μM)", "Technique": "sandwich ELISA,Flow cytometry", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "NKG2DL (MICA, MICB, ULBPs1-3)-on the surface of AML cells", "Controlled_Terms_Function_enhanced_Number_increased": "MICA; MICB; NKG2D ligand; MICA/MICB", "Immune_System-Function_inhibited/numbers_decreased": "release of soluble sNKG2DL from AML cells", "Controlled_Terms_Function_inhibited_Number_decreased": "Soluble NKG2D ligand", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1314", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "27416831", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "4T1", "Dose": "(0, 0.75, 1.5, and 3.0 μM) of decitabine for 24 and 48 h", "Technique": "Flow cytometry,qPCR", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "Her-2-neu and MHC class I molecules on tumor cells cancer testis antigens", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; HER2 / ERBB2; Cancer-testis antigens;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1377", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "24270737", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "KG-1", "Dose": "0-10 µM", "Technique": "RT-PCR analysis,Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "PD-L1, PD-L2, PD-1 and CTLA4 expression in AML cell lines,", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L2 / PDCD1LG2; PD-1 / PDCD1; CTLA-4; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1379", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "24270737", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "THP1 cells", "Dose": "0-10 µM", "Technique": "RT-PCR analysis,Flow cytometry", 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"STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single Drug", "PMID": "19997099", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung", "System": "A549 (lung)", "Dose": "GEM (1 μm)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Human leucocyte antigen class 1 on tumors", "Controlled_Terms_Function_enhanced_Number_increased": "HLA class I antigen", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1357", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase", "KEGG_Drug__ID": "D02368", "Pubchem_ID": "60750", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single Drug", "PMID": "24128051", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC(Lung)", "System": "H292 cells", "Dose": "0·05 μm", "Technique": "real-time PCR + Western blot+Flow cytometry", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "lymphokine-activated killer (LAK) cells FasL expressionon tumor cells Gemcitabine induces apoptosis of mFasL-expressing H292 cells +induces caspase-8 and caspase-3 cleavage in H292 cells", "Controlled_Terms_Function_enhanced_Number_increased": "Fas ligand / FasL / 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"Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/607", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Ribonucleotide reductase inhibition; DNA synthesis inhibition; induces ICD", "KEGG_Drug__ID": "D02368", "Pubchem_ID": "60750", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single", "PMID": "38988937", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Murine Lewis lung carcinoma (LLC)", "System": "LLC", "Dose": "2 µg/mL; 24 h", "Technique": "Western blot; flow cytometry; ELISA; apoptosis assay", "Controlled_Technique": "Increased CRT and HSP90; increased DC activation (CD11c+major histocompatibility complex (MHC)-II+), chemokines (CCL5, CXCL3, and CXCL10)", "Immune_System-Function_enhanced/numbers_increased": "CD11c / ITGAX; Calreticulin / CRT; Dendritic cells; CXCL10 / IP-10; CCL5 / RANTES", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/608", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Ribonucleotide reductase inhibition; DNA synthesis inhibition; induces ICD", "KEGG_Drug__ID": "D02368", "Pubchem_ID": "60750", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single", "PMID": "38988937", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Murine CMT-64 lung cancer cell line", "System": "CMT-64", "Dose": "2 µg/mL; 24 h", "Technique": "Western blot; flow cytometry; apoptosis assay", "Controlled_Technique": "Increased CRT and HSP90; increased DC activation (CD11c+major histocompatibility complex (MHC)-II+), chemokines (CCL5, CXCL3, and CXCL10)", "Immune_System-Function_enhanced/numbers_increased": "CD11c / ITGAX; Calreticulin / CRT; Dendritic cells; CXCL10 / IP-10; CCL5 / RANTES", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1628", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase", "KEGG_Drug__ID": "D02369", "Pubchem_ID": "60750", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single Drug", "PMID": "24128051", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC(Lung)", "System": "COLO 699", "Dose": "0·05 μm", "Technique": "real-time PCR + Western blot", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "FasL expressionon tumor cells Gemcitabine induces apoptosis of mFasL-expressing H292 cells", "Controlled_Terms_Function_enhanced_Number_increased": "Fas ligand / FasL / FASLG; 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"16-HBE", "Dose": "0·05 μm", "Technique": "real-time PCR + Western blot", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "FasL expressionon tumor cells Gemcitabine induces apoptosis of mFasL-expressing H292 cells", "Controlled_Terms_Function_enhanced_Number_increased": "Fas ligand / FasL / FASLG; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/71", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase", "KEGG_Drug__ID": "D02370", "Pubchem_ID": "60750", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single Drug", "PMID": "29872551", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "A549", "Dose": "200 nM", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD1d", "Controlled_Terms_Function_enhanced_Number_increased": "CD1d", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/632", "Drug": "CX-5461", "Drug_category": "Others/combination", "Drugbank_ID": "DB16846", "Target/s_or_mechanism_of_action": "Inhibits RNA polymerase I and rDNA transcription; induces nucleolar stress and DNA-damage response", "KEGG_Drug__ID": null, "Pubchem_ID": "12254622", "STR_LINK_(SMILES)": "CC1=NC=C(CNC(C2=C3N(C(C=CC=C4)=C4S3)C5=C(C=CC(N6CCCN(C)CC6)=N5)C2=O)=O)N=C1", "Single/Combination": "Single", "PMID": "41315184", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Human multiple-myeloma cell line", "System": "RPMI-8226", "Dose": "200 nM, 48 h", "Technique": "Flow cytometry; NK-cell CD107a degranulation assay; Western blot; qPCR", "Controlled_Technique": "Increased expression of NK-activating ligands; increased HLA-ABC", "Immune_System-Function_enhanced/numbers_increased": "Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": "HLA-E-mediated inhibition of NK-cell activity", "Immune_System-Function_inhibited/numbers_decreased": "NK cells", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "HLA-E upregulation", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1441", "Drug": "5-azacytidine and trichostatin A (TSA)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00928, DB04297", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.\n TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444, 444732", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O,\n C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Combination", "PMID": "17725605", "Cancer_Type": "Hpv16-Expressing Tumors", "Cancer_Type_Description": "Human Papilloma Virus 16-Associated Tumours", "System": "TC-1/A9 (MHC class I-deficient)", "Dose": "50 µm 5-azaC and 10 ng/ml TSA", "Technique": "Flow cytometry, quantitative real-time RT-PCR,Western blot analysis", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "MHC class I molecules apoptosis,APM genes, namely TAP-2 and LMP-7", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Apoptosis; Antigen presentation; TAP2; LMP7 / PSMB8;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/912", "Drug": "Chidamide (CS055/HBI-8000/Tucidinostat) and Rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB06334, DB00073", "Target/s_or_mechanism_of_action": "Histone deacetylase inhibitor", "KEGG_Drug__ID": "D10993, \n D02994", "Pubchem_ID": "12136798, 46505820", "STR_LINK_(SMILES)": "NC1=CC(F)=CC=C1NC(=O)C1=CC=C(CNC(=O)\\C=C\\C2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "31907371", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Diffuse Large B Cell Lymphoma (DLBCL)", "System": "Su-DHL-6", "Dose": "10 µg/ml Rituximab,5, 10, 20 and 40 µM Chidamide", "Technique": "MTT test", "Controlled_Technique": "Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/940", "Drug": "5-azacytidine+BI 836858, a fully human, Fc-engineered, anti-CD33 antibody", "Drug_category": "Others/combination", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Combination", "PMID": "27013443", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "primary AML blasts+autologous NK-cell", "Dose": "5-azacytidine (2 µM)+ BI 836858 or BI 836847 (10 μg/mL)", "Technique": "Flow cytometry, ADCC assay", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK-cell activation-natural killer ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/941", "Drug": "5-azacytidine+BI 836858, a fully human, Fc-engineered, anti-CD33 antibody", "Drug_category": "Others/combination", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Combination", "PMID": "27013443", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "primary AML blasts +allogenic NK-cell", "Dose": "5-azacytidine (2 µM)+ BI 836858 or BI 836847 (10 μg/mL)", "Technique": "Flow cytometry, ADCC assay", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK-cell activation-natural killer ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1057", "Drug": "5-fluorouracil (5-FU)+IFN-a", "Drug_category": "Others/combination", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D00584", "Pubchem_ID": "3385", "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "25368252", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": "Panc02 cells", "Dose": "5-FU (10 mM)+IFN-a (1000 IU/mL).", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "major histocompatibility complex class I and NKG2D ligands on tumor", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; NKG2D / KLRK1; NKG2D ligand", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/752", "Drug": "7A7", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29056908", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung", "System": "D122-reactive CD8+ T cells were incubated with D122", "Dose": "(1 μg/ml, 96 h)", "Technique": "ELISA,vitro lactate dehydrogenase assay", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells-mediated lysis. IFN-γ production by D122-specific CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; IFN-γ; Cytotoxicity / cytolysis; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/841", "Drug": "7A7 a surrogate antibody that recognizes murine EGFR", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29056908", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Mama", "System": "4T1", "Dose": "1 μg/ml", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC-I expression", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/860", "Drug": "7A7 a surrogate antibody that recognizes murine EGFR", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29056908", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": "CT26", "Dose": "1 μg/ml", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC-I expression", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1315", "Drug": "7A7 a surrogate antibody that recognizes murine EGFR", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29056908", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Mama", "System": "F3II", "Dose": "1 μg/ml", "Technique": "Flow cytometry, qPCR", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "MHC-I expression, H-2K and H-2D β2-m, LMP subunits, PA28α, BLH, TAPs, ERAAP1, tapasin, calnexin, calreticulin, PDI, as well as ERp57", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Tapasin; Calnexin; Calreticulin / CRT; ERp57 / PDIA3; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1328", "Drug": "7A7 a surrogate antibody that recognizes murine EGFR", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29056908", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung", "System": "D122", "Dose": "1 μg/ml", "Technique": "Flow cytometry, qPCR", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "MHC-I expression, H-2K and H-2D β2-m, LMP subunits, PA28α, BLH, TAPs, ERAAP1, tapasin, calnexin, calreticulin, PDI, as well as ERp57", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Tapasin; Calnexin; Calreticulin / CRT; ERp57 / PDIA3; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/726", "Drug": "Afatinib followed by Trastuzumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB08916, DB00072", "Target/s_or_mechanism_of_action": "Afatinib is a potent and selective, irreversible ErbB family blocker. Afatinib covalently binds to and irreversibly blocks signaling from all homo and heterodimers formed by the ErbB family members EGFR (ErbB1), HER2 (ErbB2), ErbB3 and ErbB4.\n Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D09724, D03257", "Pubchem_ID": "10184653,\n 46507516", "STR_LINK_(SMILES)": "CN(C)C\\C=C\\C(=O)NC1=C(O[C@H]2CCOC2)C=C2N=CN=C(NC3=CC(Cl)=C(F)C=C3)C2=C1", "Single/Combination": "Combination", "PMID": "28735814", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "SKBR3", "Dose": "Afatinib 2 μM concentration and a 48 h timepoint for TKI exposure", "Technique": "High content analysis, LDH-release ADCC assays", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay; LDH-releasing assays", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "decreased HER2 levels in SKBR3 (afatinib 0.8 ± 0.1 fold)", "Controlled_Terms_Function_inhibited_Number_decreased": "HER2 / ERBB2; Expression / abundance phenotype", "Immune_System_function_unaffected": "trastuzumab-mediated ADCC", "Controlled_Terms_Unaffected": "ADCC; Antibody-dependent cytotoxicity", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/727", "Drug": "Afatinib followed by Trastuzumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB08916, DB00072", "Target/s_or_mechanism_of_action": "Afatinib is a potent and selective, irreversible ErbB family blocker. Afatinib covalently binds to and irreversibly blocks signaling from all homo and heterodimers formed by the ErbB family members EGFR (ErbB1), HER2 (ErbB2), ErbB3 and ErbB4.\n Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D09724, D03257", "Pubchem_ID": "10184653,\n 46507516", "STR_LINK_(SMILES)": "CN(C)C\\C=C\\C(=O)NC1=C(O[C@H]2CCOC2)C=C2N=CN=C(NC3=CC(Cl)=C(F)C=C3)C2=C1", "Single/Combination": "Combination", "PMID": "28735814", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "MCF-7", "Dose": "Afatinib 2 μM concentration and a 48 h timepoint for TKI exposure", "Technique": "High content analysis, LDH-release ADCC assays", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay; LDH-releasing assays", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "decreased HER2 levels in SKBR3 (afatinib 0.7 ± 0.2 fold)", "Controlled_Terms_Function_inhibited_Number_decreased": "HER2 / ERBB2; Expression / abundance phenotype", "Immune_System_function_unaffected": "trastuzumab-mediated ADCC", "Controlled_Terms_Unaffected": "ADCC; Antibody-dependent cytotoxicity", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/932", "Drug": "Anti-CD3 5 ug/mL+ trametinib 10 nM", "Drug_category": "Others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "31648326", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "CD3+CD8+ cells from AML mice", "Dose": "anti-CD3 5 ug/mL+ trametinib 10 nM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD44+CD62L–,", "Controlled_Terms_Function_enhanced_Number_increased": "CD44", "Immune_System-Function_inhibited/numbers_decreased": "CD44–CD62L+", "Controlled_Terms_Function_inhibited_Number_decreased": "CD44", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/736", "Drug": "Anti-PD-1 and romidepsin", "Drug_category": "Others/combination", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "57515973", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Combination", "PMID": "26964571", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "LKR + tumor CD8 and CD4 T cells", "Dose": null, "Technique": "ELISPOT assay", "Controlled_Technique": "ELISpot/FluoroSpot assay", "Immune_System-Function_enhanced/numbers_increased": "CD8 and CD4 cells that produce IFNγ IFNγ", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/84", "Drug": "Apicidin", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Apicidin is a fungal metabolite, as well as a histone deacetylase inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": "6918328", "STR_LINK_(SMILES)": "CC[C@H](C)[C@H]1C(=O)N2CCCC[C@@H]2C(=O)N[C@H](C(=O)N[C@H](C(=O)N1)CC3=CN(C4=CC=CC=C43)OC)CCCCCC(=O)CC", "Single/Combination": "Single Drug", "PMID": "28167529", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": "SKOV3", "Dose": "0-10 μm", "Technique": "real-time RT-PCR analysis", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "proangiogenic chemokine IL-8 (CXCL-8)", "Controlled_Terms_Negative_Regulation": "IL-8 / CXCL8; IL-8/CXCL8", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/933", "Drug": "Azacitidine (AZA) in combination with allogeneic NK cells generated from CD34+ hematopoietic stem and progenitor cells (HSPC-NK cells)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Combination", "PMID": "29138222", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "THP-1 +allogeneic NK cells generated from CD34+ hematopoietic stem and progenitor cells (HSPC-NK cells)", "Dose": "0.1 to 1 µM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cell–mediated killing", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/935", "Drug": "Azacitidine (AZA) in combination with allogeneic NK cells generated from CD34+ hematopoietic stem and progenitor cells (HSPC-NK cells)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Combination", "PMID": "29138222", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "KG1a cells+allogeneic NK cells generated from CD34+ hematopoietic stem and progenitor cells (HSPC-NK cells)", "Dose": "0.1 to 1 µM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cell–mediated killing", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/936", "Drug": "Azacitidine (AZA) in combination with allogeneic NK cells generated from CD34+ hematopoietic stem and progenitor cells (HSPC-NK cells)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D03021", "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Combination", "PMID": "29138222", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "Primary AML cells obtained from 5 different patients +HSPC-NK cells", "Dose": "1 µM AZA", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cell–mediated killing", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1226", "Drug": "AZD1480", "Drug_category": "Others/combination", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Combination", "PMID": "21164517", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Myeloma", "System": "U266", "Dose": "0.5 - 3 μM AZD1480, IL-6 4ng/ml", "Technique": "Flow cytometry using Annexin V/Propidium Iodide staining", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "AZD1480 induces apoptosis of myeloma cells growth stimulated by IL-6", "Controlled_Terms_Function_enhanced_Number_increased": "IL-6; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1227", "Drug": "AZD1480", "Drug_category": "Others/combination", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Combination", "PMID": "21164517", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Myeloma", "System": "Kms.11", "Dose": "0.5 - 3 μM AZD1480, IL-6 4ng/ml", "Technique": "Flow cytometry using Annexin V/Propidium Iodide staining", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "AZD1480 induces apoptosis of myeloma cells growth stimulated by IL-6", "Controlled_Terms_Function_enhanced_Number_increased": "IL-6; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1519", "Drug": "AZD1480", "Drug_category": "Others/combination", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Combination", "PMID": "25216185", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "HCT116", "Dose": "0 - 5 μM AZD1480, IL-6 4ng/ml", "Technique": "western blot analysis, Flow cytometry using Annexin V/Propidium Iodide staining", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": "IL-6-inducible JAK2/STAT3 signaling", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6; IL-6/JAK/STAT3 signaling; STAT3; JAK2", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1520", "Drug": "AZD1480", "Drug_category": "Others/combination", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Combination", "PMID": "25216185", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "HT29", "Dose": "0 - 5 μM AZD1480, IL-6 4ng/ml", "Technique": "western blot analysis, Flow cytometry using Annexin V/Propidium Iodide staining", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": "IL-6-inducible JAK2/STAT3 signaling", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6; IL-6/JAK/STAT3 signaling; STAT3; JAK2", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1521", "Drug": "AZD1480", "Drug_category": "Others/combination", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": "16659841", "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Combination", "PMID": "25216185", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "SW480", "Dose": "0 - 5 μM AZD1480, IL-6 4ng/ml", "Technique": "western blot analysis, Flow cytometry using Annexin V/Propidium Iodide staining", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": "IL-6-inducible JAK2/STAT3 signaling", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6; IL-6/JAK/STAT3 signaling; STAT3; JAK2", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/315", "Drug": "AZD6244 (MEKi) and BMS-345541 (IKKi)", "Drug_category": "Others/combination", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": "D09666", "Pubchem_ID": "10127622", "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Combination", "PMID": "25256614", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "WM266-4", "Dose": "1μM AZD6244 (MEKi) and 0.5μM BMS-345541 (IKKi)", "Technique": "Western blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "cleavage of caspase3- apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase activation; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/316", "Drug": "AZD6244 (MEKi) and BMS-345541 (IKKi)", "Drug_category": "Others/combination", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": "D09666", "Pubchem_ID": "10127622", "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Combination", "PMID": "25256614", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "A375", "Dose": "1μM AZD6244 (MEKi) and 0.5μM BMS-345541 (IKKi)", "Technique": "Western blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "cleavage of caspase3- apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase activation; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/317", "Drug": "AZD6244 (MEKi) and BMS-345541 (IKKi)", "Drug_category": "Others/combination", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": "D09666", "Pubchem_ID": "10127622", "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Combination", "PMID": "25256614", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "BRafV600E-4434 melanoma cells", "Dose": "0.5μM AZD6244 (MEKi) and 0.1μM BMS-345541 (IKKi)", "Technique": "Western blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "cleavage of caspase3- apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase activation; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/318", "Drug": "AZD6244 (MEKi)/selumetinib and BMS-345541 (IKKi)", "Drug_category": "Others/combination", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": "D09666", "Pubchem_ID": "10127622", "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Combination", "PMID": "25256614", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "501mel human melanoma cells", "Dose": "1μM AZD6244 (MEKi) and 0.5μM BMS-345541 (IKKi)", "Technique": "Western blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "cleavage of caspase3- apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase activation; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/751", "Drug": "B7-H3 × CD3 BiAb with MEK inhibitor trametinib", "Drug_category": "Others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "32984002", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small-Cell Lung Cancer (NSCLC) And Bladder Cancer (BC)", "System": "A549, H460, T24", "Dose": "BiAb 5μg/mL.", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IFN-y", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/965", "Drug": "B7-H3 × CD3 BiAb with MEK inhibitor trametinib", "Drug_category": "Others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "32984002", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small-Cell Lung Cancer (NSCLC) And Bladder Cancer (BC)", "System": "H460, T24", "Dose": "BiAb 5μg/mL+ 10μM trametinib+ T cell", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD25, CD69", "Controlled_Terms_Function_enhanced_Number_increased": "CD25 / IL2RA; CD69", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD4+/CD8+ T\n cells", "Controlled_Terms_Unaffected": "CD4; CD8; T cells; CD8+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/260", "Drug": "B7-H3 × CD3 BiAb with MEK inhibitor trametinib", "Drug_category": "Others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "32984002", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small-Cell Lung Cancer (NSCLC) And Bladder Cancer (BC)", "System": "A549, H460, T24", "Dose": "10μM trametinib", "Technique": "Western Blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "B7-H3 expression", "Controlled_Terms_Function_enhanced_Number_increased": "B7-H3 / CD276; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": "Posphorylated MEK", "Controlled_Terms_Function_inhibited_Number_decreased": "MEK phosphorylation", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/636", "Drug": "Belantamab mafodotin (GSK2857916)", "Drug_category": "Others/combination", "Drugbank_ID": "DB15719", "Target/s_or_mechanism_of_action": "Binds BCMA (TNFRSF17) on multiple myeloma cells; delivers MMAF, inducing apoptosis. Promotes immunogenic cell death (ICD), DAMP release, and dendritic-cell maturation.", "KEGG_Drug__ID": "D11595", "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "34253590", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Human BCMA-positive NCI-H929 cells; human monocyte-derived immature dendritic cells used in co-culture experiments", "System": "NCI-H929 cells", "Dose": "0.1, 1, and 10 µg/mL; tumor cells treated for 48 h, followed by 24 h dendritic-cell co-culture", "Technique": "Flow cytometry; ELISA; extracellular ATP assay; immunoblotting", "Controlled_Technique": "calreticulin, HMGB1 and ATP release, HSP70/HSP90-associated signals, IL-8 release, and dendritic-cell maturation markers CD40, CD83, and CD86; increased PERK/eIF2α phosphorylation and BAP31 cleavage", "Immune_System-Function_enhanced/numbers_increased": "CD83; CD86; HMGB1; Calreticulin / CRT; IL-8 / CXCL8; CD40", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/634", "Drug": "BMH-21", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Inhibits RNA polymerase I, promotes degradation of the RPA194 subunit and induces nucleolar stress", "KEGG_Drug__ID": null, "Pubchem_ID": "3508054", "STR_LINK_(SMILES)": "CN(C)CCNC(=O)C1=CC=CN2C1=NC3=CC4=CC=CC=C4C=C3C2=O", "Single/Combination": "Single", "PMID": "41315184", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Human multiple-myeloma cell line", "System": "RPMI-8226", "Dose": "400 nM, 48 h", "Technique": "Flow cytometry for HLA-E, HLA-ABC, CD38; NK-cell degranulation and ADCC assays", "Controlled_Technique": "Enhanced NK-cell activation", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": "NKG2D (an activating receptor) and TIGIT (an inhibitory receptor)", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "NR", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "No significant HLA-E upregulation reported under the tested conditions", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/633", "Drug": "BMH-21", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Inhibits RNA polymerase I, promotes degradation of the RPA194 subunit and induces nucleolar stress", "KEGG_Drug__ID": null, "Pubchem_ID": "3508054", "STR_LINK_(SMILES)": "CN(C)CCNC(=O)C1=CC=CN2C1=NC3=CC4=CC=CC=C4C=C3C2=O", "Single/Combination": "Single", "PMID": "41315184", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Human multiple-myeloma cell line", "System": "SKO-007(J3)", "Dose": "400 nM, 48 h", "Technique": "Flow cytometry; NK-cell CD107a degranulation assay; IFN-γ/TNF-α measurement; Western blot; qPCR", "Controlled_Technique": "Increased NK-cell degranulation; increased IFN-γ and TNF-α production; increased NK-activating ligand expression", "Immune_System-Function_enhanced/numbers_increased": "IFN-γ; Degranulation; TNF-α / TNF; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": "NKG2D (an activating receptor) and TIGIT (an inhibitory receptor)", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "No significant HLA-E upregulation reported under the tested conditions", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/275", "Drug": "Bortezomib +mocetinostat (mgcd0103)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00188, DB11830", "Target/s_or_mechanism_of_action": "Bortezomib is a reversible inhibitor of the 26S proteasome, which is made up of a 20S core complexed with a 19S regulatory complex. Individual β-subunits allow specific catalytic action of the 20S core.\n Mocetinostat (MGCD0103) is a benzamide histone deacetylase inhibitor", "KEGG_Drug__ID": "D03150, D09641", "Pubchem_ID": "387447, 9865515", "STR_LINK_(SMILES)": "CC(C)C[C@H](NC(=O)[C@H](CC1=CC=CC=C1)NC(=O)C1=CN=CC=N1)B(O)O,\n NC1=CC=CC=C1NC(=O)C1=CC=C(CNC2=NC=CC(=N2)C2=CC=CN=C2)C=C1", "Single/Combination": "Combination", "PMID": "20880107", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Hodgkin Lymphoma", "System": "HD-LM2(of T cell origin)", "Dose": "MGCD0103 (1 μmol/l), bortezomib (20 nmol/l)", "Technique": "Western blot, Flow cyto metry", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "induction of apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": "NF-kB activation", "Controlled_Terms_Function_inhibited_Number_decreased": "NF-κB activation", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/276", "Drug": "Bortezomib +mocetinostat (mgcd0103)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00188, DB11830", "Target/s_or_mechanism_of_action": "Bortezomib is a reversible inhibitor of the 26S proteasome, which is made up of a 20S core complexed with a 19S regulatory complex. Individual β-subunits allow specific catalytic action of the 20S core.\n Mocetinostat (MGCD0103) is a benzamide histone deacetylase inhibitor", "KEGG_Drug__ID": "D03150, D09641", "Pubchem_ID": "387447, 9865515", "STR_LINK_(SMILES)": "CC(C)C[C@H](NC(=O)[C@H](CC1=CC=CC=C1)NC(=O)C1=CN=CC=N1)B(O)O,\n NC1=CC=CC=C1NC(=O)C1=CC=C(CNC2=NC=CC(=N2)C2=CC=CN=C2)C=C1", "Single/Combination": "Combination", "PMID": "20880107", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Hodgkin Lymphoma", "System": "L428 (of B cell origin)", "Dose": "MGCD0103 (1 μmol/l), bortezomib (20 nmol/l)", "Technique": "Western blot, Flow cyto metry", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "induction of apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": "NF-kB activation", "Controlled_Terms_Function_inhibited_Number_decreased": "NF-κB activation", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/277", "Drug": "Bortezomib +mocetinostat (mgcd0103)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00188, DB11830", "Target/s_or_mechanism_of_action": "Bortezomib is a reversible inhibitor of the 26S proteasome, which is made up of a 20S core complexed with a 19S regulatory complex. Individual β-subunits allow specific catalytic action of the 20S core.\n Mocetinostat (MGCD0103) is a benzamide histone deacetylase inhibitor", "KEGG_Drug__ID": "D03150, D09641", "Pubchem_ID": "387447, 9865515", "STR_LINK_(SMILES)": "CC(C)C[C@H](NC(=O)[C@H](CC1=CC=CC=C1)NC(=O)C1=CN=CC=N1)B(O)O,\n NC1=CC=CC=C1NC(=O)C1=CC=C(CNC2=NC=CC(=N2)C2=CC=CN=C2)C=C1", "Single/Combination": "Combination", "PMID": "20880107", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Hodgkin Lymphoma", "System": "KMH2(of B cell origin)", "Dose": "MGCD0103 (1 μmol/l), bortezomib (20 nmol/l)", "Technique": "Western blot, Flow cyto metry", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "induction of apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": "NF-kB activation", "Controlled_Terms_Function_inhibited_Number_decreased": "NF-κB activation", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1589", "Drug": "Cetuximab + ALT-803 ( genetically modified IL-15 plus the IL-15 receptor alpha protein (IL15Rα) fused to the Fc portion of IgG1)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "31338557", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "Cal27 +Purifed human CD56+ NK cells incubated overnight stimulated with ALT-803 (10 ng/ml)", "Dose": "100 μg/ml cetuximab", "Technique": "51Cr release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell-mediated ADCC IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/668", "Drug": "Bortezomib( a proteasome inhibitor) and SAHA( Vorinostat)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00188, DB02546", "Target/s_or_mechanism_of_action": "Bortezomib is a reversible inhibitor of the 26S proteasome, which is made up of a 20S core complexed with a 19S regulatory complex. Individual β-subunits allow specific catalytic action of the 20S core.\n Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D03150,D06320", "Pubchem_ID": "387447, 5311", "STR_LINK_(SMILES)": "CC(C)C[C@H](NC(=O)[C@H](CC1=CC=CC=C1)NC(=O)C1=CN=CC=N1)B(O)O,\n ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "25591912", "Cancer_Type": "Cervical Cancer", "Cancer_Type_Description": "Cervical Cancer", "System": "Luciferase-expressing TC-1 tumor cells +HPV16 E7-specific CTLs", "Dose": "bortezomib (3.5 nM) and SAHA (12.5 μM) for 24 h", "Technique": "IVIS luminescence imaging system for Bioluminescence signals-quantification of luminescence intensity", "Controlled_Technique": "Bioluminescence/luciferase assay; Bioluminescence/luciferase assay", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cell-mediated cytotoxicity.", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Cytotoxicity / cytolysis; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1480", "Drug": "BRAFi PLX4720+ IFNy", "Drug_category": "Others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": "24180719", "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "26943572", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer", "System": "3601R", "Dose": "BRAFi PLX4720 10μM) +mIFN-y (200ng/ml)", "Technique": "FACS, western blot", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1625", "Drug": "BRAFi PLX4720+ IFNy", "Drug_category": "Others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": "24180719", "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "26943572", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer", "System": "8505c", "Dose": "BRAFi PLX4720 (10μM )+hIFN-y (500U/ml)", "Technique": "Quantitative PCR, Western blot", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 protein expression and mRNA exxpression phospho ERK", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; ERK / MAPK; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1626", "Drug": "BRAFi PLX4720+ IFNy", "Drug_category": "Others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": "24180719", "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "26943572", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer", "System": "BCPAP", "Dose": "BRAFi PLX4720 (10μM )+hIFN-y (500U/ml)", "Technique": "Quantitative PCR, Western blot", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 protein expression and mRNA exxpression phospho ERK", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; ERK / MAPK; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1627", "Drug": "BRAFi PLX4720+ IFNy", "Drug_category": "Others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": "24180719", "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "26943572", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer", "System": "SW1736", "Dose": "BRAFi PLX4720 (10μM )+hIFN-y (500U/ml)", "Technique": "Quantitative PCR, Western blot", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 protein expression", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/85", "Drug": "Carboplatin +paclitaxel", "Drug_category": "Others/combination", "Drugbank_ID": "DB00958, DB01229", "Target/s_or_mechanism_of_action": "1. Carboplatin undergoes activation inside cells and forms reactive platinum complexes that cause the intra- and inter-strand cross-linkage of DNA molecules within the cell. 2.Pacilitaxel-Inhibition of tubulin depolymerization", "KEGG_Drug__ID": "1. D01363, 2. D00491", "Pubchem_ID": "38904, 36314", "STR_LINK_(SMILES)": "carboplatin-[H][N]([H])([H])[Pt]1(OC(=O)C2(CCC2)C(=O)O1)[N]([H])([H])[H], pacilitaxel- [H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Combination", "PMID": "20683396", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": "SKOV-3", "Dose": null, "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Macrophage chemoattractant protein-1 (MCP-1)", "Controlled_Terms_Negative_Regulation": "CCL2 / MCP-1; Macrophages", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/840", "Drug": "Carboplatin and a taxane", "Drug_category": "Others/combination", "Drugbank_ID": "DB00958", "Target/s_or_mechanism_of_action": "Carboplatin undergoes activation inside cells and forms reactive platinum complexes that cause the intra- and inter-strand cross-linkage of DNA molecules within the cell.", "KEGG_Drug__ID": "D01363", "Pubchem_ID": "38904", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt]1(OC(=O)C2(CCC2)C(=O)O1)[N]([H])([H])[H]", "Single/Combination": "Combination", "PMID": "29500278", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "MDA-MB-231 TNBC cells or BT474 HER2+ Breast cancer cells +post-NT patient sera", "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "ALDEFLUOR+ (% of MDA-MB-231) and ESA+CD44+CD24−/low (% of BT474)-)-cancer stem-like cell (CSC) phenotype and contributing to tumor relapse", "Controlled_Terms_Negative_Regulation": "CD44; ALDEFLUOR-positive cells", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/19", "Drug": "Celecoxib", "Drug_category": "Others/combination", "Drugbank_ID": "DB00482", "Target/s_or_mechanism_of_action": "celecoxib is a selective noncompetitive inhibitor of cyclooxygenase-2 (COX-2) enzyme.", "KEGG_Drug__ID": "D00567", "Pubchem_ID": "2662", "STR_LINK_(SMILES)": "CC1=CC=C(C=C1)C1=CC(=NN1C1=CC=C(C=C1)S(N)(=O)=O)C(F)(F)F", "Single/Combination": "Single Drug", "PMID": "27926489", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma", "System": "769-p", "Dose": null, "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "granulocyte-macrophage colony stimulating factor (GM-CSF)", "Controlled_Terms_Function_inhibited_Number_decreased": "GM-CSF / CSF2; Macrophages; Granulocytes", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/20", "Drug": "Celecoxib and sunitinib", "Drug_category": "Others/combination", "Drugbank_ID": "DB00482, DB01268", "Target/s_or_mechanism_of_action": "celecoxib is a selective noncompetitive inhibitor of cyclooxygenase-2 (COX-2) enzyme. \n sunitinib Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": "D00567,D06402", "Pubchem_ID": "2662, 5329102", "STR_LINK_(SMILES)": "CC1=CC=C(C=C1)C1=CC(=NN1C1=CC=C(C=C1)S(N)(=O)=O)C(F)(F)F,\n CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Combination", "PMID": "27926489", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma", "System": "769-p", "Dose": null, "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "granulocyte-macrophage colony stimulating factor (GM-CSF)", "Controlled_Terms_Function_inhibited_Number_decreased": "GM-CSF / CSF2; Macrophages; Granulocytes", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/900", "Drug": "CEP32496", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31540894", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Medullary Carcinoma", "System": "TT cells", "Dose": "CEP32496(0-100nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/966", "Drug": "CEP32496", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31540894", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung - Human Lung Adenocarcinoma", "System": "LC-2/ad", "Dose": "CEP32496(0-100nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "HLA-A,B,C", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; HLA-A", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1536", "Drug": "Cetuximab + (STING)-The intracellular DNA sensor stimulator of interferon genes", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "29496049", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "iDC+ NK + PCI15B", "Dose": "cetuximab (10ug/ml), cGAMP (10 ug/ml)-a STING activator", "Technique": "Western Blot,Flow cytometry,ELISA", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "DC maturation and NK activation phosphorylation of IRF3, IFNγ CD86, CD83 and HLA-DR and PD-L1 expression on DCs", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; MHC class II; HLA-DR; CD83; CD86; IFN-γ; Dendritic cells; PD-L1 immune checkpoint pathway; Expression / abundance phenotype; IRF3", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/201", "Drug": "Cetuximab + (STING)-The intracellular DNA sensor stimulator of interferon genes", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "29496049", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "iDC+ NK + JHU029", "Dose": "cetuximab (10ug/ml), cGAMP (10 ug/ml)-a STING activator", "Technique": "Western Blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "phosphorylation of IRF3", "Controlled_Terms_Function_enhanced_Number_increased": "IRF3", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1600", "Drug": "Cetuximab + ALT-803 ( genetically modified IL-15 plus the IL-15 receptor alpha protein (IL15Rα) fused to the Fc portion of IgG1)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "31338557", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "SCC2 + Purifed human CD56+ NK cells incubated overnight stimulated with ALT-803 (10 ng/ml)", "Dose": "100 μg/ml cetuximab", "Technique": "51Cr release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell-mediated ADCC IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1611", "Drug": "Cetuximab + ALT-803 ( genetically modified IL-15 plus the IL-15 receptor alpha protein (IL15Rα) fused to the Fc portion of IgG1)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "31338557", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "SCC47 + Purifed human CD56+ NK cells incubated overnight stimulated with ALT-803 (10 ng/ml)", "Dose": "100 μg/ml cetuximab", "Technique": "51Cr release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell-mediated ADCC IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; 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Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA,\n Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D02368,D08086, D04715, D00584, D03455", "Pubchem_ID": "60750, 60838, 149436, 3385, 46507042", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F, \n CCC1=C2CN3C(=CC4=C(COC(=O[C@]4(O)CC)C3=O)C2=NC2=CC=C(OC(=O)N3CCC(CC3)N3CCCCC3)C=C12, \n NC1=NC(=O)C2=C(NC[C@H](CNC3=CC=C(C=C3)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N2C=O)N1, \n FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "20399639", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Human Colon Carcinoma", "System": "HT29 cells rteated with drugs + IL-2-activated human PBMCs +cetuximab", "Dose": "gemcitabine at final concentration of 50 lg/ml +, levofolinic acid was added at a concentration of\n 2 microg/ml (10)4 M) +5-FU was added at a concentration of 500 microgram/ml + irinotecan at a concentration of\n 100 microgram/ml", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "cetuximab-mediated ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/372", "Drug": "Cetuximab + GILF regimen (Gem, Iri, Levofolinic acid and 5-FU)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00441\n DB00762\n DB11596\n DB00544\n DB00002", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase,\n Irinotecan inhibits the action of topoisomerase I,\n As levoleucovorin and leucovorin are analogs of tetrahydrofolate (THF), they are able to bypass DHFR reduction and act as a cellular replacement for the co-factor THF, thereby preventing these toxic side effects,\n Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA,\n Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D02368,D08086, D04715, D00584, D03455", "Pubchem_ID": "60750, 60838, 149436, 3385, 46507042", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F, \n CCC1=C2CN3C(=CC4=C(COC(=O[C@]4(O)CC)C3=O)C2=NC2=CC=C(OC(=O)N3CCC(CC3)N3CCCCC3)C=C12, \n NC1=NC(=O)C2=C(NC[C@H](CNC3=CC=C(C=C3)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N2C=O)N1, \n FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "20399639", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Human Colon Carcinoma", "System": "WiDr cells treated with drugs + IL-2-activated human PBMCs +cetuximab", "Dose": "gemcitabine at final concentration of 50 lg/ml +, levofolinic acid was added at a concentration of\n 2 microg/ml (10)4 M) +5-FU was added at a concentration of 500 microgram/ml + irinotecan at a concentration of\n 100 microgram/ml", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "cetuximab-mediated ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/373", "Drug": "Cetuximab + GILF regimen (Gem, Iri, Levofolinic acid and 5-FU)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00441\n DB00762\n DB11596\n DB00544\n DB00002", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase,\n Irinotecan inhibits the action of topoisomerase I,\n As levoleucovorin and leucovorin are analogs of tetrahydrofolate (THF), they are able to bypass DHFR reduction and act as a cellular replacement for the co-factor THF, thereby preventing these toxic side effects,\n Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA,\n Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D02368,D08086, D04715, D00584, D03455", "Pubchem_ID": "60750, 60838, 149436, 3385, 46507042", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F, \n CCC1=C2CN3C(=CC4=C(COC(=O[C@]4(O)CC)C3=O)C2=NC2=CC=C(OC(=O)N3CCC(CC3)N3CCCCC3)C=C12, \n NC1=NC(=O)C2=C(NC[C@H](CNC3=CC=C(C=C3)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N2C=O)N1, \n FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "20399639", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Human Colon Carcinoma", "System": "SW620 cells treated wirh drugs + IL-2-activated human PBMCs +Cetuximab", "Dose": "gemcitabine at final concentration of 50 lg/ml +, levofolinic acid was added at a concentration of\n 2 microg/ml (10)4 M) +5-FU was added at a concentration of 500 microgram/ml + irinotecan at a concentration of\n 100 microgram/ml", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "cetuximab-mediated ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; 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Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "ADCC of NK cells p-ERK activation", "Controlled_Terms_Function_enhanced_Number_increased": "ERK / MAPK; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/923", "Drug": "Chidamide (CS055/HBI-8000/Tucidinostat) and Rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB06334, DB00073", "Target/s_or_mechanism_of_action": "Histone deacetylase inhibitor", "KEGG_Drug__ID": "D10993, \n D02994", "Pubchem_ID": "12136798, 46505820", "STR_LINK_(SMILES)": "NC1=CC(F)=CC=C1NC(=O)C1=CC=C(CNC(=O)\\C=C\\C2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "31907371", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Diffuse Large B Cell Lymphoma (DLBCL)", "System": "Su-DHL-8", "Dose": "10 µg/ml Rituximab, 2, 4, 8 and 16 µM Chidamide", "Technique": "MTT test", "Controlled_Technique": "Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/374", "Drug": "Cetuximab + GILF regimen (Gem, Iri, Levofolinic acid and 5-FU)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00441\n DB00762\n DB11596\n DB00544\n DB00002", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase,\n Irinotecan inhibits the action of topoisomerase I,\n As levoleucovorin and leucovorin are analogs of tetrahydrofolate (THF), they are able to bypass DHFR reduction and act as a cellular replacement for the co-factor THF, thereby preventing these toxic side effects,\n Fluorouracil is an antineoplastic anti-metabolite. 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Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D03455, D08086, D04715, D00584", "Pubchem_ID": "46507042, 60838, 149436, 3385", "STR_LINK_(SMILES)": "CCC1=C2CN3C(=CC4=C(COC(=O[C@]4(O)CC)C3=O)C2=NC2=CC=C(OC(=O)N3CCC(CC3)N3CCCCC3)C=C12, \n NC1=NC(=O)C2=C(NC[C@H](CNC3=CC=C(C=C3)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N2C=O)N1, \n FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "20399639", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Human Colon Carcinoma", "System": "SW620 cells treated wirh drugs + IL-2-activated human PBMCs +Cetuximab", "Dose": "levofolinic acid was added at a concentration of 2 microg/ml (10)4 M) +5-FU was added at a concentration of 500 microgram/ml + irinotecan at a concentration of\n 100 microgram/ml", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "cetuximab-mediated ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/529", "Drug": "Emricasan", "Drug_category": "Others/combination", "Drugbank_ID": "DB05408", "Target/s_or_mechanism_of_action": "Hsp90 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": "12000240", "STR_LINK_(SMILES)": "C[C@@H](C(=O)N[C@@H](CC(=O)O)C(=O)COC1=C(C(=CC(=C1F)F)F)F)NC(=O)C(=O)NC2=CC=CC=C2C(C)(C)C", "Single/Combination": "Single", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "CTIAC11", "Dose": "10 µM; 24 h", "Technique": "ELISA, RT-qPCR", "Controlled_Technique": "Little IFN-β induction alone", "Immune_System-Function_enhanced/numbers_increased": "IFN-β", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1241", "Drug": "Cetuximab + IL-12", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "22770960", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "Cal27+ Purified NK cells were incubated overnight with IL-12", "Dose": "IL-12 (10 ng/mL),100 ug/mL of cetuximab", "Technique": "Cr-51 release assay,Flow cytometry", "Controlled_Technique": "Flow cytometry; Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "ADCC of NK cells p-ERK activation", "Controlled_Terms_Function_enhanced_Number_increased": "ERK / MAPK; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1242", "Drug": "Cetuximab + IL-12", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "22770960", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "UM-SCC74B+ + Purified NK cells were incubated overnight with IL-12", "Dose": "IL-12 (10 ng/mL),100 ug/mL of cetuximab", "Technique": "Cr-51 release assay,Flow cytometry", "Controlled_Technique": "Flow cytometry; 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Ipilimumab is a human IgG1 that binds CTLA-4, preventing the inhibition of T-cell mediated immune responses to tumors.", "KEGG_Drug__ID": "D03455, D04603", "Pubchem_ID": "46507042, 347910341", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "25832655", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Cancer (HNC)", "System": "JHU029- labeled with CFSE +peipheral NK cells + intratumoral Treg", "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "cetuximab-mediated ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/902", "Drug": "Cetuximab + motolimod", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002, DB12303", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR. Motolimod has been used in trials studying the treatment of Lymphoma, Tongue Cancer, Ovarian Cancer, Adult Solid Neoplasm, and Fallopian Tube Cancer, among others.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042, 16049404", "STR_LINK_(SMILES)": "CCCN(CCC)C(=O)C1=CC2=CC=C(C=C2N=C(N)C1)C1=CC=C(C=C1)C(=O)N1CCCC1", "Single/Combination": "Combination", "PMID": "29061643", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "UPCI:SCC090 cell cocultured with CD14+ monocytes from HNSCC patients", "Dose": "Cetuximab (10ug/ml) and motolimod (250nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD86 (an M1 marker)", "Controlled_Terms_Function_enhanced_Number_increased": "CD86", "Immune_System-Function_inhibited/numbers_decreased": "myeloid-derived suppressor cell (MDSC) CD163 (M2 marker),CD16", "Controlled_Terms_Function_inhibited_Number_decreased": "CD16 / FcγRIIIa; CD163; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "macrophage PD-L1", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; Macrophages; PD-L1 immune checkpoint pathway", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/890", "Drug": "Chidamide (CS055/HBI-8000/Tucidinostat) and Rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB06334, DB00073", "Target/s_or_mechanism_of_action": "Histone deacetylase inhibitor", "KEGG_Drug__ID": "D10993, \n D02994", "Pubchem_ID": "12136798, 46505820", "STR_LINK_(SMILES)": "NC1=CC(F)=CC=C1NC(=O)C1=CC=C(CNC(=O)\\C=C\\C2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "31907371", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Diffuse Large B Cell Lymphoma (DLBCL)", "System": "Su-DHL-10", "Dose": "10 µg/ml Rituximab,5, 10, 20 and 40 µM Chidamide", "Technique": "MTT test", "Controlled_Technique": "Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/903", "Drug": "Cetuximab + motolimod", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002, DB12303", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR. Motolimod has been used in trials studying the treatment of Lymphoma, Tongue Cancer, Ovarian Cancer, Adult Solid Neoplasm, and Fallopian Tube Cancer, among others.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042, 16049404", "STR_LINK_(SMILES)": "CCCN(CCC)C(=O)C1=CC2=CC=C(C=C2N=C(N)C1)C1=CC=C(C=C1)C(=O)N1CCCC1", "Single/Combination": "Combination", "PMID": "29061643", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "JHU029 cells cocultured with CD14+ monocytes from HNSCC patients", "Dose": "Cetuximab (10ug/ml) and motolimod (250nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD86 (an M1 marker)", "Controlled_Terms_Function_enhanced_Number_increased": "CD86", "Immune_System-Function_inhibited/numbers_decreased": "myeloid-derived suppressor cell (MDSC) CD163 (M2 marker),CD16", "Controlled_Terms_Function_inhibited_Number_decreased": "CD16 / FcγRIIIa; CD163; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "macrophage PD-L1", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; Macrophages; PD-L1 immune checkpoint pathway", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/789", "Drug": "Cetuximab + natural killer cell-activating cytokines", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "22770960", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "UM-SCC47 + Purified NK cells were incubated overnight with IL-2 (100 IU), IL-15 (10 ng/mL), or IL-21 (10 ng/mL)", "Dose": "100 ug/mL of cetuximab", "Technique": "Cr-51 release assay, ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "ADCC of NK cells IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/791", "Drug": "Cetuximab + natural killer cell-activating cytokines", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "22770960", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "Cal27+ Purified NK cells were incubated overnight with IL-2 (100 IU), IL-15 (10 ng/mL), or IL-21 (10 ng/mL)", "Dose": "100 ug/mL of cetuximab", "Technique": "Cr-51 release assay, ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "ADCC of NK cells IFN-γ,MIP-1α, RANTES, and IL-8", "Controlled_Terms_Function_enhanced_Number_increased": "IL-8 / CXCL8; IFN-γ; CCL3 / MIP-1α; CCL5 / RANTES; IL-8/CXCL8; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/792", "Drug": "Cetuximab + natural killer cell-activating cytokines", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": null, "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "UM-SCC74B+ + Purified NK cells were incubated overnight with IL-2 (100 IU), IL-15 (10 ng/mL), or IL-21 (10 ng/mL)", "Dose": "100 ug/mL of cetuximab", "Technique": "Cr-51 release assay, ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "ADCC of NK cells IFN-γ,MIP-1α, RANTES, and IL-8", "Controlled_Terms_Function_enhanced_Number_increased": "IL-8 / CXCL8; IFN-γ; CCL3 / MIP-1α; CCL5 / RANTES; IL-8/CXCL8; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/150", "Drug": "Cetuximab +IFNγ and TNFα", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "30192802", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "UM-SCC4-stimulated with 50IU/mL IFNγ and 30ng/mL TNFα", "Dose": "1μg/mL cetuximab", "Technique": "RT-qPCR,Enzyme-linked immunosorbent assay-ELISA,Western blotting", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "CCL2, CCL5, CXCL9, CXCL10 and IL-6", "Controlled_Terms_Function_enhanced_Number_increased": "IL-6; CCL2 / MCP-1; CCL5 / RANTES; CXCL10 / IP-10; CXCL9 / MIG", "Immune_System-Function_inhibited/numbers_decreased": "IL-1β Raf-MEK-ERK pathway and PI3K-AKT-mTOR, phosphorylation of p38 and ERK5", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-1 family; ERK / MAPK; AKT; PI3K", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/151", "Drug": "Cetuximab +IFNγ and TNFα", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "30192802", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "UM-SCC47-stimulated with 50IU/mL IFNγ and 30ng/mL TNFα", "Dose": "1μg/mL cetuximab", "Technique": "RT-qPCR,Enzyme-linked immunosorbent assay-ELISA,Western blotting", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "CCL2, CCL5, CXCL9, CXCL10 and IL-6", "Controlled_Terms_Function_enhanced_Number_increased": "IL-6; CCL2 / MCP-1; CCL5 / RANTES; CXCL10 / IP-10; CXCL9 / MIG", "Immune_System-Function_inhibited/numbers_decreased": "IL-1β Raf-MEK-ERK pathway and PI3K-AKT-mTOR, phosphorylation of p38 and ERK5", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-1 family; ERK / MAPK; AKT; PI3K", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/152", "Drug": "Cetuximab +IFNγ and TNFα", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "30192802", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "UM-SCC104-stimulated with 50IU/mL IFNγ and 30ng/mL TNFα", "Dose": "1μg/mL cetuximab", "Technique": "RT-qPCR,Enzyme-linked immunosorbent assay-ELISA,Western blotting", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "CCL2, CCL5, CXCL9, CXCL10 and IL-6", "Controlled_Terms_Function_enhanced_Number_increased": "IL-6; CCL2 / MCP-1; CCL5 / RANTES; CXCL10 / IP-10; CXCL9 / MIG", "Immune_System-Function_inhibited/numbers_decreased": "IL-1β Raf-MEK-ERK pathway and PI3K-AKT-mTOR, phosphorylation of p38 and ERK5", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-1 family; ERK / MAPK; AKT; PI3K", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/153", "Drug": "Cetuximab +IFNγ and TNFα", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "30192802", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "UM-SCC19-stimulated with 50IU/mL IFNγ and 30ng/mL TNFα", "Dose": "1μg/mL cetuximab", "Technique": "RT-qPCR,Enzyme-linked immunosorbent assay-ELISA,Western blotting", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "CCL2, CCL5, CXCL9, CXCL10 and IL-6", "Controlled_Terms_Function_enhanced_Number_increased": "IL-6; CCL2 / MCP-1; CCL5 / RANTES; CXCL10 / IP-10; CXCL9 / MIG", "Immune_System-Function_inhibited/numbers_decreased": "IL-1β", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-1 family", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/839", "Drug": "Cetuximab +IL-2 or IL-15", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "21308409", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast -Triple Negative Breast Cancer (TNBC))", "System": "IIB-BR-G + purified NK cells- in presence of IL-2 (100 IU/ml) or IL-15 (10 ng/ml).", "Dose": "Flow cytometry, \n assay.", "Technique": "Flow cytometry, \n assay.", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "IFN-γ NK activating receptors CD16 and NKG2D", "Controlled_Terms_Function_enhanced_Number_increased": "CD16 / FcγRIIIa; NKG2D / KLRK1; IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/895", "Drug": "Cetuximab +Poly-ICLC (a TLR3 agonist)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "30377565", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Nasopharyngeal Cancer (NPC)", "System": "DC, NK and C666-1 cells + autologous CD8 + T cells", "Dose": "10µg/ml cetuximab", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8 + T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/897", "Drug": "Cetuximab +Poly-ICLC (a TLR3 agonist)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "30377565", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Nasopharyngeal Cancer (NPC)", "System": "C666-1 + Myeloid-derived dendritic cells stimulated with 50µg/ml Poly-ICLC", "Dose": "10µg/ml cetuximab", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "DC maturation and stimulation CD83 and co-stimulatory markers CD80 and CD86-on Dendritic cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD80; CD83; CD86; CD80/CD86 costimulation; Dendritic cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1284", "Drug": "Cetuximab +Poly-ICLC (a TLR3 agonist)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "30377565", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Nasopharyngeal Cancer (NPC)", "System": "C666-1 + NK cells from healthy controls’ and NPC patients’stimulated with 10µg/ml Poly-ICLC", "Dose": "10µg/ml cetuximab", "Technique": "Flow cytometry, BATDA europium release assay,ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA); Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "CD56+ CD16+ NK cell- (ADCC) IFN-ɣ-by NK cells CD107a+ granzyme B+ high-on NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD16 / FcγRIIIa; CD56 / NCAM1; CD107a / LAMP1; ADCC; Granzyme B / GZMB; NK cells; Antibody-dependent cytotoxicity; Degranulation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/803", "Drug": "Cetuximab +VTX-2337 (motolimod)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002, DB12303", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR. Motolimod has been used in trials studying the treatment of Lymphoma, Tongue Cancer, Ovarian Cancer, Adult Solid Neoplasm, and Fallopian Tube Cancer, among others.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042, 16049404", "STR_LINK_(SMILES)": "CCCN(CCC)C(=O)C1=CC2=CC=C(C=C2N=C(N)C1)C1=CC=C(C=C1)C(=O)N1CCCC1", "Single/Combination": "Combination", "PMID": "23685782", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Cancer (HNC)", "System": "EGFR+ HNC cell lines -UM-22B + PBMC", "Dose": "VTX-2337 (250nM) ,cetuximab (10μg/mL)", "Technique": "51Cr release assays,cytokine ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Cytotoxicity/release assay; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "NK cells TNFα, IFNγ, and IL-12p40 cetuximab-mediated ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "TNF-α / TNF; IFN-γ; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/894", "Drug": "Cetuximab +VTX-2337 (motolimod)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002, DB12303", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR. Motolimod has been used in trials studying the treatment of Lymphoma, Tongue Cancer, Ovarian Cancer, Adult Solid Neoplasm, and Fallopian Tube Cancer, among others.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042, 16049404", "STR_LINK_(SMILES)": "CCCN(CCC)C(=O)C1=CC2=CC=C(C=C2N=C(N)C1)C1=CC=C(C=C1)C(=O)N1CCCC1", "Single/Combination": "Combination", "PMID": "23685782", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Cancer (HNC)", "System": "HLA-A*0201+ DC, NK cells + PCI-15B HNC cells coculture with autologous CD8+ T", "Dose": "VTX-2337 (800nM), cetuximab (10μg/mL)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD3; CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/896", "Drug": "Cetuximab +VTX-2337 (motolimod)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002, DB12303", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR. Motolimod has been used in trials studying the treatment of Lymphoma, Tongue Cancer, Ovarian Cancer, Adult Solid Neoplasm, and Fallopian Tube Cancer, among others.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042, 16049404", "STR_LINK_(SMILES)": "CCCN(CCC)C(=O)C1=CC2=CC=C(C=C2N=C(N)C1)C1=CC=C(C=C1)C(=O)N1CCCC1", "Single/Combination": "Combination", "PMID": "23685782", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Cancer (HNC)", "System": "Co-cultures of DC, NK cells and PCI-15B HNC cell", "Dose": "TLR8 agonist (VTX-2337, 800nM, 48 h), cetuximab (10μg/mL)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "DC CD80, CD83, and CD86", "Controlled_Terms_Function_enhanced_Number_increased": "CD80; CD83; CD86; CD80/CD86 costimulation; Dendritic cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/898", "Drug": "Cetuximab +VTX-2337 (motolimod)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002, DB12303", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR. Motolimod has been used in trials studying the treatment of Lymphoma, Tongue Cancer, Ovarian Cancer, Adult Solid Neoplasm, and Fallopian Tube Cancer, among others.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042, 16049404", "STR_LINK_(SMILES)": "CCCN(CCC)C(=O)C1=CC2=CC=C(C=C2N=C(N)C1)C1=CC=C(C=C1)C(=O)N1CCCC1", "Single/Combination": "Combination", "PMID": "23685782", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Cancer (HNC)", "System": "EGFR+ HNC cell lines - PCI-15B +PBMC", "Dose": "VTX-2337 (250nM) ,cetuximab (10μg/mL)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cell degranulation", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; Degranulation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1467", "Drug": "Cetuximab-based therapy", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D03455", "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "25769300", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal - Metastatic Colorectal Cancer", "System": "K562 + NK-cell from patients", "Dose": "10 μg/mL of cetuximab", "Technique": "51Cr release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell mediated ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; 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Cellular cytotoxicity/function assay", "Immune_System-Function_enhanced/numbers_increased": "PRAME-specific CTL", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; Cancer-testis antigens; PRAME antigen", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1444", "Drug": "Chidamide (CS055/HBI-8000/Tucidinostat)+decitabine", "Drug_category": "Others/combination", "Drugbank_ID": "DB06334", "Target/s_or_mechanism_of_action": "Histone deacetylase inhibitor", "KEGG_Drug__ID": "D10993", "Pubchem_ID": "12136798", "STR_LINK_(SMILES)": "NC1=CC(F)=CC=C1NC(=O)C1=CC=C(CNC(=O)\\C=C\\C2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "31934307", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Myeloid Leukemia", "System": "K562", "Dose": "4 μg/mL chidamide and 8 μmol/L decitabine", "Technique": "western blotting, Flow cytometry,RT-qPCR", "Controlled_Technique": "Flow cytometry; 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Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "cancer testis antigen- PRAME", "Controlled_Terms_Function_enhanced_Number_increased": "Cancer-testis antigens; PRAME antigen", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/49", "Drug": "Chidamide (CS055/HBI-8000/Tucidinostat)+decitabine", "Drug_category": "Others/combination", "Drugbank_ID": "DB06334", "Target/s_or_mechanism_of_action": "Histone deacetylase inhibitor", "KEGG_Drug__ID": "D10993", "Pubchem_ID": "12136798", "STR_LINK_(SMILES)": "NC1=CC(F)=CC=C1NC(=O)C1=CC=C(CNC(=O)\\C=C\\C2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "23940586", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "U937", "Dose": "chidamde (1 µM), decitabine (Dac, 0.25 mM)", "Technique": "RT-qPCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "cancer testis antigen- PRAME", "Controlled_Terms_Function_enhanced_Number_increased": "Cancer-testis antigens; PRAME antigen", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/723", "Drug": "Chidamide combined with decitabine", "Drug_category": "Others/combination", "Drugbank_ID": "DB06334, DB01262", "Target/s_or_mechanism_of_action": "Histone deacetylase inhibitor, Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D10993, D03665", "Pubchem_ID": "12136798, 451668", "STR_LINK_(SMILES)": "NC1=CC(F)=CC=C1NC(=O)C1=CC=C(CNC(=O)\\C=C\\C2=CN=CC=C2)C=C1,\n NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Combination", "PMID": "30210693", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "K562 cells were co-cultured with effector cells", "Dose": "anti-ILT2 blocking antibody (10 μg/ml) lenalidomide (LND, 1 μM)", "Technique": "calcein assay", "Controlled_Technique": "Calcein assay", "Immune_System-Function_enhanced/numbers_increased": "NK Cell Cytotoxicity", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/503", "Drug": "JQ1", "Drug_category": "Others/combination", "Drugbank_ID": "DB17021", "Target/s_or_mechanism_of_action": "BRD4 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": "46907787", "STR_LINK_(SMILES)": "CC1=C(SC2=C1C(=N[C@H](C3=NN=C(N32)C)CC(=O)OC(C)(C)C)C4=CC=C(C=C4)Cl)C", "Single/Combination": "Single", "PMID": "35517410", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": "MC38", "Dose": "0.1 μM, 48 h", "Technique": "RNA-seq, qPCR, flow cytometry", "Controlled_Technique": "H2-Kb, MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1/CD274", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 / CD274", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1207", "Drug": "Chidamide combined with decitabine", "Drug_category": "Others/combination", "Drugbank_ID": "DB06334, DB01262", "Target/s_or_mechanism_of_action": "Histone deacetylase inhibitor, Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D10993, D03665", "Pubchem_ID": "12136798, 451668", "STR_LINK_(SMILES)": "NC1=CC(F)=CC=C1NC(=O)C1=CC=C(CNC(=O)\\C=C\\C2=CN=CC=C2)C=C1,\n NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Combination", "PMID": "30210693", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "PBMCs obtained from 14 CLL patients", "Dose": "anti-ILT2 blocking antibody (10 μg/ml), lenalidomide (LND, 1 μM)", "Technique": "Flow cytometry, CFSE assay (PBMCs from 11 CLL patients)", "Controlled_Technique": "Flow cytometry; Cell proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "NK cells,NK cell proliferation in CLL, intracellular levels of perforin on NK cells CD69 on NK cells leukemic cell apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "CD69; Apoptosis; Cell proliferation; Perforin / PRF1; NK cells; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/440", "Drug": "Chloroquine (CQ)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00608", "Target/s_or_mechanism_of_action": "Raises endosomal/lysosomal pH", "KEGG_Drug__ID": "D02366", "Pubchem_ID": "2719", "STR_LINK_(SMILES)": "CCN(CC)CCCC(C)NC1=CC=NC2=CC(Cl)=CC=C12", "Single/Combination": "single", "PMID": "41019037", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast cancer", "System": "4T1", "Dose": "0–10 μM, 24 h in vitro", "Technique": "Flow cytometry", "Controlled_Technique": "MHC-I expression", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/663", "Drug": "Chloroquine (CQ)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00608", "Target/s_or_mechanism_of_action": "Raises endosomal/lysosomal pH", "KEGG_Drug__ID": "D02366", "Pubchem_ID": "2719", "STR_LINK_(SMILES)": "CCN(CC)CCCC(C)NC1=CC=NC2=CC(Cl)=CC=C12", "Single/Combination": "single", "PMID": "41019037", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "melanoma", "System": "B16F10", "Dose": "0–10 μM, 24 h in vitro", "Technique": "Flow cytometry", "Controlled_Technique": "MHC-I expression", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/874", "Drug": "Cobimetinib+anti CD40+ anti- IgM", "Drug_category": "Others/combination", "Drugbank_ID": "DB05239", "Target/s_or_mechanism_of_action": "MEK inhibitor Cobimetinib specifically binds to and inhibits the catalytic activity of MEK1, resulting in inhibition of extracellular signal-related kinase 2 (ERK2) phosphorylation and activation and decreased tumor cell proliferation. Cobimetinib and vemurafenib target two different kinases in the RAS/RAF/MEK/ERK pathway.", "KEGG_Drug__ID": "D10405", "Pubchem_ID": "16222096", "STR_LINK_(SMILES)": "OC1(CN(C1)C(=O)C1=C(NC2=C(F)C=C(I)C=C2)C(F)=C(F)C=C1)[C@@H]1CCCCN1", "Single/Combination": "Combination", "PMID": "31671149", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "Isolated splenic B cells", "Dose": "cobimetinib(0.5 μM) +anti-CD40(8 mg/ml,)+ anti-IgM((1 mg/ml)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "B10 cells, TIM1+ B cells, T2-MZP cells (CD21hi, CD23hi, and CD24hi)", "Controlled_Terms_Function_enhanced_Number_increased": "B cells; T2-MZP cells", "Immune_System-Function_inhibited/numbers_decreased": "T2-MZP cells (CD21hi, CD23hi, and CD24hi)", "Controlled_Terms_Function_inhibited_Number_decreased": "T2-MZP cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/771", "Drug": "Combined vaccine + axitinib therapy", "Drug_category": "Others/combination", "Drugbank_ID": "DB06626", "Target/s_or_mechanism_of_action": "Axitinib selectively blocks the tyrosine kinase receptors VEGFR-1 (vascular endothelial growth factor receptor), VEGFR-2, and VEGFR-3.", "KEGG_Drug__ID": "D03218", "Pubchem_ID": "6450551", "STR_LINK_(SMILES)": "CNC(=O)C1=C(SC2=CC=C3C(NN=C3\\C=C\\C3=CC=CC=N3)=C2)C=CC=C1", "Single/Combination": "Combination", "PMID": "22504156", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "MACS-isolated CD8+ T cells from TIL and TDLN were longitudinally analyzed for their ability to produce IFN-γ in response to syngenic DC pulsed with OVA254–262 (SIINFEKL) peptide for 48 hours at a 10:1 E:T ratio", "Dose": null, "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/631", "Drug": "CX-5461", "Drug_category": "Others/combination", "Drugbank_ID": "DB16846", "Target/s_or_mechanism_of_action": "Inhibits RNA polymerase I and rDNA transcription; induces nucleolar stress and DNA-damage response", "KEGG_Drug__ID": null, "Pubchem_ID": "12254622", "STR_LINK_(SMILES)": "CC1=NC=C(CNC(C2=C3N(C(C=CC=C4)=C4S3)C5=C(C=CC(N6CCCN(C)CC6)=N5)C2=O)=O)N=C1", "Single/Combination": "Single", "PMID": "41315184", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Human multiple-myeloma cell line", "System": "SKO-007(J3)", "Dose": "200 nM, 48 h", "Technique": "Flow cytometry; NK-cell CD107a degranulation assay; Western blot; qPCR", "Controlled_Technique": "Increased expression of NK-activating ligands; increased HLA-ABC", "Immune_System-Function_enhanced/numbers_increased": "Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": "HLA-E upregulation reduced NK-cell degranulation", "Immune_System-Function_inhibited/numbers_decreased": "Expression / abundance phenotype; NK cells", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "Increased HLA-E, an inhibitory NK-cell ligand", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; NK cells", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1049", "Drug": "CXCR4 inhibitor AMD 3100 /\n Plerixafor", "Drug_category": "Others/combination", "Drugbank_ID": "DB06809", "Target/s_or_mechanism_of_action": "Plerixafor inhibits the CXCR4 chemokine receptors on CD34+ cells and reversibly blocks binding of the ligand, stromal cell-derived factor-1-alpha (SDF-1α). By blocking the interaction between SDF-1α and CXCR4 with plerixafor, mobilization of progenitor cells is triggered.", "KEGG_Drug__ID": "D08971", "Pubchem_ID": "65015", "STR_LINK_(SMILES)": "C(N1CCCNCCNCCCNCC1)C1=CC=C(CN2CCCNCCNCCCNCC2)C=C1", "Single/Combination": "Single Drug", "PMID": "30802149", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": "ID8-luc cells", "Dose": "AMD3100 at 10 μg/ml", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CXCR4 and CXCL12", "Controlled_Terms_Function_inhibited_Number_decreased": "CXCR4; CXCL12 / SDF-1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1179", "Drug": "Dabrafenib+trametinib", "Drug_category": "Others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10064, D10175", "Pubchem_ID": "44462760, 11707110", "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Murine Melanoma", "System": "gp10025-33-activated pmel-1 mouse splenocytes", "Dose": "Dabrafenib: L=0.1μM, M=5μM, H=20μM and trametinib: L=0.005μM, M=0.25μM, H=1μM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "IFN-γ expressing CD3+ CD8+ cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD3; CD8; IFN-γ", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1180", "Drug": "Dacarbazine+ IFNγ", "Drug_category": "Others/combination", "Drugbank_ID": "DB00851", "Target/s_or_mechanism_of_action": "The mechanism of action is not known, but appears to exert cytotoxic effects via its action as an alkylating agent. Other theories include DNA synthesis inhibition by its action as a purine analog, and interaction with SH groups. Dacarbazine is not cell cycle-phase specific.", "KEGG_Drug__ID": "D00288", "Pubchem_ID": "5351166", "STR_LINK_(SMILES)": "CN(C)\\N=N\\C1=C(N=CN1)C(N)=O", "Single/Combination": "Combination", "PMID": "23483066", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "A375", "Dose": "20 μM dacarbazine+2000 U/mL IFNγ", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "MHC Class I molecules (HLA-A,B,C), MHC Class II molecule\n (HLA-DR)", "Controlled_Terms_Unaffected": "MHC class I; MHC class II; HLA-DR; HLA-A;", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1333", "Drug": "Decitabine (DAC, a DNA demethylation drug) and γδ T cells", "Drug_category": "Others/combination", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Combination", "PMID": "29910819", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Osteosarcoma", "System": "HOS", "Dose": "(DAC) (5 µM)", "Technique": "MTS assays,PCR and Flow cytometry", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "cytotoxic effects of γδ T cells NKG2DLs MICB and ULBP1 on OS cells", "Controlled_Terms_Function_enhanced_Number_increased": "ULBP1; MICB; Cytotoxicity / cytolysis; T cells; MICA/MICB", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1335", "Drug": "Decitabine (DAC, a DNA demethylation drug) and γδ T cells", "Drug_category": "Others/combination", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Combination", "PMID": "29910819", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Osteosarcoma", "System": "U2OS cells", "Dose": "(DAC) (5 µM)", "Technique": "PCR and Flow cytometry", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "cytotoxic effects of γδ T cells NKG2DLs MICB and ULBP1 on OS cells", "Controlled_Terms_Function_enhanced_Number_increased": "ULBP1; MICB; Cytotoxicity / cytolysis; T cells; MICA/MICB", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/133", "Drug": "Decitabine (DAC) + selinexor", "Drug_category": "Others/combination", "Drugbank_ID": "DB01262, DB11942", "Target/s_or_mechanism_of_action": "deitabine: Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses, Selinexor is a first-in-class selective inhibitor of nuclear transport (SINE) compound", "KEGG_Drug__ID": "D03665, D11222", "Pubchem_ID": "451668, \n 71481097", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1,\n FC(F)(F)C1=CC(=CC(=C1)C1=NN(\\C=C/C(=O)NNC2=NC=CN=C2)C=N1)C(F)(F)F", "Single/Combination": "Combination", "PMID": "25716206", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - 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Acute Myeloid Leukemia (AML)", "System": "MV4-11)", "Dose": "decitabine (IC50 twofold dilutions, 4 μM to 250 nM) followed by selinexor (IC50 twofold dilutions, 400nm to 25nM) for 24 hours", "Technique": "WST-1 assay,qRT-PCR, western blot", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "apoptosis,CDKN1A and FOXO3A expression levels", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis; p21 / CDKN1A; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/135", "Drug": "Decitabine (DAC) + selinexor", "Drug_category": "Others/combination", "Drugbank_ID": "DB01262, DB11942", "Target/s_or_mechanism_of_action": "deitabine: Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses, Selinexor is a first-in-class selective inhibitor of nuclear transport (SINE) compound", "KEGG_Drug__ID": "D03665, D11222", "Pubchem_ID": "451668, \n 71481097", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1,\n FC(F)(F)C1=CC(=CC(=C1)C1=NN(\\C=C/C(=O)NNC2=NC=CN=C2)C=N1)C(F)(F)F", "Single/Combination": "Combination", "PMID": "25716206", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "MOLM-13", "Dose": "decitabine (IC50 twofold dilutions, 4 μM to 250 nM) followed by selinexor (IC50 twofold dilutions, 400nm to 25nM) for 24 hours", "Technique": "WST-1 assay,qRT-PCR, western blot", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "apoptosis,CDKN1A and FOXO3A expression levels", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis; p21 / CDKN1A; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/937", "Drug": "Decitabine (DAC) in combination with allogeneic NK cells generated from CD34+ hematopoietic stem and progenitor cells (HSPC-NK cells)", "Drug_category": "Others/combination", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Combination", "PMID": "29138222", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "THP-1 +allogeneic NK cells generated from CD34+ hematopoietic stem and progenitor cells (HSPC-NK cells)", "Dose": "0.01 to 0.1 µM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cell–mediated killing", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/938", "Drug": "Decitabine (DAC) in combination with allogeneic NK cells generated from CD34+ hematopoietic stem and progenitor cells (HSPC-NK cells)", "Drug_category": "Others/combination", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Combination", "PMID": "29138222", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "KG1a cells+allogeneic NK cells generated from CD34+ hematopoietic stem and progenitor cells (HSPC-NK cells)", "Dose": "0.01 to 0.1 µM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cell–mediated killing", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/939", "Drug": "Decitabine (DAC) in combination with allogeneic NK cells generated from CD34+ hematopoietic stem and progenitor cells (HSPC-NK cells)", "Drug_category": "Others/combination", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Combination", "PMID": "29138222", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "Primary AML cells obtained from 5 different patients +HSPC-NK cells", "Dose": "0.1 µM DAC", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cell–mediated killing", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/942", "Drug": "Decitabine (DAC)+BI 836858, a fully human, Fc-engineered, anti-CD33 antibody", "Drug_category": "Others/combination", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Combination", "PMID": "27013443", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "primary AML blasts +autologous NK-cell", "Dose": "DAC (500 nM)+ BI 836858 or BI 836847 (10 μg/mL)", "Technique": "Flow cytometry, ADCC assay", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK-cell activation-natural killer ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/943", "Drug": "Decitabine (DAC)+BI 836858, a fully human, Fc-engineered, anti-CD33 antibody", "Drug_category": "Others/combination", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": "D03665", "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Combination", "PMID": "27013443", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "primary AML blasts +allogenic NK-cell", "Dose": "DAC (500 nM)+ BI 836858 or BI 836847 (10 μg/mL)", "Technique": "Flow cytometry, ADCC assay", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK-cell activation-natural killer ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/859", "Drug": "Decitabine + Vorinostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB01262, DB02546", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses.\n Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D03665, D06320", "Pubchem_ID": "451668, 5311", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1\n ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "22461695", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Carcinoma", "System": "LS411N", "Dose": "0 - 1 μM (both drugs) + FasL (200 ng/ml)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "FasL-induced apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Fas ligand / FasL / FASLG; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1436", "Drug": "Decitabine + Vorinostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB01262, DB02546", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses.\n Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D03665, D06320", "Pubchem_ID": "451668, 5311", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1\n ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "22461695", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Carcinoma", "System": "LS411N", "Dose": "0 - 1 μM (both drugs)", "Technique": "Flow cytometry, RT PCR, Western blotting analysis", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "Fas protein level on the tumor cell surface, BNIP3 and Bik ,FasL-induced apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "CD95 / Fas / FAS; Fas ligand / FasL / FASLG; Apoptosis; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": "Bcl-xL protein", "Controlled_Terms_Function_inhibited_Number_decreased": "BCL-xL / BCL2L1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1219", "Drug": "Decitabine and Vorinostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB01262, DB02546", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses.\n Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D03665, D06320", "Pubchem_ID": "451668, 5311", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1\n ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "28881658", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "HL-60", "Dose": "0.1 μM DAC, 0.25 μM and 0.75 μM VOR", "Technique": "Annexin V PI staining-Flow cytometry", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "apoptotic cell death, caspase 8, 9 and 3/7 activity", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-8; Caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1523", "Drug": "Decitabine and Vorinostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB01262, DB02546", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses.\n Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D03665, D06320", "Pubchem_ID": "451668, 5311", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1\n ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "28881658", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": "OCI-AML3", "Dose": "0.1 μM DAC, 0.25 μM and 0.75 μM VOR", "Technique": "Annexin V PI staining-Flow cytometry, western blot", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "apoptotic cell death, caspase 8, 9 and 3/7 activity", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-8; Caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1203", "Drug": "Depsipeptide (FK228) or Romidepsin +FasL", "Drug_category": "Others/combination", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "57515973", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Combination", "PMID": "18185535", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "B16/F10", "Dose": "depsipeptide (5 nM) and recombinant FLAG-tagged FasL (10 ng/ ml ) and multimerized with anti-FLAG M2 antibodies (1 mg/ ml ) for 16 hours.", "Technique": "Flow cytometry,Caspase-Glo 3/7 Assay system (Promega)", "Controlled_Technique": "Flow cytometry; Apoptosis/cell viability assay; Bioluminescence/luciferase assay; Caspase-Glo3/7 Assay", "Immune_System-Function_enhanced/numbers_increased": "apoptotic cell death after Fas–FasL crosslinking, (whereas B16/ F10 cells were resistant to apoptosis with Fas crosslinking alone), Caspase-3/7 activity", "Controlled_Terms_Function_enhanced_Number_increased": "CD95 / Fas / FAS; Fas ligand / FasL / FASLG; Caspase-3; Caspase activation; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/930", "Drug": "Depsipeptide ++tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)", "Drug_category": "Others/combination", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": "D06637", "Pubchem_ID": "57515973", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Combination", "PMID": "16818655", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "CD19+ CLL cells", "Dose": "0.5 to 1μM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "BID, DR5, and p73 CD154", "Controlled_Terms_Function_enhanced_Number_increased": "TRAIL-R2 / DR5 / TNFRSF10B; BID", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/97", "Drug": "Depsipeptide and 5-fluorouracil", "Drug_category": "Others/combination", "Drugbank_ID": "DB06176,\n DB00544", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor. Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D06637, D00584", "Pubchem_ID": "57515973, 3385", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C, FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "27509880", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": "HCT-116", "Dose": "Dep (1 nM)", "Technique": "caspase-3 activation assay, qRT-PCR method", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "MHC class II genes, including HLA-DPB1, HLA-DQB1, HLA-DRA, and HLA-DRB1", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class II; HLA-DR;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "MHC class I genes including HLA-A, HLA-B-HLA-C", "Controlled_Terms_Unaffected": "MHC class I; HLA-A; HLA-B; HLA-C;", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/98", "Drug": "Depsipeptide and 5-fluorouracil", "Drug_category": "Others/combination", "Drugbank_ID": "DB06176,\n DB00544", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor. Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D06637, D00584", "Pubchem_ID": "57515973, 3385", "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C, FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "27509880", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": "HCT-116", "Dose": "5-FU (1.75 µM) + Dep (1 nM)", "Technique": "caspase-3 activation assay, qRT-PCR method", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "MHC class II genes, including HLA-DPB1, HLA-DQB1, HLA-DRA, and HLA-DRB1 caspase-3/7 activation", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class II; HLA-DR; Caspase-3; Caspase activation;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/765", "Drug": "Dex with IMiD1", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "12036884", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "MM.1S cells", "Dose": "1 µM of both drugs", "Technique": "The DNA binding activity of NF-κB in MM.1S cells was quantified by enzyme-linked immunosorbent assay using the Trans-AM NF-κB p65 Transcription Factor Assay Kit", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "NF-κB", "Controlled_Terms_Function_inhibited_Number_decreased": "NF-κB", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/442", "Drug": "DM1 (emtansine)", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "40175391", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "HER2-positive", "System": "Au565 cells", "Dose": "Titrated concentrations; 3-day ICD experiment", "Technique": "ATP, HMGB1, calreticulin assays", "Controlled_Technique": "Extracellular ATP release, HMGB1 release, Surface calreticulin (CRT)  on tumor cells undergoing ICD", "Immune_System-Function_enhanced/numbers_increased": "HMGB1; Calreticulin / CRT; Immunogenic cell death", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/968", "Drug": "Docetaxel+cisplatin", "Drug_category": "Others/combination", "Drugbank_ID": "1. DB01248 (APRD00932) 2. DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "1. Inhibition of tubulin depolymerization, 2. Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": "1. D07866, 2. D00275", "Pubchem_ID": "96024562", "STR_LINK_(SMILES)": "[H][C@@]12C[C@H](O)[C@@]3(C)C(=O)[C@H](O)C4=C(C)[C@H](C[C@@](O)([C@@H](OC(=O)C5=CC=CC=C5)[C@]3([H])[C@@]1(CO2)OC(C)=O)C4(C)C)OC(=O)[C@H](O)[C@@H](NC(=O)OC(C)(C)C)C1=CC=CC=C2", "Single/Combination": "Combination", "PMID": "24868562", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Nonsmall-Cell Lung Cancer (NSCLC)", "System": "PBMCs from NSCLC patients+docetaxe", "Dose": "1 μg/mL", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "T reg", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/622", "Drug": "Doxorubicin + Celecoxib", "Drug_category": "Others/combination", "Drugbank_ID": "DB00997 + DB00482", "Target/s_or_mechanism_of_action": "Doxorubicin induces DNA damage and immunogenic cell death; celecoxib inhibits COX-2 and suppresses PI3K/AKT-associated IDO1 expression", "KEGG_Drug__ID": "D03899+D00567", "Pubchem_ID": "31703 + 2662", "STR_LINK_(SMILES)": "COC1=CC=CC2=C1C(=O)C1=C(O)C3=C(C[C@](O)(C[C@@H]3O[C@H]3C[C@H](N)[C@H](O)[C@H](C)O3)C(=O)CO)C(O)=C1C2=O and CC1=CC(=NN1C2=CC=C(C=C2)S(=O)(=O)N)C3=CC=C(C=C3)C(F)(F)F", "Single/Combination": "Combination", "PMID": "38988937", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Murine Lewis lung carcinoma (LLC) cell line", "System": "LLC", "Dose": "25 mg/kg; 50 mg/kg", "Technique": "Flow cytometry; ROS assay; apoptosis assay; Western blot", "Controlled_Technique": "DOX-associated ICD; celecoxib may enhance ROS-associated ER stress and antitumor immunogenicity", "Immune_System-Function_enhanced/numbers_increased": "Reactive oxygen species / ROS; Immunogenic cell death", "Controlled_Terms_Function_enhanced_Number_increased": "IDO1-associated immunosuppression may decrease", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "Reduced IDO1-associated negative immune regulation", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/623", "Drug": "Doxorubicin + Celecoxib", "Drug_category": "Others/combination", "Drugbank_ID": "DB00997 + DB00482", "Target/s_or_mechanism_of_action": "Doxorubicin induces DNA damage and immunogenic cell death; celecoxib inhibits COX-2 and suppresses PI3K/AKT-associated IDO1 expression", "KEGG_Drug__ID": "D03899+D00567", "Pubchem_ID": "31703 + 2662", "STR_LINK_(SMILES)": "COC1=CC=CC2=C1C(=O)C1=C(O)C3=C(C[C@](O)(C[C@@H]3O[C@H]3C[C@H](N)[C@H](O)[C@H](C)O3)C(=O)CO)C(O)=C1C2=O and CC1=CC(=NN1C2=CC=C(C=C2)S(=O)(=O)N)C3=CC=C(C=C3)C(F)(F)F", "Single/Combination": "Combination", "PMID": "38988937", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Murine CMT-64 lung cancer cell line", "System": "CMT-64", "Dose": "25 mg/kg; 50 mg/kg", "Technique": "Flow cytometry; ROS assay; apoptosis assay; Western blot", "Controlled_Technique": "DOX-associated ICD; celecoxib may enhance ROS-associated ER stress and antitumor immunogenicity", "Immune_System-Function_enhanced/numbers_increased": "Reactive oxygen species / ROS; Immunogenic cell death", "Controlled_Terms_Function_enhanced_Number_increased": "IDO1-associated immunosuppression may decrease", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "Reduced IDO1-associated negative immune regulation", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/519", "Drug": "Emricasan", "Drug_category": "Others/combination", "Drugbank_ID": "DB05408", "Target/s_or_mechanism_of_action": "Hsp90 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": "12000240", "STR_LINK_(SMILES)": "C[C@@H](C(=O)N[C@@H](CC(=O)O)C(=O)COC1=C(C(=CC(=C1F)F)F)F)NC(=O)C(=O)NC2=CC=CC=C2C(C)(C)C", "Single/Combination": "Single", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "MC38", "Dose": "10 µM; 24 h", "Technique": "ELISA, RT-qPCR", "Controlled_Technique": "Little IFN-β induction alone", "Immune_System-Function_enhanced/numbers_increased": "IFN-β", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/522", "Drug": "Emricasan", "Drug_category": "Others/combination", "Drugbank_ID": "DB05408", "Target/s_or_mechanism_of_action": "Hsp90 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": "12000240", "STR_LINK_(SMILES)": "C[C@@H](C(=O)N[C@@H](CC(=O)O)C(=O)COC1=C(C(=CC(=C1F)F)F)F)NC(=O)C(=O)NC2=CC=CC=C2C(C)(C)C", "Single/Combination": "Single", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "HT29", "Dose": "10 µM; 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ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/358", "Drug": "Entinostat + Avelumab ( anti-PD-1)", "Drug_category": "Others/combination", "Drugbank_ID": "DB11841, DB11951", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM).\n Avelumab binds PD-L1 through the FG loops 7 and blocks the interaction between PD-L1 and its receptors PD-1 and B7.1.", "KEGG_Drug__ID": "D06320, \n D10817", "Pubchem_ID": "5311, \n 347911260", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "30377559", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate", "System": "DU145 +NK cells purified from two healthy donor PBMCs", "Dose": "entinostat (500 nM) for 72 hours, , Avelumab - 2 ng/mL", "Technique": "111In-release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK lysis and ADCC-mediated lysis", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; 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ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/69", "Drug": "Entinostat + Avelumab ( anti-PD-1)", "Drug_category": "Others/combination", "Drugbank_ID": "DB11841, DB11945", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM).\n Avelumab binds PD-L1 through the FG loops 7 and blocks the interaction between PD-L1 and its receptors PD-1 and B7.1.", "KEGG_Drug__ID": "D06320, \n D10817", "Pubchem_ID": "5311, \n 347911260", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "30377559", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung - Small Cell Lung Cancer", "System": "H1882 +NK cells purified from two healthy donor PBMCs", "Dose": "entinostat (500 nM) for 72 hours, , Avelumab - 2 ng/mL", "Technique": "111In-release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK lysis and ADCC-mediated lysis", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/80", "Drug": "Entinostat + Avelumab ( anti-PD-1)", "Drug_category": "Others/combination", "Drugbank_ID": "DB11841, DB11946", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM).\n Avelumab binds PD-L1 through the FG loops 7 and blocks the interaction between PD-L1 and its receptors PD-1 and B7.1.", "KEGG_Drug__ID": "D06320, \n D10817", "Pubchem_ID": "5311, \n 347911260", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "30377559", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCL", "System": "NCI-H441+NK cells purified from two healthy donor PBMCs", "Dose": "entinostat (500 nM) for 72 hours, , Avelumab - 2 ng/mL", "Technique": "111In-release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK lysis and ADCC-mediated lysis", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/91", "Drug": "Entinostat + Avelumab ( anti-PD-1)", "Drug_category": "Others/combination", "Drugbank_ID": "DB11841, DB11947", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM).\n Avelumab binds PD-L1 through the FG loops 7 and blocks the interaction between PD-L1 and its receptors PD-1 and B7.1.", "KEGG_Drug__ID": "D06320, \n D10817", "Pubchem_ID": "5311, \n 347911260", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "30377559", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCL", "System": "NCI-H460 +NK cells purified from two healthy donor PBMCs", "Dose": "entinostat (500 nM) for 72 hours, , Avelumab - 2 ng/mL", "Technique": "111In-release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK lysis and ADCC-mediated lysis", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1048", "Drug": "Entinostat and azacytidine", "Drug_category": "Others/combination", "Drugbank_ID": "DB11841, DB00928", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers.\n As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D09338,\n D03021", "Pubchem_ID": "4261, 9444", "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1, \n NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Combination", "PMID": "28498806", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": "ID8", "Dose": "entinostat-5 μM, azacytidine-150 nM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC II expression", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class II; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1249", "Drug": "Erlotinib+cetuximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00530,DB00002", "Target/s_or_mechanism_of_action": "Erlotinib inhibits the intracellular phosphorylation of tyrosine kinase associated with the epidermal growth factor receptor (EGFR). Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D07907, D03455", "Pubchem_ID": "176870, 46507042", "STR_LINK_(SMILES)": "COCCOC1=CC2=C(C=C1OCCOC)C(NC1=CC(=CC=C1)C#C)=NC=N2", "Single/Combination": "Combination", "PMID": "31546690", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": "IGROV-1 co-incubated with purified unstimulated NK cells", "Dose": "Cetuximab - 1 µg/mL+erlotinib (1 µM) for 7 days and 6 weeks", "Technique": "Flow cytometry, ELISpot assay", "Controlled_Technique": "Flow cytometry; ELISpot/FluoroSpot assay", "Immune_System-Function_enhanced/numbers_increased": "NK cytotoxicity and NK-specific tumor cell lysis", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "IFNγ,NK-activating cytokine IL18 MHC class I polypeptide-related sequence A (MICA) and MHC class I polypeptide-related sequence B (MICB)", "Controlled_Terms_Negative_Regulation": "MHC class I; MICA; MICB; IL-18; IFN-γ; ; MICA/MICB", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1250", "Drug": "Erlotinib+cetuximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00530,DB00002", "Target/s_or_mechanism_of_action": "Erlotinib inhibits the intracellular phosphorylation of tyrosine kinase associated with the epidermal growth factor receptor (EGFR). Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D07907, D03455", "Pubchem_ID": "176870, 46507042", "STR_LINK_(SMILES)": "COCCOC1=CC2=C(C=C1OCCOC)C(NC1=CC(=CC=C1)C#C)=NC=N2", "Single/Combination": "Combination", "PMID": "31546690", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": "SKOV-3-1 co-incubated with purified unstimulated NK cells", "Dose": "Cetuximab - 1 µg/mL+erlotinib (1 µM) for 7 days and 6 weeks", "Technique": "Flow cytometry, ELISpot assay", "Controlled_Technique": "Flow cytometry; ELISpot/FluoroSpot assay", "Immune_System-Function_enhanced/numbers_increased": "NK cytotoxicity and NK-specific tumor cell lysis", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "IFNγ- MHC class I polypeptide-related sequence A (MICA) and MHC class I polypeptide-related sequence B (MICB)", "Controlled_Terms_Negative_Regulation": "MHC class I; MICA; MICB; IFN-γ; ; MICA/MICB", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/875", "Drug": "FOLFIRI+cetuximab", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "27135741", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "Lim1215-KRAS WT, BRAF WT", "Dose": "The concentrations used for FOLFIRI single component were: calcium levofolinate (20 µM), 5-fluorouracil (20 µM) and irinotecan (60 µM),cetuximab (10 μg/mL)", "Technique": "Flow cytometry, westen blot", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "eIF2-α phosphorylation and phagocytosis - markers of Immunogenic cell death", "Controlled_Terms_Function_enhanced_Number_increased": "Immunogenic cell death; Phagocytosis / trogocytosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/876", "Drug": "FOLFIRI+cetuximab", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "27135741", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "OXCO-2", "Dose": "The concentrations used for FOLFIRI single component were: calcium levofolinate (20 µM), 5-fluorouracil (20 µM) and irinotecan (60 µM),cetuximab (10 μg/mL)", "Technique": "Flow cytometry, westen blot", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "eIF2-α phosphorylation and phagocytosis - markers of Immunogenic cell death", "Controlled_Terms_Function_enhanced_Number_increased": "Immunogenic cell death; Phagocytosis / trogocytosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/877", "Drug": "FOLFIRI+cetuximab", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "27135741", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "Caco-2", "Dose": "The concentrations used for FOLFIRI single component were: calcium levofolinate (20 µM), 5-fluorouracil (20 µM) and irinotecan (60 µM),cetuximab (10 μg/mL)", "Technique": "Flow cytometry, westen blot", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "eIF2-α phosphorylation and phagocytosis - markers of Immunogenic cell death", "Controlled_Terms_Function_enhanced_Number_increased": "Immunogenic cell death; Phagocytosis / trogocytosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/878", "Drug": "FOLFIRI+cetuximab", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "27135741", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "HCT116-KRAS mut", "Dose": "The concentrations used for FOLFIRI single component were: calcium levofolinate (20 µM), 5-fluorouracil (20 µM) and irinotecan (60 µM),cetuximab (10 μg/mL)", "Technique": "Flow cytometry, westen blot", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "eIF2-α phosphorylation and phagocytosis - markers of Immunogenic cell death", "Controlled_Terms_Function_enhanced_Number_increased": "Immunogenic cell death; Phagocytosis / trogocytosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/880", "Drug": "FOLFIRI+cetuximab", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "27135741", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "Lim1215 KRASG12D-KRAS mut", "Dose": "The concentrations used for FOLFIRI single component were: calcium levofolinate (20 µM), 5-fluorouracil (20 µM) and irinotecan (60 µM),cetuximab (10 μg/mL)", "Technique": "Flow cytometry, westen blot", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "eIF2-α phosphorylation and phagocytosis - markers of Immunogenic cell death", "Controlled_Terms_Function_enhanced_Number_increased": "Immunogenic cell death; Phagocytosis / trogocytosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/881", "Drug": "FOLFIRI+cetuximab", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "27135741", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "(CT26) expressing human EGFR (hEGFR-CT26)", "Dose": "The concentrations used for FOLFIRI single component were: calcium levofolinate (20 µM), 5-fluorouracil (20 µM) and irinotecan (60 µM),cetuximab (10 μg/mL)", "Technique": "Flow cytometry, westen blot", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "ER stress response and phagocytosis-markers of Immunogenic cell death", "Controlled_Terms_Function_enhanced_Number_increased": "Immunogenic cell death; Phagocytosis / trogocytosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/882", "Drug": "FOLFIRI+cetuximab", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "27135741", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "DiFi", "Dose": "The concentrations used for FOLFIRI single component were: calcium levofolinate (20 µM), 5-fluorouracil (20 µM) and irinotecan (60 µM),cetuximab (10 μg/mL)", "Technique": "Flow cytometry, westen blot,global mass-spectrometry-based quantitative proteomics using a technique called stable isotope labeling by amino acids in cell culture (SILAC)", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "ER stress response and the translocation of CRT and ERp57 to the cell surface- markers of Immunogenic cell death", "Controlled_Terms_Function_enhanced_Number_increased": "Immunogenic cell death; Calreticulin / CRT; ERp57 / PDIA3", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1570", "Drug": "FOLFIRI+cetuximab", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "27135741", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "DiFi+ DCs", "Dose": "The concentrations used for FOLFIRI single component were: calcium levofolinate (20 µM), 5-fluorouracil (20 µM) and irinotecan (60 µM),cetuximab (10 μg/mL)", "Technique": "confocal microscopy", "Controlled_Technique": "Microscopy; Confocal microscopy", "Immune_System-Function_enhanced/numbers_increased": "phagocytosis by dendritic cells-of tumor cells", "Controlled_Terms_Function_enhanced_Number_increased": "Dendritic cells; Phagocytosis / trogocytosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/621", "Drug": "Gemcitabine + Celecoxib", "Drug_category": "Others/combination", "Drugbank_ID": "DB00441 + DB00482", "Target/s_or_mechanism_of_action": "Ribonucleotide reductase/DNA synthesis inhibition by GEM; COX-2/PGE2 and PI3K/AKT/IDO1 pathway suppression by celecoxib; increased ROS and ER stress", "KEGG_Drug__ID": "D02368+D00567", "Pubchem_ID": "60750 + 2662", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F and CC1=CC(=NN1C2=CC=C(C=C2)S(=O)(=O)N)C3=CC=C(C=C3)C(F)(F)F", "Single/Combination": "Combination", "PMID": "38988937", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Murine CMT-64 lung cancer cell line", "System": "CMT-64", "Dose": "GEM 2 µg/mL and celecoxib 40 µM; 24 h", "Technique": "Flow cytometry; ROS assay; Western blot; apoptosis assay", "Controlled_Technique": "Increased ROS and apoptosis; enhanced GEM-associated ICD", "Immune_System-Function_enhanced/numbers_increased": "Apoptosis; Reactive oxygen species / ROS; Immunogenic cell death", "Controlled_Terms_Function_enhanced_Number_increased": "Reduced IDO1-associated immunosuppression", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "celecoxib suppresses the IDO1-mediated negative immune-regulatory pathway", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/620", "Drug": "Gemcitabine + Celecoxib", "Drug_category": "Others/combination", "Drugbank_ID": "DB00441 + DB00482", "Target/s_or_mechanism_of_action": "Ribonucleotide reductase/DNA synthesis inhibition by GEM; COX-2/PGE2 and PI3K/AKT/IDO1 pathway suppression by celecoxib; increased ROS and ER stress", "KEGG_Drug__ID": "D02368+D00567", "Pubchem_ID": "60750 + 2662", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F and CC1=CC(=NN1C2=CC=C(C=C2)S(=O)(=O)N)C3=CC=C(C=C3)C(F)(F)F", "Single/Combination": "Combination", "PMID": "38988937", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Murine Lewis lung carcinoma (LLC) cell line", "System": "LLC", "Dose": "GEM 2 µg/mL and celecoxib 40 µM; 24 h", "Technique": "Flow cytometry; ROS assay; Western blot; apoptosis assay", "Controlled_Technique": "Increased ROS and apoptosis; enhanced GEM-associated ICD; increased tumor immunogenicity and potential DC activation", "Immune_System-Function_enhanced/numbers_increased": "Apoptosis; Reactive oxygen species / ROS; Immunogenic cell death; Dendritic cells", "Controlled_Terms_Function_enhanced_Number_increased": "Reduced IDO1-associated immunosuppression; reduced tumor-cell survival", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "celecoxib suppresses the IDO1-mediated negative immune-regulatory pathway", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/179", "Drug": "GILF regimen (Gem, Iri, Levofolinic acid and 5-FU)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00441\n DB00762\n DB11596\n DB00544", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase\n Irinotecan inhibits the action of topoisomerase I\n As levoleucovorin and leucovorin are analogs of tetrahydrofolate (THF), they are able to bypass DHFR reduction and act as a cellular replacement for the co-factor THF, thereby preventing these toxic side effects\n Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D02368,D08086, D04715, D00584", "Pubchem_ID": "60750, 60838, 149436, 3385", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F, \n CCC1=C2CN3C(=CC4=C(COC(=O[C@]4(O)CC)C3=O)C2=NC2=CC=C(OC(=O)N3CCC(CC3)N3CCCCC3)C=C12, \n NC1=NC(=O)C2=C(NC[C@H](CNC3=CC=C(C=C3)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N2C=O)N1, \n FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "20399639", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Human Colon Carcinoma", "System": "HT29", "Dose": "gemcitabine at final concentration of 50 lg/ml +, levofolinic acid was added at a concentration of\n 2 microg/ml (10)4 M) +5-FU was added at a concentration of 500 microgram/ml + irinotecan at a concentration of\n 100 microgram/ml", "Technique": "cytofluorimetric and Western blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "up-regulation of EGFR on tumor cells", "Controlled_Terms_Function_enhanced_Number_increased": "EGFR; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/181", "Drug": "GILF regimen (Gem, Iri, Levofolinic acid and 5-FU)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00441\n DB00762\n DB11596\n DB00544", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase\n Irinotecan inhibits the action of topoisomerase I\n As levoleucovorin and leucovorin are analogs of tetrahydrofolate (THF), they are able to bypass DHFR reduction and act as a cellular replacement for the co-factor THF, thereby preventing these toxic side effects\n Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D02368,D08086, D04715, D00584", "Pubchem_ID": "60750, 60838, 149436, 3385", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F, \n CCC1=C2CN3C(=CC4=C(COC(=O[C@]4(O)CC)C3=O)C2=NC2=CC=C(OC(=O)N3CCC(CC3)N3CCCCC3)C=C12, \n NC1=NC(=O)C2=C(NC[C@H](CNC3=CC=C(C=C3)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N2C=O)N1, \n FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "20399639", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Human Colon Carcinoma", "System": "WiDr", "Dose": "gemcitabine at final concentration of 50 lg/ml +, levofolinic acid was added at a concentration of\n 2 microg/ml (10)4 M) +5-FU was added at a concentration of 500 microgram/ml + irinotecan at a concentration of\n 100 microgram/ml", "Technique": "cytofluorimetric and Western blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "up-regulation of EGFR on tumor cells", "Controlled_Terms_Function_enhanced_Number_increased": "EGFR; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/182", "Drug": "GILF regimen (Gem, Iri, Levofolinic acid and 5-FU)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00441\n DB00762\n DB11596\n DB00544", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase\n Irinotecan inhibits the action of topoisomerase I\n As levoleucovorin and leucovorin are analogs of tetrahydrofolate (THF), they are able to bypass DHFR reduction and act as a cellular replacement for the co-factor THF, thereby preventing these toxic side effects\n Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D02368,D08086, D04715, D00584", "Pubchem_ID": "60750, 60838, 149436, 3385", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F, \n CCC1=C2CN3C(=CC4=C(COC(=O[C@]4(O)CC)C3=O)C2=NC2=CC=C(OC(=O)N3CCC(CC3)N3CCCCC3)C=C12, \n NC1=NC(=O)C2=C(NC[C@H](CNC3=CC=C(C=C3)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N2C=O)N1, \n FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "20399639", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Human Colon Carcinoma", "System": "SW620", "Dose": "gemcitabine at final concentration of 50 lg/ml +, levofolinic acid was added at a concentration of\n 2 microg/ml (10)4 M) +5-FU was added at a concentration of 500 microgram/ml + irinotecan at a concentration of\n 100 microgram/ml", "Technique": "cytofluorimetric and Western blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "up-regulation of EGFR on tumor cells", "Controlled_Terms_Function_enhanced_Number_increased": "EGFR; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/625", "Drug": "Glaucocalyxin A", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Inhibits STAT3 phosphorylation/activation; induces apoptosis and G2/M cell-cycle arrest", "KEGG_Drug__ID": null, "Pubchem_ID": "10471963", "STR_LINK_(SMILES)": "C[C@@]12CCC(=O)C([C@H]1C[C@H]([C@]34[C@H]2CC[C@H]([C@H]3O)C(=C)C4=O)O)(C)C", "Single/Combination": "Single", "PMID": "34923957", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Human plasma-cell malignancy", "System": "RPMI-8226", "Dose": "0–80 μM for 24, 48 and 72 h; apoptosis assays at 10 μM for 24 h", "Technique": "Annexin V-FITC/PI flow cytometry, Western blot, qPCR", "Controlled_Technique": "cleaved PARP and cleaved caspase-3, caspase 3 mRNA", "Immune_System-Function_enhanced/numbers_increased": "PARP cleavage / PARP; Caspase-3", "Controlled_Terms_Function_enhanced_Number_increased": "anti-apoptosis-related protein (Bcl-2) , decreased the levels of p-STAT3. STAT3", "Immune_System-Function_inhibited/numbers_decreased": "Apoptosis; Expression / abundance phenotype; BCL-2; STAT3", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/626", "Drug": "Glaucocalyxin A", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Inhibits STAT3 phosphorylation; reduces anti-apoptotic Bcl-2 and increases caspase-associated apoptosis", "KEGG_Drug__ID": null, "Pubchem_ID": "10471963", "STR_LINK_(SMILES)": "C[C@@]12CCC(=O)C([C@H]1C[C@H]([C@]34[C@H]2CC[C@H]([C@H]3O)C(=C)C4=O)O)(C)C", "Single/Combination": "Single", "PMID": "34923957", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Human plasma-cell malignancy", "System": "LP1", "Dose": "0–80 μM for 24, 48 and 72 h; selected apoptosis experiments at 10 μM for 24 h", "Technique": "Annexin V-FITC/PI flow cytometry, Western blot, qPCR", "Controlled_Technique": "cleaved PARP and cleaved caspase-3, caspase 3 mRNA", "Immune_System-Function_enhanced/numbers_increased": "PARP cleavage / PARP; Caspase-3", "Controlled_Terms_Function_enhanced_Number_increased": "anti-apoptosis-related protein (Bcl-2) , decreased the levels of p-STAT3. STAT3", "Immune_System-Function_inhibited/numbers_decreased": "Apoptosis; Expression / abundance phenotype; BCL-2; STAT3", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/627", "Drug": "Glaucocalyxin A", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Inhibits STAT3 phosphorylation and promotes apoptosis", "KEGG_Drug__ID": null, "Pubchem_ID": "10471963", "STR_LINK_(SMILES)": "C[C@@]12CCC(=O)C([C@H]1C[C@H]([C@]34[C@H]2CC[C@H]([C@H]3O)C(=C)C4=O)O)(C)C", "Single/Combination": "Single", "PMID": "34923957", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Human plasma-cell malignancy", "System": "U266", "Dose": "0–80 μM for 24, 48 and 72 h; selected apoptosis experiments at 10 μM for 24 h", "Technique": "Annexin V-FITC/PI flow cytometry, Western blot, qPCR", "Controlled_Technique": "cleaved PARP and cleaved caspase-3, caspase 3 mRNA", "Immune_System-Function_enhanced/numbers_increased": "PARP cleavage / PARP; Caspase-3", "Controlled_Terms_Function_enhanced_Number_increased": "anti-apoptosis-related protein (Bcl-2) , decreased the levels of p-STAT3. STAT3", "Immune_System-Function_inhibited/numbers_decreased": "Apoptosis; Expression / abundance phenotype; BCL-2; STAT3", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/504", "Drug": "JQ1", "Drug_category": "Others/combination", "Drugbank_ID": "DB17021", "Target/s_or_mechanism_of_action": "BRD4 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": "46907787", "STR_LINK_(SMILES)": "CC1=C(SC2=C1C(=N[C@H](C3=NN=C(N32)C)CC(=O)OC(C)(C)C)C4=CC=C(C=C4)Cl)C", "Single/Combination": "Single", "PMID": "35517410", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": "HCT116", "Dose": "0.1 μM", "Technique": "Flow cytometry", "Controlled_Technique": "HLA-ABC, MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I", "Controlled_Terms_Function_enhanced_Number_increased": "surface PD-L1", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 / CD274", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/628", "Drug": "Glaucocalyxin A", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Inhibits STAT3 phosphorylation and activation; induces apoptosis", "KEGG_Drug__ID": null, "Pubchem_ID": "10471963", "STR_LINK_(SMILES)": "C[C@@]12CCC(=O)C([C@H]1C[C@H]([C@]34[C@H]2CC[C@H]([C@H]3O)C(=C)C4=O)O)(C)C", "Single/Combination": "Single", "PMID": "34923957", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Human plasma-cell malignancy", "System": "OCI-MY5", "Dose": "0–80 μM for 24, 48 and 72 h; selected apoptosis experiments at 10 μM for 24 h", "Technique": "Annexin V-FITC/PI flow cytometry, Western blot, qPCR", "Controlled_Technique": "cleaved PARP and cleaved caspase-3, caspase 3 mRNA", "Immune_System-Function_enhanced/numbers_increased": "PARP cleavage / PARP; Caspase-3", "Controlled_Terms_Function_enhanced_Number_increased": "anti-apoptosis-related protein (Bcl-2) , decreased the levels of p-STAT3. STAT3", "Immune_System-Function_inhibited/numbers_decreased": "Apoptosis; Expression / abundance phenotype; BCL-2; STAT3", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/629", "Drug": "Glaucocalyxin A", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Inhibits STAT3 phosphorylation; reduces STAT3-associated survival signaling", "KEGG_Drug__ID": null, "Pubchem_ID": "10471963", "STR_LINK_(SMILES)": "C[C@@]12CCC(=O)C([C@H]1C[C@H]([C@]34[C@H]2CC[C@H]([C@H]3O)C(=C)C4=O)O)(C)C", "Single/Combination": "Single", "PMID": "34923957", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Human plasma-cell malignancy", "System": "OPM2", "Dose": "0–80 μM for 24, 48 and 72 h; selected apoptosis experiments at 10 μM for 24 h", "Technique": "Annexin V-FITC/PI flow cytometry, Western blot, qPCR", "Controlled_Technique": "cleaved PARP and cleaved caspase-3, caspase 3 mRNA", "Immune_System-Function_enhanced/numbers_increased": "PARP cleavage / PARP; Caspase-3", "Controlled_Terms_Function_enhanced_Number_increased": "anti-apoptosis-related protein (Bcl-2) , decreased the levels of p-STAT3. STAT3", "Immune_System-Function_inhibited/numbers_decreased": "Apoptosis; Expression / abundance phenotype; BCL-2; STAT3", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/630", "Drug": "Glaucocalyxin A", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Inhibits STAT3 phosphorylation; reduces STAT3-associated survival signaling", "KEGG_Drug__ID": null, "Pubchem_ID": "10471963", "STR_LINK_(SMILES)": "C[C@@]12CCC(=O)C([C@H]1C[C@H]([C@]34[C@H]2CC[C@H]([C@H]3O)C(=C)C4=O)O)(C)C", "Single/Combination": "Single", "PMID": "34923957", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Human plasma-cell malignancy", "System": "KMS11", "Dose": "10 μM for 24 h in the reported STAT3/apoptosis experiments", "Technique": "Annexin V-FITC/PI flow cytometry, Western blot, qPCR", "Controlled_Technique": "cleaved PARP and cleaved caspase-3, caspase 3 mRNA", "Immune_System-Function_enhanced/numbers_increased": "PARP cleavage / PARP; Caspase-3", "Controlled_Terms_Function_enhanced_Number_increased": "anti-apoptosis-related protein (Bcl-2) , decreased the levels of p-STAT3. STAT3", "Immune_System-Function_inhibited/numbers_decreased": "Apoptosis; Expression / abundance phenotype; BCL-2; STAT3", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1003", "Drug": "Ibrutinib", "Drug_category": "Others/combination", "Drugbank_ID": "DB09053", "Target/s_or_mechanism_of_action": "Ibrutinib is an inhibitor of Bruton’s tyrosine kinase (BTK).", "KEGG_Drug__ID": "D10223", "Pubchem_ID": "24821094", "STR_LINK_(SMILES)": "NC1=NC=NC2=C1C(=NN2[C@@H]1CCCN(C1)C(=O)C=C)C1=CC=C(OC2=CC=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "26660519", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma", "System": "H11 tumor cells were incubated with ibrutinib (1 µM) for 24 hours and then cocultured with splenocytes or purified splenic T cells from mice that had been treated with the ibrutinib/CpG combination", "Dose": "ibrutinib (1 µM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/183", "Drug": "IFL (irinotecan + 5-fluoruracil + levofolinic acid)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00762, DB11596, DB00544", "Target/s_or_mechanism_of_action": "Irinotecan inhibits the action of topoisomerase I\n As levoleucovorin and leucovorin are analogs of tetrahydrofolate (THF), they are able to bypass DHFR reduction and act as a cellular replacement for the co-factor THF, thereby preventing these toxic side effects\n Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D08086, D04715, D00584", "Pubchem_ID": "60838, 149436, 3385", "STR_LINK_(SMILES)": "CCC1=C2CN3C(=CC4=C(COC(=O[C@]4(O)CC)C3=O)C2=NC2=CC=C(OC(=O)N3CCC(CC3)N3CCCCC3)C=C12, \n NC1=NC(=O)C2=C(NC[C@H](CNC3=CC=C(C=C3)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N2C=O)N1, \n FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "20399639", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Human Colon Carcinoma", "System": "HT29", "Dose": "levofolinic acid was added at a concentration of 2 microg/ml (10)4 M) +5-FU was added at a concentration of 500 microgram/ml + irinotecan at a concentration of\n 100 microgram/ml", "Technique": "cytofluorimetric and Western blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "up-regulation of EGFR on tumor cells", "Controlled_Terms_Function_enhanced_Number_increased": "EGFR; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/184", "Drug": "IFL (irinotecan + 5-fluoruracil + levofolinic acid)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00762, DB11596, DB00544", "Target/s_or_mechanism_of_action": "Irinotecan inhibits the action of topoisomerase I\n As levoleucovorin and leucovorin are analogs of tetrahydrofolate (THF), they are able to bypass DHFR reduction and act as a cellular replacement for the co-factor THF, thereby preventing these toxic side effects\n Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": "D08086, D04715, D00584", "Pubchem_ID": "60838, 149436, 3385", "STR_LINK_(SMILES)": "CCC1=C2CN3C(=CC4=C(COC(=O[C@]4(O)CC)C3=O)C2=NC2=CC=C(OC(=O)N3CCC(CC3)N3CCCCC3)C=C12, \n NC1=NC(=O)C2=C(NC[C@H](CNC3=CC=C(C=C3)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N2C=O)N1, \n FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "20399639", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Human Colon Carcinoma", "System": "SW620", "Dose": "levofolinic acid was added at a concentration of 2 microg/ml (10)4 M) +5-FU was added at a concentration of 500 microgram/ml + irinotecan at a concentration of\n 100 microgram/ml", "Technique": "cytofluorimetric and Western blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "up-regulation of EGFR on tumor cells", "Controlled_Terms_Function_enhanced_Number_increased": "EGFR; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1438", "Drug": "IFN-γ + MEK inhibitor trametinib", "Drug_category": "Others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10175", "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "30546955", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "SCCVII mouse cells", "Dose": "trametinib (30 nM), IFN-γ (1 ng/ml)", "Technique": "Flow cytometry,qRT-PCR, Western blotting", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "CXCL9 and CXCL10 MHC-encoded class I molecule H-2Kk", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; CXCL10 / IP-10; CXCL9 / MIG;", "Immune_System-Function_inhibited/numbers_decreased": "Erk1/2 activation", "Controlled_Terms_Function_inhibited_Number_decreased": "ERK / MAPK", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1450", "Drug": "ILT2 Blockade(HP-F1 antibody, which blocks the interaction between ILT2 and its ligands)", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "30619281", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "HL60", "Dose": "0-8 µM", "Technique": "CCK-8 assay,Flow cytometry,westen blot, DNA ladder assay and a Flow cytometry analysis with Annexin V/PI double staining,Western blotting,qRT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Cell viability/proliferation assay; Apoptosis/cell viability assay; Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "antiproliferation activity,Cell cycle arrest,p21 protein,apoptosis-Bax protein increased", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis; Cell-cycle arrest; Cell proliferation; BAX; p21 / CDKN1A", "Immune_System-Function_inhibited/numbers_decreased": "Bcl-2 and Procaspase-3", "Controlled_Terms_Function_inhibited_Number_decreased": "BCL-2", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1451", "Drug": "ILT2 Blockade(HP-F1 antibody, which blocks the interaction between ILT2 and its ligands) + IL-2", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "30619281", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "NB4", "Dose": "0-8 µM", "Technique": "CCK-8 assay,Flow cytometry,westen blot, DNA ladder assay and a Flow cytometry analysis with Annexin V/PI double staining,Western blotting,qRT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Cell viability/proliferation assay; Apoptosis/cell viability assay; Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "antiproliferation activity,Cell cycle arrest,p21 protein,apoptosis-Bax protein increased", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis; Cell-cycle arrest; Cell proliferation; BAX; p21 / CDKN1A", "Immune_System-Function_inhibited/numbers_decreased": "Bcl-2 and Procaspase-3", "Controlled_Terms_Function_inhibited_Number_decreased": "BCL-2", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1452", "Drug": "ILT2 Blockade(HP-F1 antibody, which blocks the interaction between ILT2 and its ligands) + IL-2", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "30619281", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "HL60", "Dose": "chidamide (0.5 μM) combined with decitabine (5 μM) for 72 h", "Technique": "CCK-8 assay,Flow cytometry,westen blot, DNA ladder assay and a Flow cytometry analysis with Annexin V/PI double staining,Western blotting,qRT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Cell viability/proliferation assay; Apoptosis/cell viability assay; Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "antiproliferation activity,Cell cycle arrest,p21 protein,apoptosis-Bax protein increased", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis; Cell-cycle arrest; Cell proliferation; BAX; p21 / CDKN1A", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1453", "Drug": "ILT2 Blockade(HP-F1 antibody, which blocks the interaction between ILT2 and its ligands) and lenalidomide", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "30619281", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "NB4", "Dose": "chidamide (0.5 μM) combined with decitabine (5 μM) for 72 h", "Technique": "CCK-8 assay,Flow cytometry,westen blot, DNA ladder assay and a Flow cytometry analysis with Annexin V/PI double staining,Western blotting,qRT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Cell viability/proliferation assay; Apoptosis/cell viability assay; Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "antiproliferation activity,Cell cycle arrest,p21 protein,apoptosis-Bax protein increased", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis; Cell-cycle arrest; Cell proliferation; BAX; p21 / CDKN1A", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/564", "Drug": "Irinotecan+ AZD7762", "Drug_category": "Others/combination", "Drugbank_ID": "DB00762", "Target/s_or_mechanism_of_action": "Inhibits TOP1 ;Chk1/Chk2 inhibition", "KEGG_Drug__ID": "D08086", "Pubchem_ID": "60838", "STR_LINK_(SMILES)": "CCC1=C2CN3C(=CC4=C(C3=O)COC(=O)[C@@]4(CC)O)C2=NC5=C1C=C(C=C5)OC(=O)N6CCC(CC6)N7CCCCC7", "Single/Combination": "Combination", "PMID": "36589674", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": "SW620", "Dose": "IRI 25 µg/mL; 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Ricolinostat (ACY-1215) is an orally available selective HDAC6 inhibitor", "KEGG_Drug__ID": "D10661", "Pubchem_ID": "46907787, 53340666", "STR_LINK_(SMILES)": "O=C(C[C@H]1C2=NN=C(N2C3=C(C(C4=CC=C(C=C4)Cl)=N1)C(C)=C(S3)C)C)OC(C)(C)C,\n ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "31015208", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "LP-1", "Dose": "500 nM JQ1, 3 μM ricolinostat", "Technique": "immunoblotting, Flow cytometry", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "apoptosis induction-caspase-3 cleavage and DNA fragmentation", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase activation; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": "c-MYC and BCL-2 expression", "Controlled_Terms_Function_inhibited_Number_decreased": "BCL-2; FOS / c-MYC; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/281", "Drug": "JQ1 (BET inhibitor) in combination with ricolinostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB12376", "Target/s_or_mechanism_of_action": "JQ1 is a thienotriazolodiazepine and a potent inhibitor of the BET family of bromodomain proteins which include BRD2, BRD3, BRD4, and the testis-specific protein BRDT in mammals. BET inhibitors structurally similar to JQ1 are being tested in clinical trials for a variety of cancers including NUT midline carcinoma. Ricolinostat (ACY-1215) is an orally available selective HDAC6 inhibitor", "KEGG_Drug__ID": "D10661", "Pubchem_ID": "46907787, 53340666", "STR_LINK_(SMILES)": "O=C(C[C@H]1C2=NN=C(N2C3=C(C(C4=CC=C(C=C4)Cl)=N1)C(C)=C(S3)C)C)OC(C)(C)C,\n ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "31015208", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "OPM-2", "Dose": "500 nM JQ1, 3 μM ricolinostat", "Technique": "immunoblotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "apoptosis induction-caspase-3 cleavage and DNA fragmentation", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase activation; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": "c-MYC and BCL-2 expression", "Controlled_Terms_Function_inhibited_Number_decreased": "BCL-2; FOS / c-MYC; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/282", "Drug": "JQ1 (BET inhibitor) in combination with ricolinostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB12376", "Target/s_or_mechanism_of_action": "JQ1 is a thienotriazolodiazepine and a potent inhibitor of the BET family of bromodomain proteins which include BRD2, BRD3, BRD4, and the testis-specific protein BRDT in mammals. BET inhibitors structurally similar to JQ1 are being tested in clinical trials for a variety of cancers including NUT midline carcinoma. Ricolinostat (ACY-1215) is an orally available selective HDAC6 inhibitor", "KEGG_Drug__ID": "D10661", "Pubchem_ID": "46907787, 53340666", "STR_LINK_(SMILES)": "O=C(C[C@H]1C2=NN=C(N2C3=C(C(C4=CC=C(C=C4)Cl)=N1)C(C)=C(S3)C)C)OC(C)(C)C,\n ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "31015208", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "RPMI-8226", "Dose": "500 nM JQ1, 3 μM ricolinostat", "Technique": "immunoblotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "apoptosis induction-caspase-3 cleavage and DNA fragmentation", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase activation; Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": "c-MYC and BCL-2 expression", "Controlled_Terms_Function_inhibited_Number_decreased": "BCL-2; FOS / c-MYC; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1145", "Drug": "JQ1 (BET inhibitor) in combination with vorinostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "JQ1 is a thienotriazolodiazepine and a potent inhibitor of the BET family of bromodomain proteins which include BRD2, BRD3, BRD4, and the testis-specific protein BRDT in mammals. BET inhibitors structurally similar to JQ1 are being tested in clinical trials for a variety of cancers including NUT midline carcinoma. Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "46907787, 5311", "STR_LINK_(SMILES)": "O=C(C[C@H]1C2=NN=C(N2C3=C(C(C4=CC=C(C=C4)Cl)=N1)C(C)=C(S3)C)C)OC(C)(C)C,\n ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "31015208", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "LP-1", "Dose": "500 nM JQ1, 1 μM vorinostat", "Technique": "MTT assay", "Controlled_Technique": "Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "antimyeloma activity", "Controlled_Terms_Function_enhanced_Number_increased": "Antimyeloma activity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1156", "Drug": "JQ1 (BET inhibitor) in combination with vorinostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "JQ1 is a thienotriazolodiazepine and a potent inhibitor of the BET family of bromodomain proteins which include BRD2, BRD3, BRD4, and the testis-specific protein BRDT in mammals. BET inhibitors structurally similar to JQ1 are being tested in clinical trials for a variety of cancers including NUT midline carcinoma. Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "46907787, 5311", "STR_LINK_(SMILES)": "O=C(C[C@H]1C2=NN=C(N2C3=C(C(C4=CC=C(C=C4)Cl)=N1)C(C)=C(S3)C)C)OC(C)(C)C,\n ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "31015208", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "OPM-2", "Dose": "500 nM JQ1, 1 μM vorinostat", "Technique": "MTT assay", "Controlled_Technique": "Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "antimyeloma activity", "Controlled_Terms_Function_enhanced_Number_increased": "Antimyeloma activity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1167", "Drug": "JQ1 (BET inhibitor) in combination with vorinostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "JQ1 is a thienotriazolodiazepine and a potent inhibitor of the BET family of bromodomain proteins which include BRD2, BRD3, BRD4, and the testis-specific protein BRDT in mammals. BET inhibitors structurally similar to JQ1 are being tested in clinical trials for a variety of cancers including NUT midline carcinoma. Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": "D06320", "Pubchem_ID": "46907787, 5311", "STR_LINK_(SMILES)": "O=C(C[C@H]1C2=NN=C(N2C3=C(C(C4=CC=C(C=C4)Cl)=N1)C(C)=C(S3)C)C)OC(C)(C)C,\n ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "31015208", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "primary CD138+ cells collected from patients with MM (n = 10)", "Dose": "500 nM JQ1, 1 μM vorinostat", "Technique": "MTT assay", "Controlled_Technique": "Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "antimyeloma activity", "Controlled_Terms_Function_enhanced_Number_increased": "Antimyeloma activity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/963", "Drug": "JQ1, an inhibitor of the BET family of bromodomain proteins", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "JQ1 is a thienotriazolodiazepine and a potent inhibitor of the BET family of bromodomain proteins which include BRD2, BRD3, BRD4, and the testis-specific protein BRDT in mammals. BET inhibitors structurally similar to JQ1 are being tested in clinical trials for a variety of cancers including NUT midline carcinoma.", "KEGG_Drug__ID": null, "Pubchem_ID": "46907787", "STR_LINK_(SMILES)": "O=C(C[C@H]1C2=NN=C(N2C3=C(C(C4=CC=C(C=C4)Cl)=N1)C(C)=C(S3)C)C)OC(C)(C)C", "Single/Combination": "Single Drug", "PMID": "28408401", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": "FOXP3+ Tregs present within dissociated tumors from NSCLC patients", "Dose": "2.5μm", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "FOXP3, CTLA-4, and PD-1", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-1 / PDCD1; CTLA-4; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/533", "Drug": "Luminespib + Emricasan", "Drug_category": "Others/combination", "Drugbank_ID": "DB05408", "Target/s_or_mechanism_of_action": "Hsp90 inhibition+Inhibits caspases, including caspase-associated apoptotic signaling", "KEGG_Drug__ID": null, "Pubchem_ID": "135539077 + 12000240", "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C and C[C@@H](C(=O)N[C@@H](CC(=O)O)C(=O)COC1=C(C(=CC(=C1F)F)F)F)NC(=O)C(=O)NC2=CC=CC=C2C(C)(C)C", "Single/Combination": "Single", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "Panc02", "Dose": "0.5 + 10 µM; 24 h", "Technique": "ELISA, RT-qPCR", "Controlled_Technique": "Increased IFN-β, CXCL10, ISG15, and type I IFN signaling", "Immune_System-Function_enhanced/numbers_increased": "IFN-β; CXCL10 / IP-10", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/728", "Drug": "Lapatinib followed by Trastuzumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB01259, DB00072", "Target/s_or_mechanism_of_action": "Lapatinib is a 4-anilinoquinazoline kinase inhibitor of the intracellular tyrosine kinase domains of both epidermal growth factor receptor (HER1/EGFR/ERBB1) and human epidermal growth factor receptor type 2 (HER2/ERBB2)with a dissociation half-life of ≥300 minutes.\n Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D04024, D03257", "Pubchem_ID": "208908, 46507516", "STR_LINK_(SMILES)": "CS(=O(=O)CCNCC1=CC=C(O1)C1=CC2=C(C=C1)N=CN=C2NC1=CC(Cl)=C(OCC2=CC(F)=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "28735814", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "MCF-7", "Dose": "Lapatinib 2 μM concentration and a 48 h timepoint for TKI exposure", "Technique": "High content analysis, LDH-release ADCC assays", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay; LDH-releasing assays", "Immune_System-Function_enhanced/numbers_increased": "increased HER2 levels in MCF-7 (1.3 ± 0.1 fold increase)", "Controlled_Terms_Function_enhanced_Number_increased": "HER2 / ERBB2; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "trastuzumab-mediated ADCC", "Controlled_Terms_Unaffected": "ADCC; Antibody-dependent cytotoxicity", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/729", "Drug": "Lapatinib followed by Trastuzumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB01259, DB00072", "Target/s_or_mechanism_of_action": "Lapatinib is a 4-anilinoquinazoline kinase inhibitor of the intracellular tyrosine kinase domains of both epidermal growth factor receptor (HER1/EGFR/ERBB1) and human epidermal growth factor receptor type 2 (HER2/ERBB2)with a dissociation half-life of ≥300 minutes.\n Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D04024, D03257", "Pubchem_ID": "208908, 46507516", "STR_LINK_(SMILES)": "CS(=O(=O)CCNCC1=CC=C(O1)C1=CC2=C(C=C1)N=CN=C2NC1=CC(Cl)=C(OCC2=CC(F)=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "28735814", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "SKBR3", "Dose": "Lapatinib 2 μM concentration and a 48 h timepoint for TKI exposure", "Technique": "High content analysis, LDH-release ADCC assays", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay; LDH-releasing assays", "Immune_System-Function_enhanced/numbers_increased": "increased HER2 levels in SKBR3\n (2.1 ± 0.6 fold increase)", "Controlled_Terms_Function_enhanced_Number_increased": "HER2 / ERBB2; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "trastuzumab-mediated ADCC", "Controlled_Terms_Unaffected": "ADCC; Antibody-dependent cytotoxicity", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/730", "Drug": "Lapatinib followed by Trastuzumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB01259, DB00072", "Target/s_or_mechanism_of_action": "Lapatinib is a 4-anilinoquinazoline kinase inhibitor of the intracellular tyrosine kinase domains of both epidermal growth factor receptor (HER1/EGFR/ERBB1) and human epidermal growth factor receptor type 2 (HER2/ERBB2)with a dissociation half-life of ≥300 minutes.\n Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D04024, D03257", "Pubchem_ID": "208908, 46507516", "STR_LINK_(SMILES)": "CS(=O(=O)CCNCC1=CC=C(O1)C1=CC2=C(C=C1)N=CN=C2NC1=CC(Cl)=C(OCC2=CC(F)=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "28735814", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "PBMC samples displaying higher direct cytotoxicity against K562,", "Dose": "Lapatinib", "Technique": "High content analysis, LDH-release ADCC assays", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay; LDH-releasing assays", "Immune_System-Function_enhanced/numbers_increased": "increase in trastuzumab-mediated ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1178", "Drug": "Lenalidomide (CC-5013, IMiD3) + anti-CD40 SGN-40", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "16357183", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "MM.1S cells", "Dose": "lenalidomide-1 µM and anti-CD40 SGN-40= 2-10µg", "Technique": "MTT assay", "Controlled_Technique": "Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "MM cell death", "Controlled_Terms_Function_enhanced_Number_increased": "Multiple myeloma cell death", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1189", "Drug": "Lenalidomide (CC-5013, IMiD3) + anti-CD40 SGN-40", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "16357183", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "MM1R", "Dose": "lenalidomide-10 µM and anti-CD40 SGN-40= 2-10µg", "Technique": "MTT assay", "Controlled_Technique": "Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "MM cell death", "Controlled_Terms_Function_enhanced_Number_increased": "Multiple myeloma cell death", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/236", "Drug": "Lenalidomide (CC-5013, IMiD3) + anti-CD40 SGN-40", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "16357183", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "MM patient PBMCs + autologous MM cell lysis", "Dose": "SGN-40 (1 µg/mL), lenalidomide (2 µM/L)", "Technique": "calcein-AM release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "antibody-dependent cell-mediated cytotoxicity (ADCC)", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; Antibody-dependent cytotoxicity;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1215", "Drug": "Lenalidomide (CC-5013, IMiD3) + anti-CD40 SGN-40", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "16357183", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "12BM", "Dose": "lenalidomide-10 µM and anti-CD40 SGN-40= 2-10µg", "Technique": "MTT assay, Flow cytometry", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "MM cell death, cleavage of caspase-3, caspase-8, and\n PARP -markers of apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase-8; Caspase activation; Apoptosis; PARP cleavage / PARP; Multiple myeloma cell death", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1216", "Drug": "Lenalidomide (CC-5013, IMiD3) + anti-CD40 SGN-40", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "16357183", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "28BM", "Dose": "lenalidomide-10 µM and anti-CD40 SGN-40= 2-10µg", "Technique": "MTT assay, Flow cytometry", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "MM cell death, cleavage of caspase-3, caspase-8, and\n PARP -markers of apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase-8; Caspase activation; Apoptosis; PARP cleavage / PARP; Multiple myeloma cell death", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1243", "Drug": "Lenalidomide (CC-5013, IMiD3) + anti-CD40 SGN-40", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "16357183", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "12BM + freshly isolated PBMC effectors at E/T\n ratios of 5:1, 10:1, and 40:1", "Dose": "SGN-40 (2 µg/mL), lenalidomide (2 µM/L)", "Technique": "calcein-AM release assay, Flow cytometry", "Controlled_Technique": "Flow cytometry; Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "CD56+ CD3+ NK cells, double-positive NK cells (CD16+CD56+CD3+as well as LFA 1+CD56+CD3+) antibody-dependent cell-mediated cytotoxicity (ADCC)", "Controlled_Terms_Function_enhanced_Number_increased": "CD3; CD16 / FcγRIIIa; CD56 / NCAM1; LFA-1; Cytotoxicity / cytolysis; ADCC; NK cells; Antibody-dependent cytotoxicity;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/576", "Drug": "Luminespib + Z-VAD-FMK", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Hsp90 inhibition combined with broad caspase inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": "5497174", "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C and C[C@@H](C(=O)N[C@@H](CC(=O)OC)C(=O)CF)NC(=O)[C@H](C(C)C)NC(=O)OCC1=CC=CC=C1", "Single/Combination": "combination", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "MC38", "Dose": "0.5 + 20 µM; 24 h", "Technique": "RT-qPCR, immunoblotting", "Controlled_Technique": "Increased IFN-β and downstream signaling", "Immune_System-Function_enhanced/numbers_increased": "IFN-β", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1244", "Drug": "Lenalidomide (CC-5013, IMiD3) + anti-CD40 SGN-40", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "16357183", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "12BM + freshly isolated PBMC effectors at E/T\n ratios of 5:1, 10:1, and 40:1", "Dose": "SGN-40 (2 µg/mL), lenalidomide (2 µM/L)", "Technique": "calcein-AM release assay, Flow cytometry", "Controlled_Technique": "Flow cytometry; Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "CD56+ CD3+ NK cells, double-positive NK cells (CD16+CD56+CD3+as well as LFA 1+CD56+CD3+) antibody-dependent cell-mediated cytotoxicity (ADCC)", "Controlled_Terms_Function_enhanced_Number_increased": "CD3; CD16 / FcγRIIIa; CD56 / NCAM1; LFA-1; Cytotoxicity / cytolysis; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1033", "Drug": "Lenalidomide + defucosylated version (YB-AHM) of humanized monoclonal antibody against HM1.24 (CD317)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "24386306", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "BMMCs from MM patient", "Dose": "Len (3 µM) for 24 hours, and incubated in the presence of YB-AHM (0.1 µg/mL) for 24 hours", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1035", "Drug": "Lenalidomide + defucosylated version (YB-AHM) of humanized monoclonal antibody against HM1.24 (CD317)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "24386306", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "RPMI 8226 and KMS-11 cells exhibitING SP fractions (MM drug-resistant) + PBMCs from 3 normal donors", "Dose": "Len (3 µM) , YB-AHM (0.1 µg/mL) combination for 24 hours", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "ADCC activity against SP cells HM1.24 (CD317)", "Controlled_Terms_Function_enhanced_Number_increased": "CD317 / HM1.24; ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1224", "Drug": "Lenalidomide + defucosylated version (YB-AHM) of humanized monoclonal antibody against HM1.24 (CD317)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "24386306", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "PBMCs from 3 normal donors + RPMI 8226 cell", "Dose": "YB-AHM (0.1 µg/mL) for 4 hours, Len (3 µM) for 48 hours", "Technique": "Flow cytometric PKH26 assay. ADCC activity was determined by percentages of 7AAD+ dead cells in PKH26-labeled target MM cells", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1225", "Drug": "Lenalidomide + defucosylated version (YB-AHM) of humanized monoclonal antibody against HM1.24 (CD317)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "24386306", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "PBMCs from patient with MM + RPMI 8226 cell", "Dose": "YB-AHM (0.1 µg/mL) for 4 hours, Len (3 µM) for 48 hours", "Technique": "Flow cytometric PKH26 assay. ADCC activity was determined by percentages of 7AAD+ dead cells in PKH26-labeled target MM cells", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1027", "Drug": "Lenalidomide + IFN-γ", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "KMS-11", "Dose": "Lenalidomide 1.0 or 0.1 μM and 100 U/ml of IFN-γ", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1028", "Drug": "Lenalidomide + IFN-γ", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "MM.1S cells", "Dose": "Lenalidomide 1.0 or 0.1 μM and 100 U/ml of IFN-γ", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1029", "Drug": "Lenalidomide + IFN-γ", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "OPM-2", "Dose": "Lenalidomide 1.0 or 0.1 μM and 100 U/ml of IFN-γ", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1030", "Drug": "Lenalidomide + IFN-γ + panobinostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB06603", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D04687, D10019", "Pubchem_ID": "216326, 6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Combination", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "MM.1S cells", "Dose": "Lenalidomide 1.0 or 0.1 μM and 100 U/ml of IFN-γ +25 nM panobinostat", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1031", "Drug": "Lenalidomide + IFN-γ + panobinostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB06603", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D04687, D10019", "Pubchem_ID": "216326, 6918837", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O,\n CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Combination", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "KMS-11", "Dose": "Lenalidomide 1.0 or 0.1 μM and 100 U/ml of IFN-γ +25 nM panobinostat", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1032", "Drug": "Lenalidomide + IFN-γ + panobinostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB06603", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D04687, D10019", "Pubchem_ID": "216326, 6918837", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "OPM-2", "Dose": "Lenalidomide 1.0 or 0.1 μM and 100 U/ml of IFN-γ +25 nM panobinostat", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/778", "Drug": "Lenalidomide + IL21 )", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "27287425", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "Raji cells followed by γ-irradiation (to prevent further cell proliferation) + purified T lymphocytes from healthy donors", "Dose": "SAHA (2.5 µM)", "Technique": "ELISA , [3H]-thymidine uptake assay for T cell proliferation", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Cell viability/proliferation assay; Cell proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "T cell proliferation", "Controlled_Terms_Function_enhanced_Number_increased": "Cell proliferation; T cells; T-cell proliferation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1026", "Drug": "Lenalidomide +IPH2101", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB06049", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n The therapeutic principle of IPH 2101 (NN 1975) is based on the activation of Natural Killer (NK) cells by a monoclonal antibody which blocks the NK’s KIR inhibitory receptors, thereby potentiating NK cells anti-cancer action.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "22031859", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "Primary MM cells", "Dose": "5μM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "UBLP-1", "Controlled_Terms_Function_enhanced_Number_increased": "ULBP1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1047", "Drug": "Lenalidomide +IPH2101", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB06049", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n The therapeutic principle of IPH 2101 (NN 1975) is based on the activation of Natural Killer (NK) cells by a monoclonal antibody which blocks the NK’s KIR inhibitory receptors, thereby potentiating NK cells anti-cancer action.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "22031859", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "U266", "Dose": "5μM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MICA , DR4, ULBP-2, CD112", "Controlled_Terms_Function_enhanced_Number_increased": "CD112 / Nectin-2 / PVRL2; ULBP2; MICA; TRAIL-R1 / DR4 / TNFRSF10A;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "ULBP-1, CD155, ULBP-3, and ULBP-4", "Controlled_Terms_Unaffected": "CD155 / PVR; ULBP1; ULBP3; ULBP4", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/408", "Drug": "Lenalidomide +IPH2101", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB06049", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n The therapeutic principle of IPH 2101 (NN 1975) is based on the activation of Natural Killer (NK) cells by a monoclonal antibody which blocks the NK’s KIR inhibitory receptors, thereby potentiating NK cells anti-cancer action.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "22031859", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "primary MM cells+ Healthy NK cells", "Dose": "5μM lenalidomide+30 μg/mL IPH2101", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "IFN-y", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/409", "Drug": "Lenalidomide +IPH2101", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB06049", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n The therapeutic principle of IPH 2101 (NN 1975) is based on the activation of Natural Killer (NK) cells by a monoclonal antibody which blocks the NK’s KIR inhibitory receptors, thereby potentiating NK cells anti-cancer action.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "22031859", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "patient-derived NK cells+ autologous MM tumor cells", "Dose": "5μM lenalidomide+30 μg/mL IPH2101", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "IFN-y", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/713", "Drug": "Lenalidomide +rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB00073", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Rituximab is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes.", "KEGG_Drug__ID": "D04687, \n D02994", "Pubchem_ID": "216326, \n 46505820", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "18628480", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Mantle Cell Lymphoma (MCL)", "System": "CD20+ Jeko-1 (rituximab-coated)", "Dose": "(0.001-10 10 µM/L), 20 µg/mL rituximab", "Technique": "lactate dehydrogenase release assay", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell cytotoxicity, ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, 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"D04687, \n D02994", "Pubchem_ID": "216326, \n 46505820", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "18628480", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - NHL", "System": "Namalwa(rituximab-coated NHL cell lines) + Purified NK cells", "Dose": "(0.001-10 10 µM/L), 20 µg/mL rituximab", "Technique": "lactate dehydrogenase release assay", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell cytotoxicity, ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/719", "Drug": "Lenalidomide +rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB00073", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Rituximab is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes.", "KEGG_Drug__ID": "D04687, \n D02994", "Pubchem_ID": "216326, \n 46505820", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "18628480", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - NHL", "System": "primary tumor cells derived from three patients with B-CLL who have been treated with fludarabine plus cyclophosphamide, two of whom had relapsed after treatment + Purified NK cells", "Dose": "(0.001-10 10 µM/L), 20 µg/mL rituximab", "Technique": "lactate dehydrogenase release assay", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell cytotoxicity, ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; NK cells; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/264", "Drug": "PI3K inhibitor (LY294002; )", "Drug_category": "PI3K inhibitor", "Drugbank_ID": "DB02656", "Target/s_or_mechanism_of_action": "Protein kinase inhibitors, the mode of action of LY294002 is through competition with ATP for binding the PI3K active site", "KEGG_Drug__ID": "C15195", "Pubchem_ID": "3973", "STR_LINK_(SMILES)": "O=C1C=C(OC2=C1C=CC=C2C1=CC=CC=C1)N1CCOCC1", "Single/Combination": "Single Drug", "PMID": "26637667", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC", "System": "H157", "Dose": "1 µmol/L", "Technique": "Western Blotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 expression", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/720", "Drug": "Lenalidomide +rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB00073", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Rituximab is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes.", "KEGG_Drug__ID": "D04687, \n D02994", "Pubchem_ID": "216326, \n 46505820", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "18628480", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - NHL", "System": "Raji (rituximab-coated NHL cell lines) + Purified NK cells", "Dose": "(0.001-10 10 µM/L), 20 µg/mL rituximab", "Technique": "lactate dehydrogenase release assay", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell cytotoxicity, monocyte-mediated lysis, ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; NK cells; 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engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes.", "KEGG_Drug__ID": "D04687, \n D02994", "Pubchem_ID": "216326, \n 46505820", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "18628480", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - NHL", "System": "Farage (rituximab-coated NHL cell lines) +Purified NK cells", "Dose": "(0.001-10 10 µM/L), 20 µg/mL rituximab", "Technique": "lactate dehydrogenase release assay", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell cytotoxicity, monocyte-mediated lysis,ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; NK cells; Monocytes; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1380", "Drug": "Lenalidomide +rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB00073", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Rituximab is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes.", "KEGG_Drug__ID": "D04687, \n D02994", "Pubchem_ID": "216326, \n 46505820", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "18772452", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "Raji cells", "Dose": "(250 nM)", "Technique": "Time course RT-PCR,Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "TNF-related costimulatory molecules - 4-1BB ligand (4-1BBL/TNFSF9),4-1BBL", "Controlled_Terms_Function_enhanced_Number_increased": "4-1BB / CD137; 4-1BB ligand / TNFSF9; TNF-α / TNF; CD80/CD86 costimulation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/44", "Drug": "Lenalidomide +rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB00073", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Rituximab is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes.", "KEGG_Drug__ID": "D04687, \n D02994", "Pubchem_ID": "216326, \n 46505820", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "25313353", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "U937", "Dose": "(250 nM)", "Technique": "Time course RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "TNF-related costimulatory molecules - 4-1BB ligand (4-1BBL/TNFSF9)", "Controlled_Terms_Function_enhanced_Number_increased": "4-1BB / CD137; 4-1BB ligand / TNFSF9; TNF-α / TNF; CD80/CD86 costimulation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/117", "Drug": "Lenalidomide +rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB00073", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Rituximab is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes.", "KEGG_Drug__ID": "D04687, \n D02994", "Pubchem_ID": "216326, \n 46505820", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "18772452", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "Jurkat T cells (JA16 clone)", "Dose": "(500 nM)", "Technique": "Transcription Low Density Array,RT-PCR analysis,quantitative real time RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "TNF-related costimulatory molecules - 4-1BB ligand (4-1BBL/TNFSF9) p21/WAF/CDKN1A cell cycle inhibitor", "Controlled_Terms_Function_enhanced_Number_increased": "4-1BB / CD137; 4-1BB ligand / TNFSF9; TNF-α / TNF; p21 / CDKN1A; CD80/CD86 costimulation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1004", "Drug": "Lenalidomide and\n pomalidomide", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB08910", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Promalidomide is an immunomodulatory agent with antineoplastic activity. It is shown to inhibit the proliferation and induce apoptosis of various tumour cells.", "KEGG_Drug__ID": "D04687, D08976", "Pubchem_ID": "216326, 134780", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O,\n NC1=CC=CC2=C1C(=O)N(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "28881567", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Kaposi Sarcoma And Primary Effusion Lymphoma (PEL)", "System": "BCBL-1", "Dose": "10 μM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "MHC-1", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/780", "Drug": "Lenalidomide and alemtuzumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480,DB00087", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Campath binds to the CD52 antigen present on most B and T lymphocytes. This binding leads to antibody-dependent lysis of leukemic cells.", "KEGG_Drug__ID": "D04687, \n D02802", "Pubchem_ID": "216326, 46507379", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "27815572", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "Raji cells followed by γ-irradiation (to prevent further cell proliferation) + purified T lymphocytes from healthy donors", "Dose": "(250 nM)", "Technique": "ELISA , [3H]-thymidine uptake assay for T cell proliferation", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Cell viability/proliferation assay; Cell proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "T cell proliferation", "Controlled_Terms_Function_enhanced_Number_increased": "Cell proliferation; T cells; T-cell proliferation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/207", "Drug": "Lenalidomide and IL-2", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D04687", "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "30619281", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "Jurkat", "Dose": "0.25 µM/L,TRAIL-(20 and 100 ng/mL, respectively)", "Technique": "Western blotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "TRAIL-induced apoptosis-phosphatidylserine externalization, processing of caspase-3 to its catalytically active large subunits (p19/p17) and cleavage of PARP", "Controlled_Terms_Function_enhanced_Number_increased": "TRAIL; Caspase-3; Caspase activation; Apoptosis; PARP cleavage / PARP", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/501", "Drug": "Macrocarpal I", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Binds TUBB2B (beta-tubulin) and PARP1; disrupts microtubule polymerization and DNA repair; activates PERK/eIF2A/ATF4/CHOP signaling and induces immunogenic cell death", "KEGG_Drug__ID": null, "Pubchem_ID": "10028546", "STR_LINK_(SMILES)": "CC(C)C[C@@H]([C@@H]1CC[C@@]([C@H]2[C@]1(CC[C@H](C2)C(C)(C)O)C)(C)O)C3=C(C(=C(C(=C3O)C=O)O)C=O)O", "Single/Combination": "Single", "PMID": "39987121", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Human colorectal adenocarcinoma cell line", "System": "DLD1", "Dose": "10, 50 and 100 µM in specified assays; 50 µM used for time-course and selected mechanistic assays", "Technique": "Immunofluorescence; flow cytometry; HMGB1 reporter assay; extracellular ATP assay; apoptosis and ferroptosis assays; western blot", "Controlled_Technique": "expression of ICD-associated DAMPs (CRT, HMGB1, and ATP)", "Immune_System-Function_enhanced/numbers_increased": "HMGB1; Calreticulin / CRT; Immunogenic cell death; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": "Induced tumor-cell apoptosis and ferroptosis; inhibited microtubule polymerization and PARP1 activity", "Immune_System-Function_inhibited/numbers_decreased": "Apoptosis", "Controlled_Terms_Function_inhibited_Number_decreased": "NR", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "NR", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1245", "Drug": "Lenalidomide-rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB00002", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D04687, D03455", "Pubchem_ID": "216326, 46507042", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "30767211", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Follicular Lymphoma (FL)", "System": "RL", "Dose": "1 μmol/l lenalidomide and 1 μg/ml rituximab", "Technique": "Apoptosis analysis by Annexin V and TO-PRO-3 staining", "Controlled_Technique": "Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "ADCC 57%", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1256", "Drug": "Lenalidomide-rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB00002", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D04687, D03455", "Pubchem_ID": "216326, 46507042", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "30767211", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Follicular Lymphoma (FL)", "System": "DOHH2", "Dose": "1 μmol/l lenalidomide and 1 μg/ml rituximab", "Technique": "Apoptosis analysis by Annexin V and TO-PRO-3 staining", "Controlled_Technique": "Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "ADCC 69%", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/403", "Drug": "Lenalidomide-rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB00002", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": "D04687, D03455", "Pubchem_ID": "216326, 46507042", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "30767211", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Follicular Lymphoma (FL)", "System": "PBMCs from FL patients", "Dose": null, "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "interferon-y (IFN-y), granulocyte macrophage\n colony-stimulating factor (GM-CSF) and\n tumour necrosis factor-a (TNF-a)", "Controlled_Terms_Function_enhanced_Number_increased": "TNF-α / TNF; GM-CSF / CSF2; Macrophages; Granulocytes; IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/743", "Drug": "Lenalidomide+thalidomide+pomalidomide", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB01041, DB08910", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Previous research indicate that thalidomide binds to cerebron, a component of the E3 ubiquitin ligase complex, to selectively degrade the transcription factor IKZF3 and IKZF1. These 2 transcription factors are vital for the proliferation and survival of malignant myeloma cells.\n Promalidomide is an immunomodulatory agent with antineoplastic activity. It is shown to inhibit the proliferation and induce apoptosis of various tumour cells.", "KEGG_Drug__ID": "D04687, D00754, D08976", "Pubchem_ID": "216326, 5426, 134780", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O\n O=C1N(C2CCC(=O)NC2=O)C(=O)C2=CC=CC=C12\n NC1=CC=CC2=C1C(=O)N(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "19638977", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "CT26 cells", "Dose": "0.01 to 30 mM.", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "VEGF", "Controlled_Terms_Function_inhibited_Number_decreased": "VEGF", "Immune_System_function_unaffected": "IP10 and TIMP1", "Controlled_Terms_Unaffected": "CXCL10 / IP-10", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/518", "Drug": "Luminespib (AUY922)", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Hsp90 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": "135539077", "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C", "Single/Combination": "Single", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "MC38", "Dose": "0.5 µM; 24 h", "Technique": "ELISA, RT-qPCR", "Controlled_Technique": "Marginal IFN-β induction", "Immune_System-Function_enhanced/numbers_increased": "IFN-β", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/521", "Drug": "Luminespib (AUY922)", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Hsp90 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": "135539077", "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C", "Single/Combination": "Single", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "HT29", "Dose": "0.5 µM; 24 h", "Technique": "ELISA, RT-qPCR", "Controlled_Technique": "Marginal IFN-β induction", "Immune_System-Function_enhanced/numbers_increased": "IFN-β", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/525", "Drug": "Luminespib (AUY922)", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Hsp90 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": "135539077", "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C", "Single/Combination": "Single", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "CT26", "Dose": "0.5 µM; 24 h", "Technique": "ELISA, RT-qPCR", "Controlled_Technique": "Marginal IFN-β induction", "Immune_System-Function_enhanced/numbers_increased": "IFN-β", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/528", "Drug": "Luminespib (AUY922)", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Hsp90 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": "135539077", "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C", "Single/Combination": "Single", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "CTIAC11", "Dose": "0.5 µM; 24 h", "Technique": "ELISA, RT-qPCR", "Controlled_Technique": "Marginal IFN-β induction", "Immune_System-Function_enhanced/numbers_increased": "IFN-β", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/531", "Drug": "Luminespib (AUY922)", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Hsp90 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": "135539077", "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C", "Single/Combination": "Single", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "Panc02", "Dose": "0.5 µM; 24 h", "Technique": "ELISA, RT-qPCR", "Controlled_Technique": "Marginal IFN-β induction", "Immune_System-Function_enhanced/numbers_increased": "IFN-β", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/520", "Drug": "Luminespib + Emricasan", "Drug_category": "Others/combination", "Drugbank_ID": "DB05408", "Target/s_or_mechanism_of_action": "Hsp90 inhibition+Inhibits caspases, including caspase-associated apoptotic signaling", "KEGG_Drug__ID": null, "Pubchem_ID": "135539077 + 12000240", "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C and C[C@@H](C(=O)N[C@@H](CC(=O)O)C(=O)COC1=C(C(=CC(=C1F)F)F)F)NC(=O)C(=O)NC2=CC=CC=C2C(C)(C)C", "Single/Combination": "Single", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "MC38", "Dose": "0.5 + 10 µM; 24 h", "Technique": "ELISA, RT-qPCR", "Controlled_Technique": "Increased IFN-β, CXCL10, ISG15, and type I IFN signaling", "Immune_System-Function_enhanced/numbers_increased": "IFN-β; CXCL10 / IP-10", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/523", "Drug": "Luminespib + Emricasan", "Drug_category": "Others/combination", "Drugbank_ID": "DB05408", "Target/s_or_mechanism_of_action": "Hsp90 inhibition+Inhibits caspases, including caspase-associated apoptotic signaling", "KEGG_Drug__ID": null, "Pubchem_ID": "135539077 + 12000240", "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C and C[C@@H](C(=O)N[C@@H](CC(=O)O)C(=O)COC1=C(C(=CC(=C1F)F)F)F)NC(=O)C(=O)NC2=CC=CC=C2C(C)(C)C", "Single/Combination": "Single", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "HT29", "Dose": "0.5 + 10 µM; 24 h", "Technique": "ELISA, RT-qPCR", "Controlled_Technique": "Increased IFN-β, CXCL10, ISG15, and type I IFN signaling", "Immune_System-Function_enhanced/numbers_increased": "IFN-β; CXCL10 / IP-10", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/527", "Drug": "Luminespib + Emricasan", "Drug_category": "Others/combination", "Drugbank_ID": "DB05408", "Target/s_or_mechanism_of_action": "Hsp90 inhibition+Inhibits caspases, including caspase-associated apoptotic signaling", "KEGG_Drug__ID": null, "Pubchem_ID": "135539077 + 12000240", "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C and C[C@@H](C(=O)N[C@@H](CC(=O)O)C(=O)COC1=C(C(=CC(=C1F)F)F)F)NC(=O)C(=O)NC2=CC=CC=C2C(C)(C)C", "Single/Combination": "Single", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "CT26", "Dose": "0.5 + 10 µM; 24 h", "Technique": "ELISA, RT-qPCR", "Controlled_Technique": "Increased IFN-β, CXCL10, ISG15, and type I IFN signaling", "Immune_System-Function_enhanced/numbers_increased": "IFN-β; CXCL10 / IP-10", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/530", "Drug": "Luminespib + Emricasan", "Drug_category": "Others/combination", "Drugbank_ID": "DB05408", "Target/s_or_mechanism_of_action": "Hsp90 inhibition+Inhibits caspases, including caspase-associated apoptotic signaling", "KEGG_Drug__ID": null, "Pubchem_ID": "135539077 + 12000240", "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C and C[C@@H](C(=O)N[C@@H](CC(=O)O)C(=O)COC1=C(C(=CC(=C1F)F)F)F)NC(=O)C(=O)NC2=CC=CC=C2C(C)(C)C", "Single/Combination": "Single", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": "CTIAC11", "Dose": "0.5 + 10 µM; 24 h", "Technique": "ELISA, RT-qPCR", "Controlled_Technique": "Increased IFN-β, CXCL10, ISG15, and type I IFN signaling", "Immune_System-Function_enhanced/numbers_increased": "IFN-β; CXCL10 / IP-10", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/500", "Drug": "Macrocarpal I", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Binds TUBB2B (beta-tubulin) and PARP1; disrupts microtubule polymerization and DNA repair; activates PERK/eIF2A/ATF4/CHOP signaling and induces immunogenic cell death", "KEGG_Drug__ID": null, "Pubchem_ID": "10028546", "STR_LINK_(SMILES)": "CC(C)C[C@@H]([C@@H]1CC[C@@]([C@H]2[C@]1(CC[C@H](C2)C(C)(C)O)C)(C)O)C3=C(C(=C(C(=C3O)C=O)O)C=O)O", "Single/Combination": "Single", "PMID": "39987121", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Human colorectal adenocarcinoma cell line", "System": "SW620", "Dose": "10, 50 and 100 µM in specified assays; 50 µM used for time-course and selected mechanistic assays", "Technique": "Immunofluorescence; flow cytometry; HMGB1 reporter assay; extracellular ATP assay, western blot", "Controlled_Technique": "expression of ICD-associated DAMPs (CRT, HMGB1, and ATP), activating the PERK/eIF2A/ATF4/CHOP signaling pathway, induces apoptosis and ferroptosis in tumor cells", "Immune_System-Function_enhanced/numbers_increased": "Apoptosis; HMGB1; eIF2α / EIF2S1; Calreticulin / CRT; Immunogenic cell death; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": "Induced tumor-cell apoptosis and ferroptosis; inhibited microtubule polymerization and PARP1 activity", "Immune_System-Function_inhibited/numbers_decreased": "Apoptosis", "Controlled_Terms_Function_inhibited_Number_decreased": "NR", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "NR", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/761", "Drug": "MC1568", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "HDAC Inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": "11381449", "STR_LINK_(SMILES)": "CN1C=C(C=C1/C=C/C(=O)NO)/C=C/C(=O)C2=CC(=CC=C2)F", "Single/Combination": "Single Drug", "PMID": "27614429", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Mantle Cell Lymphoma (MCL)", "System": "JeKo-1 + co-cultured with DN32.D3 and N38-3C3", "Dose": "50 nM MC1568 for 4 h,", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "CD1D-mediated antigen presentation IL-2 levels", "Controlled_Terms_Function_enhanced_Number_increased": "CD1d; IL-2; Antigen presentation; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1620", "Drug": "MEKi PD0325901", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "26943572", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer", "System": "SW1736", "Dose": "MEKi PD0325901 10μM", "Technique": "Quantitative PCR, Western blot", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 protein expression", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1621", "Drug": "MEKi PD0325901+IFN-y", "Drug_category": "Others/combination", "Drugbank_ID": "DB07101", "Target/s_or_mechanism_of_action": "PD0325901 is a selective, cell permeable inhibitor of the MEK/ERK pathway that inhibits the activation and downstream signaling of MEK.", "KEGG_Drug__ID": null, "Pubchem_ID": "9826528", "STR_LINK_(SMILES)": "[H][C@@](O)(CO)CONC(=O)C1=C(NC2=CC=C(I)C=C2F)C(F)=C(F)C=C1", "Single/Combination": "Combination", "PMID": "26943572", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer", "System": "8505c", "Dose": "MEKi PD0325901(10μM )+hIFN-y (500U/ml)", "Technique": "Quantitative PCR, Western blot", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 protein expression and mRNA exxpression phospho ERK", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; ERK / MAPK; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1623", "Drug": "MEKi PD0325901+IFN-y", "Drug_category": "Others/combination", "Drugbank_ID": "DB07101", "Target/s_or_mechanism_of_action": "PD0325901 is a selective, cell permeable inhibitor of the MEK/ERK pathway that inhibits the activation and downstream signaling of MEK.", "KEGG_Drug__ID": null, "Pubchem_ID": "9826528", "STR_LINK_(SMILES)": "[H][C@@](O)(CO)CONC(=O)C1=C(NC2=CC=C(I)C=C2F)C(F)=C(F)C=C1", "Single/Combination": "Combination", "PMID": "26943572", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer", "System": "BCPAP", "Dose": "MEKi PD0325901(10μM )+hIFN-y (500U/ml)", "Technique": "Quantitative PCR, Western blot", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 protein expression and mRNA exxpression phospho ERK", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; ERK / MAPK; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1624", "Drug": "MEKi PD0325901+IFN-y", "Drug_category": "Others/combination", "Drugbank_ID": "DB07101", "Target/s_or_mechanism_of_action": "PD0325901 is a selective, cell permeable inhibitor of the MEK/ERK pathway that inhibits the activation and downstream signaling of MEK.", "KEGG_Drug__ID": null, "Pubchem_ID": "9826528", "STR_LINK_(SMILES)": "[H][C@@](O)(CO)CONC(=O)C1=C(NC2=CC=C(I)C=C2F)C(F)=C(F)C=C1", "Single/Combination": "Combination", "PMID": "26943572", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer", "System": "SW1736", "Dose": "MEKi PD0325901(10μM )+hIFN-y (500U/ml)", "Technique": "Quantitative PCR, Western blot", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 protein expression", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/582", "Drug": "Melarsoprol (MEL)", "Drug_category": "Others/combination", "Drugbank_ID": "DB12864", "Target/s_or_mechanism_of_action": "DNA damage; activates cGAS–STING–TBK1–IRF3 signaling, promoting IFN-β production", "KEGG_Drug__ID": "D00832", "Pubchem_ID": "10311", "STR_LINK_(SMILES)": "C1C(S[As](S1)C2=CC=C(C=C2)NC3=NC(=NC(=N3)N)N)CO", "Single/Combination": "Single", "PMID": "40528981", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "mouse HCC cell line", "System": "Hepa1–6", "Dose": "20 µmol/L in vitro", "Technique": "Western blot, RT-qPCR, ELISA, cGAS–STING signaling", "Controlled_Technique": "expression of IFN-β mRNA and protein,", "Immune_System-Function_enhanced/numbers_increased": "IFN-β; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/583", "Drug": "Melarsoprol (MEL)", "Drug_category": "Others/combination", "Drugbank_ID": "DB12864", "Target/s_or_mechanism_of_action": "DNA damage; activates cGAS–STING–TBK1–IRF3 signaling, promoting IFN-β production", "KEGG_Drug__ID": "D00832", "Pubchem_ID": "10311", "STR_LINK_(SMILES)": "C1C(S[As](S1)C2=CC=C(C=C2)NC3=NC(=NC(=N3)N)N)CO", "Single/Combination": "Single", "PMID": "40528981", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Human HCC cell line", "System": "HepG2", "Dose": "20 µmol/L in vitro", "Technique": "Western blot, RT-qPCR, ELISA, cGAS–STING signaling", "Controlled_Technique": "expression of IFN-β mRNA and protein,", "Immune_System-Function_enhanced/numbers_increased": "IFN-β; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/586", "Drug": "Melarsoprol (MEL)+Lenalidomide (LEN)", "Drug_category": "Others/combination", "Drugbank_ID": "DB12864+DB00480", "Target/s_or_mechanism_of_action": "DNA damage; activates cGAS–STING–TBK1–IRF3 signaling, promoting IFN-β production", "KEGG_Drug__ID": "D00832+\t\nD04687", "Pubchem_ID": "10311+216326", "STR_LINK_(SMILES)": "C1C(S[As](S1)C2=CC=C(C=C2)NC3=NC(=NC(=N3)N)N)CO and C1CC(=O)NC(=O)C1N2CC3=C(C2=O)C=CC=C3N", "Single/Combination": "combination", "PMID": "40528981", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "mouse HCC cell line", "System": "Hepa1–6", "Dose": "20 µmol/L in vitro  and 40 µmol/L in vitro", "Technique": "Western blot, RT-qPCR, ELISA, cGAS–STING signaling", "Controlled_Technique": "maintenance of IFN-β", "Immune_System-Function_enhanced/numbers_increased": "IFN-β", "Controlled_Terms_Function_enhanced_Number_increased": "reduction of TNF-α", "Immune_System-Function_inhibited/numbers_decreased": "TNF-α / TNF", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/587", "Drug": "Melarsoprol (MEL)+Lenalidomide (LEN)", "Drug_category": "Others/combination", "Drugbank_ID": "DB12864+DB00480", "Target/s_or_mechanism_of_action": "DNA damage; 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PD-L1 / CD274", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "Increased PD-L1 may promote inhibitory immune-checkpoint signaling", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 immune checkpoint pathway; Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/690", "Drug": "Mitomycin C (MMC)", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "DNA crosslinking and inhibition of DNA synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "40380807", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "gastric cancer cell line", "System": "SNU-1", "Dose": "0.85μM", "Technique": "Flow cytometry; Western blot", "Controlled_Technique": "Increased cell-surface PD-L1 and MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; PD-L1 / CD274", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "Increased PD-L1 may promote inhibitory immune-checkpoint signaling", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 immune checkpoint pathway; Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1428", "Drug": "MMC (mitomycin)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00305", "Target/s_or_mechanism_of_action": "Mitomycin is activated in vivo to a bifunctional and trifunctional alkylating agent. Binding to DNA leads to cross-linking and inhibition of DNA synthesis and function. Mitomycin is cell cycle phase-nonspecific.", "KEGG_Drug__ID": "D00208", "Pubchem_ID": "5746", "STR_LINK_(SMILES)": "[H][C@]12CN3C4=C([C@@H](COC(N)=O)[C@@]3(OC)[C@@]1([H])N2)C(=O)C(N)=C(C)C4=O", "Single/Combination": "Single Drug", "PMID": "16957513", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": "Colon cancer (SW480) cells", "Dose": "MMC (mitomycin) IC 50: 3.12ug/ml", "Technique": "Immunocytochemistry\n and Flow cytometry, RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunocytochemistry (ICC)", "Immune_System-Function_enhanced/numbers_increased": "Fas, FasL", "Controlled_Terms_Function_enhanced_Number_increased": "CD95 / Fas / FAS; Fas ligand / FasL / FASLG", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/834", "Drug": "MPT0G612", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "a Novel HDAC6 Inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31652644", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "DLD-1", "Dose": "0-5 µM", "Technique": "SRB and MTT assay", "Controlled_Technique": "Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "antiproliferation activity", "Controlled_Terms_Function_enhanced_Number_increased": "Cell proliferation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/845", "Drug": "MPT0G612", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "a Novel HDAC6 Inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31652644", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "HT-29", "Dose": "0-5 µM", "Technique": "SRB and MTT assay, propidium iodide (PI) staining", "Controlled_Technique": "Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "apoptosis, antiproliferation activity, apoptotic cell death-related proteins (cleaved PARP and caspase 3/8/9), cell cycle arrest", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; 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Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "IL-8 and CCL2", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-8 / CXCL8; CCL2 / MCP-1; IL-8/CXCL8", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/931", "Drug": "MS-275 (entinostat) ++tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)", "Drug_category": "Others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": "D09338", "Pubchem_ID": "4261", "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "16818655", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "PBMCs", "Dose": "2.5-7.5 mg/day", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "BID, DR5, and p73 CD154", "Controlled_Terms_Function_enhanced_Number_increased": "TRAIL-R2 / DR5 / TNFRSF10B; BID", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/724", "Drug": "Neratinib followed by Trastuzumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB11828, DB00072", "Target/s_or_mechanism_of_action": "Neratinib binds to and irreversibly inhibits EGFR, HER2, and HER4 [FDA Label]. This prevents auotphoshorylation of tyrosine residues on the receptor and reduces oncogenic signalling through the mitogen-activated protein kinase and Akt pathways.\n Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "9915743, 46507516", "STR_LINK_(SMILES)": "CCOC1=C(NC(=O)\\C=C\\CN(C)C)C=C2C(NC3=CC=C(OCC4=CC=CC=N4)C(Cl)=C3)=C(C=NC2=C1)C#N", "Single/Combination": "Combination", "PMID": "28735814", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "SKBR3", "Dose": "Neratinib 2 μM concentration and a 48 h timepoint for TKI exposure", "Technique": "High content analysis, LDH-release ADCC assays", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay; LDH-releasing assays", "Immune_System-Function_enhanced/numbers_increased": "trastuzumab-mediated ADCC", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": "decreased HER2 levels in SKBR3 (neratinib\n 0.6 ± 0.1 fold)", "Controlled_Terms_Function_inhibited_Number_decreased": "HER2 / ERBB2; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/725", "Drug": "Neratinib followed by Trastuzumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB11828, DB00072", "Target/s_or_mechanism_of_action": "Neratinib binds to and irreversibly inhibits EGFR, HER2, and HER4 [FDA Label]. This prevents auotphoshorylation of tyrosine residues on the receptor and reduces oncogenic signalling through the mitogen-activated protein kinase and Akt pathways.\n Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "9915743, 46507516", "STR_LINK_(SMILES)": "CCOC1=C(NC(=O)\\C=C\\CN(C)C)C=C2C(NC3=CC=C(OCC4=CC=CC=N4)C(Cl)=C3)=C(C=NC2=C1)C#N", "Single/Combination": "Combination", "PMID": "28735814", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "MCF-7", "Dose": "Neratinib 2 μM concentration and a 48 h timepoint for TKI exposure", "Technique": "High content analysis, LDH-release ADCC assays", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay; LDH-releasing assays", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "decreased HER2 levels in SKBR3 (0.3 ± 0.1 fold)", "Controlled_Terms_Function_inhibited_Number_decreased": "HER2 / ERBB2; Expression / abundance phenotype", "Immune_System_function_unaffected": "trastuzumab-mediated ADCC", "Controlled_Terms_Unaffected": "ADCC; Antibody-dependent cytotoxicity", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/208", "Drug": "Ofatumumab and lenalidomide", "Drug_category": "Others/combination", "Drugbank_ID": "DB06650, DB00480", "Target/s_or_mechanism_of_action": "Ofatumumab is an anti-CD20 monoclonal antibody that binds to the small and large extracellular loops of the CD20 molecule. The Fab domain of ofatumumab binds to CD20, and this drug-target interaction does not result in immediate shedding and internalization of CD20 from the plasma membrane of B lymphocytes\n In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": "D09314, D04687", "Pubchem_ID": "347910355, 216326", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "26733610", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "K562 cells", "Dose": "0.25 µM/L,TRAIL-(20 and 100 ng/mL, respectively)", "Technique": "Western blotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "TRAIL-induced apoptosis-phosphatidylserine externalization, processing of caspase-3 to its catalytically active large subunits (p19/p17) and cleavage of PARP", "Controlled_Terms_Function_enhanced_Number_increased": "TRAIL; Caspase-3; Caspase activation; Apoptosis; PARP cleavage / PARP", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/655", "Drug": "Olaparib", "Drug_category": "Others/combination", "Drugbank_ID": "DB09074", "Target/s_or_mechanism_of_action": "Inhibits PARP1/2-mediated DNA repair", "KEGG_Drug__ID": "D09730", "Pubchem_ID": "23725625", "STR_LINK_(SMILES)": "C1CC1C(=O)N2CCN(CC2)C(=O)C3=C(C=CC(=C3)CC4=NNC(=O)C5=CC=CC=C54)F", "Single/Combination": "Single", "PMID": "40986050", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": null, "System": "SW684", "Dose": "5 µM", "Technique": "gene expression; flow cytometry", "Controlled_Technique": "POU5F1 mRNA", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "percentage of OCT4+ cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/656", "Drug": "Olaparib", "Drug_category": "Others/combination", "Drugbank_ID": "DB09074", "Target/s_or_mechanism_of_action": "Inhibits PARP1/2-mediated DNA repair", "KEGG_Drug__ID": "D09730", "Pubchem_ID": "23725625", "STR_LINK_(SMILES)": "C1CC1C(=O)N2CCN(CC2)C(=O)C3=C(C=CC(=C3)CC4=NNC(=O)C5=CC=CC=C54)F", "Single/Combination": "Single", "PMID": "40986050", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": null, "System": "402.91", "Dose": "5 µM", "Technique": "gene expression; flow cytometry", "Controlled_Technique": "POU5F1 mRNA", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "percentage of OCT4+ cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/658", "Drug": "Olaparib", "Drug_category": "Others/combination", "Drugbank_ID": "DB09074", "Target/s_or_mechanism_of_action": "Inhibits PARP1/2-mediated DNA repair", "KEGG_Drug__ID": "D09730", "Pubchem_ID": "23725625", "STR_LINK_(SMILES)": "C1CC1C(=O)N2CCN(CC2)C(=O)C3=C(C=CC(=C3)CC4=NNC(=O)C5=CC=CC=C54)F", "Single/Combination": "Single", "PMID": "40986050", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": null, "System": "DMR", "Dose": "5 µM in vitro; animal dose NR", "Technique": "gene expression; flow cytometry", "Controlled_Technique": "POU5F1 mRNA", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "percentage of OCT4+ cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/659", "Drug": "Olaparib", "Drug_category": "Others/combination", "Drugbank_ID": "DB09074", "Target/s_or_mechanism_of_action": "Inhibits PARP1/2-mediated DNA repair", "KEGG_Drug__ID": "D09730", "Pubchem_ID": "23725625", "STR_LINK_(SMILES)": "C1CC1C(=O)N2CCN(CC2)C(=O)C3=C(C=CC(=C3)CC4=NNC(=O)C5=CC=CC=C54)F", "Single/Combination": "Single", "PMID": "40986050", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": null, "System": "MES-SA", "Dose": "5 µM", "Technique": "gene expression; flow cytometry", "Controlled_Technique": "POU5F1 mRNA", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "percentage of OCT4+ cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/660", "Drug": "Olaparib", "Drug_category": "Others/combination", "Drugbank_ID": "DB09074", "Target/s_or_mechanism_of_action": "Inhibits PARP1/2-mediated DNA repair", "KEGG_Drug__ID": "D09730", "Pubchem_ID": "23725625", "STR_LINK_(SMILES)": "C1CC1C(=O)N2CCN(CC2)C(=O)C3=C(C=CC(=C3)CC4=NNC(=O)C5=CC=CC=C54)F", "Single/Combination": "Single", "PMID": "40986050", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": null, "System": "S018", "Dose": "5 µM", "Technique": "gene expression; flow cytometry", "Controlled_Technique": "POU5F1 mRNA", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "percentage of OCT4+ cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/661", "Drug": "Olaparib", "Drug_category": "Others/combination", "Drugbank_ID": "DB09074", "Target/s_or_mechanism_of_action": "Inhibits PARP1/2-mediated DNA repair", "KEGG_Drug__ID": "D09730", "Pubchem_ID": "23725625", "STR_LINK_(SMILES)": "C1CC1C(=O)N2CCN(CC2)C(=O)C3=C(C=CC(=C3)CC4=NNC(=O)C5=CC=CC=C54)F", "Single/Combination": "Single", "PMID": "40986050", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": null, "System": "S006", "Dose": "5 µM", "Technique": "gene expression; flow cytometry", "Controlled_Technique": "POU5F1 mRNA", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "percentage of OCT4+ cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/717", "Drug": "Olaparib", "Drug_category": "Others/combination", "Drugbank_ID": "DB09074", "Target/s_or_mechanism_of_action": "Inhibits PARP1/2-mediated DNA repair", "KEGG_Drug__ID": "D09730", "Pubchem_ID": "23725625", "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "40986050", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Sarcoma", "System": "HT-1080", "Dose": "5 µM", "Technique": "gene expression; flow cytometry", "Controlled_Technique": "POU5F1 mRNA", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "percentage of OCT4+ cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/486", "Drug": "Olaparib + AZD1775", "Drug_category": "Others/combination", "Drugbank_ID": "DB09074 + DB11740", "Target/s_or_mechanism_of_action": "Combined PARP and WEE1 inhibition increases replication catastrophe/DNA damage and activates cGAS–STING signaling", "KEGG_Drug__ID": "D09713 + D11361", "Pubchem_ID": "23725625 + 24856436", "STR_LINK_(SMILES)": "CN1CCN(CC1)C2=NC3=C(N2C4=CC=CC=C4C5=CC=CC=C5)C=CC(=C3)C(=O)N and CN1CCN(CC1)C2=CC=C(C=C2)NC3=NC4=C(C(=O)N(C4=CC=C3)CC=C)N(C5=CC=CC(=C5)C(C)(C)O)", "Single/Combination": "Combination", "PMID": "37582853", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "BRCA1/2-wildtype TNBC", "System": "HCC1806", "Dose": "olaparib 1 µM (5 µM MDA-MB-231) + AZD1775 200 nM; 72 h", "Technique": "Chou–Talalay synergy; clonogenic assay; RNA-seq; western blot; flow cytometry; tumor growth; survival; immune profiling", "Controlled_Technique": "STING/pTBK1/pIRF3 signaling,  CXCL10, IFIT3, ISG15, MX1, OAS2, OASL, TNF,  MHC-I/II genes expression and antigen-processing genes expression Tap1, , TAPBP, PSMB9, tumor-cell surface MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; TNF-α / TNF; CXCL10 / IP-10; TAP1; Tapasin; LMP2 / PSMB9; Antigen presentation; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "PD-L1 increased", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/487", "Drug": "Olaparib + AZD1775", "Drug_category": "Others/combination", "Drugbank_ID": "DB09074 + DB11740", "Target/s_or_mechanism_of_action": "Combined PARP and WEE1 inhibition increases replication catastrophe/DNA damage and activates cGAS–STING signaling", "KEGG_Drug__ID": "D09713 + D11361", "Pubchem_ID": "23725625 + 24856436", "STR_LINK_(SMILES)": "CN1CCN(CC1)C2=NC3=C(N2C4=CC=CC=C4C5=CC=CC=C5)C=CC(=C3)C(=O)N and CN1CCN(CC1)C2=CC=C(C=C2)NC3=NC4=C(C(=O)N(C4=CC=C3)CC=C)N(C5=CC=CC(=C5)C(C)(C)O)", "Single/Combination": "Combination", "PMID": "37582853", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "BRCA1/2-wildtype TNBC", "System": "MDA-MB-468", "Dose": "olaparib 1 µM (5 µM MDA-MB-231) + AZD1775 200 nM; 72 h", "Technique": "Chou–Talalay synergy; clonogenic assay; RNA-seq; western blot; flow cytometry; tumor growth; survival; immune profiling", "Controlled_Technique": "STING/pTBK1/pIRF3 signaling,  CXCL10, IFIT3, ISG15, MX1, OAS2, OASL, TNF,  MHC-I/II genes expression and antigen-processing genes expression Tap1, , TAPBP, PSMB9, tumor-cell surface MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; TNF-α / TNF; CXCL10 / IP-10; TAP1; Tapasin; LMP2 / PSMB9; Antigen presentation; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "PD-L1 increased", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/488", "Drug": "Olaparib + AZD1775", "Drug_category": "Others/combination", "Drugbank_ID": "DB09074 + DB11740", "Target/s_or_mechanism_of_action": "Combined PARP and WEE1 inhibition increases replication catastrophe/DNA damage and activates cGAS–STING signaling", "KEGG_Drug__ID": "D09713 + D11361", "Pubchem_ID": "23725625 + 24856436", "STR_LINK_(SMILES)": "CN1CCN(CC1)C2=NC3=C(N2C4=CC=CC=C4C5=CC=CC=C5)C=CC(=C3)C(=O)N and CN1CCN(CC1)C2=CC=C(C=C2)NC3=NC4=C(C(=O)N(C4=CC=C3)CC=C)N(C5=CC=CC(=C5)C(C)(C)O)", "Single/Combination": "Combination", "PMID": "37582853", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "BRCA1/2-wildtype TNBC", "System": "MDA-MB-231", "Dose": "olaparib 1 µM (5 µM MDA-MB-231) + AZD1775 200 nM; 72 h", "Technique": "Chou–Talalay synergy; clonogenic assay; RNA-seq; western blot; flow cytometry; tumor growth; survival; immune profiling", "Controlled_Technique": "STING/pTBK1/pIRF3 signaling,  CXCL10, IFIT3, ISG15, MX1, OAS2, OASL, TNF,  MHC-I/II genes expression and antigen-processing genes expression Tap1, , TAPBP, PSMB9, tumor-cell surface MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; TNF-α / TNF; CXCL10 / IP-10; TAP1; Tapasin; LMP2 / PSMB9; Antigen presentation; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "PD-L1 increased", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/489", "Drug": "Olaparib + AZD1775", "Drug_category": "Others/combination", "Drugbank_ID": "DB09074 + DB11740", "Target/s_or_mechanism_of_action": "Combined PARP and WEE1 inhibition increases replication catastrophe/DNA damage and activates cGAS–STING signaling", "KEGG_Drug__ID": "D09713 + D11361", "Pubchem_ID": "23725625 + 24856436", "STR_LINK_(SMILES)": "CN1CCN(CC1)C2=NC3=C(N2C4=CC=CC=C4C5=CC=CC=C5)C=CC(=C3)C(=O)N and CN1CCN(CC1)C2=CC=C(C=C2)NC3=NC4=C(C(=O)N(C4=CC=C3)CC=C)N(C5=CC=CC(=C5)C(C)(C)O)", "Single/Combination": "Combination", "PMID": "37582853", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "BRCA1/2-wildtype TNBC", "System": "MDA-MB-436", "Dose": "olaparib 1 µM (5 µM MDA-MB-231) + AZD1775 200 nM; 72 h", "Technique": "Chou–Talalay synergy; clonogenic assay; RNA-seq; western blot; flow cytometry; tumor growth; survival; immune profiling", "Controlled_Technique": "STING/pTBK1/pIRF3 signaling,  CXCL10, IFIT3, ISG15, MX1, OAS2, OASL, TNF,  MHC-I/II genes expression and antigen-processing genes expression Tap1, , TAPBP, PSMB9, tumor-cell surface MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; TNF-α / TNF; CXCL10 / IP-10; TAP1; Tapasin; LMP2 / PSMB9; Antigen presentation; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "PD-L1 increased", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/644", "Drug": "Tuvusertib (M1774)", "Drug_category": "Others/combination", "Drugbank_ID": "DB18790", "Target/s_or_mechanism_of_action": "ATR inhibitor", "KEGG_Drug__ID": "D12882", "Pubchem_ID": "90199447", "STR_LINK_(SMILES)": "CN1C=NC=C1C2=C(C=NC=C2NC(=O)C3=C4N=CC(=CN4N=C3N)F)F", "Single/Combination": "Single", "PMID": "41417226", "Cancer_Type": "Prostate", "Cancer_Type_Description": "DU145", "System": "Human NK cells", "Dose": "0.5 µM, 48 h pretreatment of tumor cells", "Technique": "flow cytometry; NK-cell lysis assay using xCELLigence RTCA", "Controlled_Technique": "TRAIL-R2 , NKG2D ligand ULBP-1", "Immune_System-Function_enhanced/numbers_increased": "TRAIL; NKG2D / KLRK1; TRAIL-R2 / DR5 / TNFRSF10B", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "TRAIL-R1", "Immune_System_function_unaffected": "TRAIL", "Controlled_Terms_Unaffected": "PD-L1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/490", "Drug": "Olaparib + AZD1775", "Drug_category": "Others/combination", "Drugbank_ID": "DB09074 + DB11740", "Target/s_or_mechanism_of_action": "Combined PARP and WEE1 inhibition increases replication catastrophe/DNA damage and activates cGAS–STING signaling", "KEGG_Drug__ID": "D09713 + D11361", "Pubchem_ID": "23725625 + 24856436", "STR_LINK_(SMILES)": "CN1CCN(CC1)C2=NC3=C(N2C4=CC=CC=C4C5=CC=CC=C5)C=CC(=C3)C(=O)N and CN1CCN(CC1)C2=CC=C(C=C2)NC3=NC4=C(C(=O)N(C4=CC=C3)CC=C)N(C5=CC=CC(=C5)C(C)(C)O)", "Single/Combination": "Combination", "PMID": "37582853", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "BRCA1/2-wildtype TNBC", "System": "MDA-MB-453", "Dose": "olaparib 1 µM (5 µM MDA-MB-231) + AZD1775 200 nM; 72 h", "Technique": "Chou–Talalay synergy; clonogenic assay; RNA-seq; western blot; flow cytometry; tumor growth; survival; immune profiling", "Controlled_Technique": "STING/pTBK1/pIRF3 signaling,  CXCL10, IFIT3, ISG15, MX1, OAS2, OASL, TNF,  MHC-I/II genes expression and antigen-processing genes expression Tap1, , TAPBP, PSMB9, tumor-cell surface MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; TNF-α / TNF; CXCL10 / IP-10; TAP1; Tapasin; LMP2 / PSMB9; Antigen presentation; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "PD-L1 increased", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1036", "Drug": "Panobinostat + IFN-γ-", "Drug_category": "Others/combination", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Combination", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "OPM-2", "Dose": "25 nM panobinostat and 100 U/ml of IFN-γ", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1447", "Drug": "Panobinostat + IFN-γ-", "Drug_category": "Others/combination", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Combination", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "KMS-11", "Dose": "25 nM panobinostat and 100 U/ml of IFN-γ", "Technique": "Flow cytometry,RT-PCR,western bloting", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "phosphorylated STAT1 (p-STAT1),IFN-γR1", "Controlled_Terms_Function_enhanced_Number_increased": "STAT1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1448", "Drug": "Panobinostat + IFN-γ-", "Drug_category": "Others/combination", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D10019", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Combination", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "MM.1S cells", "Dose": "25 nM panobinostat and 100 U/ml of IFN-γ", "Technique": "Flow cytometry,RT-PCR,western bloting", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "phosphorylated STAT1 (p-STAT1),IFN-γR1", "Controlled_Terms_Function_enhanced_Number_increased": "STAT1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1549", "Drug": "Pemetrexed + sildenafil", "Drug_category": "Others/combination", "Drugbank_ID": "DB00642, DB00203", "Target/s_or_mechanism_of_action": "Pemetrexed is an antifolate containing the pyrrolopyrimidine-based nucleus that exerts its antineoplastic activity by disrupting folate-dependent metabolic processes essential for cell replication. \n sildenafil is a potent and selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5) in the corpus cavernosum, where PDE5 is responsible for degradation of cGMP", "KEGG_Drug__ID": "D07472, \n D08514", "Pubchem_ID": "446556, \n 5212", "STR_LINK_(SMILES)": "NC1=NC(=O)C2=C(NC=C2CCC2=CC=C(C=C2)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N1,\n CCCC1=NN(C)C2=C1N=C(NC2=O)C1=CC(=CC=C1OCC)S(=O)(=O)N1CCN(C)CC1", "Single/Combination": "Combination", "PMID": "28812434", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": "Afatinib-resistant H1975 cells", "Dose": "[pemetrexed (1 uM) + sildenafil (2 uM)", "Technique": "immuno-fluorescence", "Controlled_Technique": "Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "MHCA", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1, PD-L2 and ODC", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; PD-L2 / PDCD1LG2; PD-L1 immune checkpoint pathway", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1550", "Drug": "Pemetrexed + sildenafil", "Drug_category": "Others/combination", "Drugbank_ID": "DB00642, DB00203", "Target/s_or_mechanism_of_action": "Pemetrexed is an antifolate containing the pyrrolopyrimidine-based nucleus that exerts its antineoplastic activity by disrupting folate-dependent metabolic processes essential for cell replication. \n sildenafil is a potent and selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5) in the corpus cavernosum, where PDE5 is responsible for degradation of cGMP", "KEGG_Drug__ID": "D07472, \n D08514", "Pubchem_ID": "446556, \n 5212", "STR_LINK_(SMILES)": "NC1=NC(=O)C2=C(NC=C2CCC2=CC=C(C=C2)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N1,\n CCCC1=NN(C)C2=C1N=C(NC2=O)C1=CC(=CC=C1OCC)S(=O)(=O)N1CCN(C)CC1", "Single/Combination": "Combination", "PMID": "28812434", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": "LLC cells", "Dose": "[pemetrexed (1 uM) + sildenafil (2 uM)", "Technique": "immuno-fluorescence", "Controlled_Technique": "Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "MHCA", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1, PD-L2 and ODC", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; 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Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC Class I molecules (HLA-A,B,C)", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; HLA-A;", "Immune_System-Function_inhibited/numbers_decreased": "Phospho-ERK", "Controlled_Terms_Function_inhibited_Number_decreased": "ERK / MAPK", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1168", "Drug": "Pmel-1 ACT+Dobrafenib+ Trametinib", "Drug_category": "Others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D10064, D10175", "Pubchem_ID": "44462760, 11707110", "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Gp10025-33–activated pmel-1 mouse splenocytes", "Dose": "D (0.1 mM)/T (0.005 mM),", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD3+CD8+ IFN-Y", "Controlled_Terms_Function_inhibited_Number_decreased": "CD3; 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It is shown to inhibit the proliferation and induce apoptosis of various tumour cells.", "KEGG_Drug__ID": "D08976", "Pubchem_ID": "134780", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1C(=O)N(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "KMS-11", "Dose": "pomalidomide 1.0 or 0.1 μM and 100 U/ml of IFN-γ", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1038", "Drug": "Pomalidomide + IFN-γ", "Drug_category": "Others/combination", "Drugbank_ID": "DB08910", "Target/s_or_mechanism_of_action": "Promalidomide is an immunomodulatory agent with antineoplastic activity. 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It is shown to inhibit the proliferation and induce apoptosis of various tumour cells.", "KEGG_Drug__ID": "D08976", "Pubchem_ID": "134780", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1C(=O)N(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "OPM-2", "Dose": "pomalidomide 1.0 or 0.1 μM and 100 U/ml of IFN-γ", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1040", "Drug": "Pomalidomide + IFN-γ + panobinostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB08910, DB06603", "Target/s_or_mechanism_of_action": "Promalidomide is an immunomodulatory agent with antineoplastic activity. 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It is shown to inhibit the proliferation and induce apoptosis of various tumour cells.\n Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": "D08976, D10019", "Pubchem_ID": "134780, 6918837", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1C(=O)N(C1CCC(=O)NC1=O)C2=O,\n CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Combination", "PMID": "30956773", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": "OPM-2", "Dose": "pomalidomide 1.0 or 0.1 μM and 100 U/ml of IFN-γ +25 nM panobinostat", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression by MM cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; 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Fluorouracil is an antineoplastic anti-metabolite. 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Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "Ifng, Ifngr1 Cd274 (Pdl1) and Pdcd1lg2 (Pdl2) tumor programmed cell death 1 ligand 1 (PD-L1) level, phosphorylation of STAT1 and its downstream transcription factor IRF1", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L2 / PDCD1LG2; CD274; IFN-γ; STAT1; IRF-1; PD-L1 immune checkpoint pathway; Expression / abundance phenotype; IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/190", "Drug": "SGI-1027 (SGI)", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "32079180", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "HCT116", "Dose": null, "Technique": "immunoblotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "tumor programmed cell death 1 ligand 1 (PD-L1) level", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; 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Polymerase chain reaction (PCR/qPCR); Cell co-culture/transwell assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "MDSCs IL-10 Arg1, TGF-β, cyclooxygenase 2 (COX2), IDO1, IDO2, and NOS2", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-10; TGF-β; IDO1/IDO; NOS2 / iNOS; ARG1 / arginase-1; COX-2 / PTGS2; Myeloid-derived suppressor cells / MDSCs; TGF-β / TGF-beta", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1306", "Drug": "Sorafenib + TLR3 agonist: lysine-stabilized polyinosinic-polycytidylic-acid (poly-ICLC)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "26287667", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": "SNU449", "Dose": "50 μg/ml poly-ICLC and 15 μM Sorafenib", "Technique": "Flow cytometry,Microscopy", "Controlled_Technique": "Flow cytometry; Microscopy", "Immune_System-Function_enhanced/numbers_increased": "Apoptosis-(Annexin-V and Topro-3-positive cells)", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis; Annexin V", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1307", "Drug": "Sorafenib + TLR3 agonist: lysine-stabilized polyinosinic-polycytidylic-acid (poly-ICLC)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "26287667", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": "SNU475", "Dose": "50 μg/ml poly-ICLC and 15 μM Sorafenib", "Technique": "Flow cytometry,Microscopy", "Controlled_Technique": "Flow cytometry; Microscopy", "Immune_System-Function_enhanced/numbers_increased": "Apoptosis-(Annexin-V and Topro-3-positive cells)", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis; Annexin V", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/434", "Drug": "TAK-117", "Drug_category": "PI3K inhibitor", "Drugbank_ID": "DB14935", "Target/s_or_mechanism_of_action": "Selective PI3Kα/p110α inhibition", "KEGG_Drug__ID": "—", "Pubchem_ID": "70798655", "STR_LINK_(SMILES)": "TAK-117 canonical SMILES", "Single/Combination": "Single", "PMID": "39258533", "Cancer_Type": "Bladder cancer", "Cancer_Type_Description": "Bladder cancer", "System": "T24", "Dose": "3.5 µM, 48 h", "Technique": "qRT-PCR, western blot", "Controlled_Technique": "PD-L1 mRNA increased", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 / CD274", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "PD-L1 mRNA increased", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1362", "Drug": "Sorafenib + TLR3 agonist: lysine-stabilized polyinosinic-polycytidylic-acid (poly-ICLC)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "26287667", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": "Hepa 1-6 cells", "Dose": "50 μg/ml poly-ICLC and 15 μM Sorafenib", "Technique": "Flow cytometry,Microscopy,densitometry, western blot,quantitative-PCR", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Immunostaining/image analysis; Microscopy", "Immune_System-Function_enhanced/numbers_increased": "Apoptosis-(Annexin-V and Topro-3-positive cells)", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis; Annexin V", "Immune_System-Function_inhibited/numbers_decreased": "phosphorylations of AKT (Ser473), MEK1/2 (Ser217/221) and ERK1/2 (Thr202/Tyr204), Survivin gene (BIRC5)", "Controlled_Terms_Function_inhibited_Number_decreased": "ERK / MAPK; MEK1/2 / MAP2K1/2; AKT; Survivin / BIRC5", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1483", "Drug": "Sorafenib and YC-1, a soluble guanylyl cyclase (sGC) activator", "Drug_category": "Others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "24418169", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": "HepG2", "Dose": "(5 μmol/L) and YC-1 (10 μmol/L)", "Technique": "Flow cytometry, western blot analysis", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "S cell cycle arrest, apoptosis-Increased activation of PARP ,extrinsic or death receptor pathway, which activates caspase 8,SHP-1 activity", "Controlled_Terms_Function_enhanced_Number_increased": "SHP-1 / PTPN6; Caspase-8; Caspase activation; Apoptosis; Cell-cycle arrest; PARP cleavage / PARP", "Immune_System-Function_inhibited/numbers_decreased": "(p-STAT3),(p-ERK1/2), cyclin D1 and survivin", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6/JAK/STAT3 signaling; STAT3; ERK / MAPK; Survivin / BIRC5; Cyclin D1 / CCND1; STAT3 phosphorylation", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1484", "Drug": "Sorafenib and YC-1, a soluble guanylyl cyclase (sGC) activator", "Drug_category": "Others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "24418169", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": "BEL-7402", "Dose": "(5 μmol/L) and YC-1 (10 μmol/L)", "Technique": "Flow cytometry, western blot analysis", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "S cell cycle arrest, apoptosis-Increased activation of PARP ,extrinsic or death receptor pathway, which activates caspase 8,SHP-1 activity", "Controlled_Terms_Function_enhanced_Number_increased": "SHP-1 / PTPN6; Caspase-8; Caspase activation; Apoptosis; Cell-cycle arrest; PARP cleavage / PARP", "Immune_System-Function_inhibited/numbers_decreased": "(p-STAT3),(p-ERK1/2), cyclin D1 and survivin", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6/JAK/STAT3 signaling; STAT3; ERK / MAPK; Survivin / BIRC5; Cyclin D1 / CCND1; STAT3 phosphorylation", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1485", "Drug": "Sorafenib and YC-1, a soluble guanylyl cyclase (sGC) activator", "Drug_category": "Others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "24418169", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": "HCCLM3 cells", "Dose": "(5 μmol/L) and YC-1 (10 μmol/L)", "Technique": "Flow cytometry, western blot analysis", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "S cell cycle arrest, apoptosis-Increased activation of PARP ,extrinsic or death receptor pathway, which activates caspase 8,SHP-1 activity", "Controlled_Terms_Function_enhanced_Number_increased": "SHP-1 / PTPN6; Caspase-8; Caspase activation; Apoptosis; Cell-cycle arrest; PARP cleavage / PARP", "Immune_System-Function_inhibited/numbers_decreased": "(p-STAT3),(p-ERK1/2), cyclin D1 and survivin", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6/JAK/STAT3 signaling; STAT3; ERK / MAPK; Survivin / BIRC5; Cyclin D1 / CCND1; STAT3 phosphorylation", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1184", "Drug": "Sorafenib+ IFNγ", "Drug_category": "Others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "23483066", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "A375", "Dose": "10 μM Sorafenib+2000 U/mL IFNγ", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC Class I molecules (HLA-A,B,C)", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; HLA-A;", "Immune_System-Function_inhibited/numbers_decreased": "MHC Class II molecule\n (HLA-DR)", "Controlled_Terms_Function_inhibited_Number_decreased": "MHC class II; HLA-DR;", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/319", "Drug": "Taxol", "Drug_category": "Others/combination", "Drugbank_ID": "DB01229 (APRD00259, DB05261, DB05927, DB05526, DB05281)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": "D00491", "Pubchem_ID": "36314", "STR_LINK_(SMILES)": "[H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Single Drug", "PMID": "12389115", "Cancer_Type": "Urethera", "Cancer_Type_Description": "Urothelial - Human Urothelial Cancer", "System": "T24", "Dose": "Taxol 0.8 microg/ml", "Technique": "Western blot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "Fas and FasL", "Controlled_Terms_Unaffected": "CD95 / Fas / FAS; Fas ligand / FasL / FASLG", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/677", "Drug": "Tazemetostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB12887", "Target/s_or_mechanism_of_action": "EZH2 inhibition → reduced H3K27me3-mediated transcriptional repression", "KEGG_Drug__ID": "D11444", "Pubchem_ID": "66558664", "STR_LINK_(SMILES)": "CCN(C1CCOCC1)C2=CC(=CC(=C2C)C(=O)NCC3=C(C=C(NC3=O)C)C)C4=CC=C(C=C4)CN5CCOCC5", "Single/Combination": "Single", "PMID": "33316946", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Human uveal melanoma", "System": "OMM1", "Dose": "5 µM, 48 h", "Technique": "Flow cytometry, qPCR", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "HLA-I surface expression unaffected", "Immune_System_function_unaffected": "Expression / abundance phenotype; MHC class I", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/678", "Drug": "Tazemetostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB12887", "Target/s_or_mechanism_of_action": "EZH2 inhibition → reduced H3K27me3-mediated transcriptional repression", "KEGG_Drug__ID": "D11444", "Pubchem_ID": "66558664", "STR_LINK_(SMILES)": "CCN(C1CCOCC1)C2=CC(=CC(=C2C)C(=O)NCC3=C(C=C(NC3=O)C)C)C4=CC=C(C=C4)CN5CCOCC5", "Single/Combination": "Single", "PMID": "33316946", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Human uveal melanoma", "System": "OMM2.5", "Dose": "5 µM, 48 h", "Technique": "Flow cytometry, qPCR", "Controlled_Technique": "Slight increase in HLA-A mRNA", "Immune_System-Function_enhanced/numbers_increased": "HLA-A", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "HLA-I surface expression unaffected", "Immune_System_function_unaffected": "Expression / abundance phenotype; MHC class I", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/679", "Drug": "Tazemetostat", "Drug_category": "Others/combination", "Drugbank_ID": "DB12887", "Target/s_or_mechanism_of_action": "EZH2 inhibition → reduced H3K27me3-mediated transcriptional repression", "KEGG_Drug__ID": "D11444", "Pubchem_ID": "66558664", "STR_LINK_(SMILES)": "CCN(C1CCOCC1)C2=CC(=CC(=C2C)C(=O)NCC3=C(C=C(NC3=O)C)C)C4=CC=C(C=C4)CN5CCOCC5", "Single/Combination": "Single", "PMID": "33316946", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Human uveal melanoma", "System": "MP38", "Dose": "5 µM, 48 h", "Technique": "Flow cytometry, qPCR", "Controlled_Technique": "Slight increase in HLA-A mRNA", "Immune_System-Function_enhanced/numbers_increased": "HLA-A", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "HLA-I surface expression unaffected", "Immune_System_function_unaffected": "Expression / abundance phenotype; MHC class I", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1171", "Drug": "Temozolomide+ IFNγ", "Drug_category": "Others/combination", "Drugbank_ID": "DB00853", "Target/s_or_mechanism_of_action": "TMZ is a DNA alkylating agent known to induce cell cycle arrest at G2/M and to eventually lead to apoptosis.", "KEGG_Drug__ID": "D06067", "Pubchem_ID": "5394", "STR_LINK_(SMILES)": "CN1N=NC2=C(N=CN2C1=O)C(N)=O", "Single/Combination": "Combination", "PMID": "23483066", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "A375", "Dose": "10 μM temozolomide+2000 U/mL IFNγ", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "MHC Class I molecules (HLA-A,B,C), MHC Class II molecule\n (HLA-DR)", "Controlled_Terms_Unaffected": "MHC class I; MHC class II; HLA-DR; HLA-A;", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/481", "Drug": "TPH104-conditioned medium", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Products released by TPH104-treated tumor cells stimulate dendritic-cell maturation", "KEGG_Drug__ID": "NR", "Pubchem_ID": "18326651", "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "33919653", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Mouse bone-marrow-derived dendritic cells (BMDCs) exposed to conditioned medium from treated MDA-MB-231 cells", "System": "MDA-MB-231 media+ BMDCs", "Dose": "Conditioned medium from cells treated with 1 or 5 µM TPH104; BMDC exposure for 48 h", "Technique": "Flow cytometry, qPCR, ELISA", "Controlled_Technique": "CD86-high and MHC-II-high BMDC populations increased; TNF-α mRNA increased by 67%, IL-6 by 327%, and IL-12A by 45% at 5 µM conditioned-medium treatment", "Immune_System-Function_enhanced/numbers_increased": "CD86; MHC class II; TNF-α / TNF; IL-6", "Controlled_Terms_Function_enhanced_Number_increased": "CD86-low and MHC-II-low BMDC populations decreased", "Immune_System-Function_inhibited/numbers_decreased": "Expression / abundance phenotype; MHC class II; CD86; Dendritic cells", "Controlled_Terms_Function_inhibited_Number_decreased": "Total CD11c+ population and IL-1β expression showed no significant change", "Immune_System_function_unaffected": "Expression / abundance phenotype; CD11c / ITGAX", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1185", "Drug": "Vemurafenib+IFN-y", "Drug_category": "Others/combination", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": "D09996", "Pubchem_ID": "42611257", "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Combination", "PMID": "23483066", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "A375", "Dose": "625 nM vemurafenib+2000 U/mL IFNγ", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC Class I molecules (HLA-A,B,C), β2\n microblobulin, MHC Class II molecules (HLA-D,R)", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; MHC class II; HLA-A;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/492", "Drug": "Trabectedin + IL-12", "Drug_category": "Others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "DNA minor-groove binding; DNA damage", "KEGG_Drug__ID": "D06199", "Pubchem_ID": "108150", "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39777457", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Human TNBC", "System": "MDA-MB-436", "Dose": "10 ng/mL + 2.5 nmol/L", "Technique": "RT-PCR, flow cytometery", "Controlled_Technique": "CD69 expression, IFN-γ (IFNG) and granzyme B (GZMB), T-BET (Tbx21),TRAIL (TNFSF10) and Fas ligand (FASLG), lymphotactin (XCL1), Phospho-STAT4 levels , increased NK-cell cytotoxicity, higher levels of IFN-γ, TNF-α and granzyme B", "Immune_System-Function_enhanced/numbers_increased": "TRAIL; Granzyme B / GZMB; IFN-γ; TNF-α / TNF; Cytotoxicity / cytolysis; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "AN", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "trabectedin has a direct stimulatory effect on NK cells and can be combined with IL-12 to activate NK cells in the presence of TNBC", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "NK cells; IL-12", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/493", "Drug": "Trabectedin + IL-12", "Drug_category": "Others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "DNA minor-groove binding; DNA damage", "KEGG_Drug__ID": "D06199", "Pubchem_ID": "108150", "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39777457", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Human TNBC", "System": "MDA-MB-231", "Dose": "10 ng/mL + 2.5 nmol/L", "Technique": "RT-PCR, flow cytometery", "Controlled_Technique": "CD69 expression, IFN-γ (IFNG) and granzyme B (GZMB), T-BET (Tbx21),TRAIL (TNFSF10) and Fas ligand (FASLG), lymphotactin (XCL1), Phospho-STAT4 levels , increased NK-cell cytotoxicity, higher levels of IFN-γ, TNF-α and granzyme B", "Immune_System-Function_enhanced/numbers_increased": "TRAIL; Granzyme B / GZMB; IFN-γ; TNF-α / TNF; Cytotoxicity / cytolysis; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "AN", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "trabectedin has a direct stimulatory effect on NK cells and can be combined with IL-12 to activate NK cells in the presence of TNBC", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "NK cells; IL-12", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/494", "Drug": "Trabectedin + IL-12", "Drug_category": "Others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "DNA minor-groove binding; DNA damage", "KEGG_Drug__ID": "D06199", "Pubchem_ID": "108150", "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39777457", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Human TNBC", "System": "MDA-MB-468", "Dose": "10 ng/mL + 2.5 nmol/L", "Technique": "RT-PCR, flow cytometery", "Controlled_Technique": "CD69 expression, IFN-γ (IFNG) and granzyme B (GZMB), T-BET (Tbx21),TRAIL (TNFSF10) and Fas ligand (FASLG), lymphotactin (XCL1), Phospho-STAT4 levels , increased NK-cell cytotoxicity, higher levels of IFN-γ, TNF-α and granzyme B", "Immune_System-Function_enhanced/numbers_increased": "TRAIL; Granzyme B / GZMB; IFN-γ; TNF-α / TNF; Cytotoxicity / cytolysis; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "AN", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "trabectedin has a direct stimulatory effect on NK cells and can be combined with IL-12 to activate NK cells in the presence of TNBC", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "NK cells; IL-12", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/495", "Drug": "Trabectedin + IL-12", "Drug_category": "Others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "DNA minor-groove binding; DNA damage", "KEGG_Drug__ID": "D06199", "Pubchem_ID": "108150", "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39777457", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Human TNBC", "System": "K562", "Dose": "10 ng/mL + 2.5 nmol/L", "Technique": "Human NK-cell cytotoxicity assay", "Controlled_Technique": "increased NK-cell cytotoxicity", "Immune_System-Function_enhanced/numbers_increased": "Cytotoxicity / cytolysis", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "AN", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "trabectedin has a direct stimulatory effect on NK cells and can be combined with IL-12 to activate NK cells in the presence of TNBC", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "NK cells; 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Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC-1 pSTAT1, pSTAT3, STAT3, and pSTAT5", "Controlled_Terms_Function_enhanced_Number_increased": "IL-6/JAK/STAT3 signaling; STAT3; ; STAT3 phosphorylation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "PD-L1", "Controlled_Terms_Unaffected": "PD-L1 / CD274; PD-L1 immune checkpoint pathway", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/346", "Drug": "Trametinib+Lapatinib", "Drug_category": "Others/combination", "Drugbank_ID": "DB08911, DB01259", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity. \n Lapatinib is a 4-anilinoquinazoline kinase inhibitor of the intracellular tyrosine kinase domains of both epidermal growth factor receptor (HER1/EGFR/ERBB1) and human epidermal growth factor receptor type 2 (HER2/ERBB2)with a dissociation half-life of ≥300 minutes.", "KEGG_Drug__ID": "D10175, D04024", "Pubchem_ID": "11707110, 208908", "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1,\n CS(=O(=O)CCNCC1=CC=C(O1)C1=CC2=C(C=C1)N=CN=C2NC1=CC(Cl)=C(OCC2=CC(F)=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "33062958", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "MMTV-Neu cells", "Dose": "trametinib (50 nM) + Lapatinib (0.1 μM)", "Technique": "Flow cytometery, Immunoblot", "Controlled_Technique": "Western blot/immunoblot analysis; Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "pSTAT1, pSTAT3, STAT3", "Controlled_Terms_Function_enhanced_Number_increased": "IL-6/JAK/STAT3 signaling; STAT3; STAT3 phosphorylation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "MHC-I and PD-L1", "Controlled_Terms_Unaffected": "PD-L1 / CD274; MHC class I; PD-L1 immune checkpoint pathway;", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/693", "Drug": "Trastuzumab deruxtecan (T-DXd)", "Drug_category": "Others/combination", "Drugbank_ID": "DB14962", "Target/s_or_mechanism_of_action": "HER2 targeting; TOP1 inhibition; 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PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/443", "Drug": "Trastuzumab deruxtecan (T-DXd)", "Drug_category": "Others/combination", "Drugbank_ID": "DB14962", "Target/s_or_mechanism_of_action": "Fcγ-receptor activation; antibody-dependent cellular phagocytosis (ADCP); ICD", "KEGG_Drug__ID": "D11529", "Pubchem_ID": "384585505", "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "40175391", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "HER2-positive", "System": "Au565 cells with human macrophages or mouse bone-marrow-derived macrophages", "Dose": null, "Technique": "Phagocytosis flow cytometry; ELISA; flow cytometry", "Controlled_Technique": "Macrophage HLA-A2, HLA-DR, CD80, CD40 and CCR7; antigen-presentation and chemokine genes; inflammatory cytokines", "Immune_System-Function_enhanced/numbers_increased": "CD80; HLA-DR; Macrophages; CD40", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "CD47 upregulation was observed after DXd treatment", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; CD47", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/444", "Drug": "Trastuzumab deruxtecan (T-DXd)", "Drug_category": "Others/combination", "Drugbank_ID": "DB14962", "Target/s_or_mechanism_of_action": "Fcγ-receptor activation; antibody-dependent cellular phagocytosis (ADCP); ICD", "KEGG_Drug__ID": "D11529", "Pubchem_ID": "384585505", "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "40175391", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "HER2-positive", "System": "Human dendritic cells + Au565 cells", "Dose": null, "Technique": "Phagocytosis flow cytometry; ELISA; flow cytometry", "Controlled_Technique": "Macrophage HLA-A2, HLA-DR, CD80, CD40 and CCR7; antigen-presentation and chemokine genes; inflammatory cytokines", "Immune_System-Function_enhanced/numbers_increased": "CD80; HLA-DR; Macrophages; CD40", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "CD47 upregulation was observed after DXd treatment", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; CD47", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/692", "Drug": "Trastuzumab deruxtecan (T-DXd)", "Drug_category": "Others/combination", "Drugbank_ID": "DB14962", "Target/s_or_mechanism_of_action": "HER2 targeting; TOP1 inhibition; DNA damage and cGAS–STING/type-I IFN pathway activation", "KEGG_Drug__ID": "D11529", "Pubchem_ID": "384585505", "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "39449023", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Human gastric adenocarcinoma; very low HER2 expression", "System": "SNU-601", "Dose": "Multiple concentrations; assay-specific", "Technique": "immunoblotting", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "PD-L1 upregulation", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/695", "Drug": "Trastuzumab deruxtecan (T-DXd)", "Drug_category": "Others/combination", "Drugbank_ID": "DB14962", "Target/s_or_mechanism_of_action": "HER2 targeting; TOP1 inhibition; DNA damage and cGAS–STING/type-I IFN pathway activation", "KEGG_Drug__ID": "D11529", "Pubchem_ID": "384585505", "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "39449023", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Human gastric adenocarcinoma; HER2-amplified", "System": "SNU-216", "Dose": "Assay-specific concentrations; see article methods", "Technique": "immunoblotting", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "PD-L1 upregulation", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1055", "Drug": "Trastuzumab+ Anti CD137 mAB", "Drug_category": "Others/combination", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "30596643", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": "NK+Capan-1 (HER2-high-expressing cell line) + αCD137 (Anti-CD137 mAb), effector/target (E/T) ratio was set at 10:1", "Dose": "10 μg/ml of Tmab +10 μg/ml αCD137", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "cell surface CD69 of NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD69; NK cells", "Immune_System-Function_inhibited/numbers_decreased": "perforin—and granzyme-B- double-positive NK cells", "Controlled_Terms_Function_inhibited_Number_decreased": "Granzyme B / GZMB; Perforin / PRF1; NK cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1562", "Drug": "Trastuzumab+ Anti CD137 mAB", "Drug_category": "Others/combination", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": "D03257", "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "30596643", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": "NK+ Panc-1 (HER2-low-expressing cell line) + αCD137 (Anti-CD137 mAb), effector/target (E/T) ratio was set at 10:1", "Dose": "10 μg/ml of Tmab + 10 μg/ml αCD137", "Technique": "LDH-releasing assays", "Controlled_Technique": "LDH-releasing assays", "Immune_System-Function_enhanced/numbers_increased": "enhanced Tmab-mediated ADCC against Panc-1", "Controlled_Terms_Function_enhanced_Number_increased": "ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/944", "Drug": "Trichostatin A +tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)", "Drug_category": "Others/combination", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": "444732", "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Combination", "PMID": "16818655", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "PBMCs obtained from 10 CLL patients", "Dose": "lenalidomide (LND; 1 μM) and IL-2 (50 U/mL)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "HLA-E expression", "Controlled_Terms_Function_enhanced_Number_increased": "Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": "classical MHC class I", "Controlled_Terms_Function_inhibited_Number_decreased": "MHC class I;", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/647", "Drug": "Tuvusertib (M1774)", "Drug_category": "Others/combination", "Drugbank_ID": "DB18790", "Target/s_or_mechanism_of_action": "ATR inhibitor", "KEGG_Drug__ID": "D12882", "Pubchem_ID": "90199447", "STR_LINK_(SMILES)": "CN1C=NC=C1C2=C(C=NC=C2NC(=O)C3=C4N=CC(=CN4N=C3N)F)F", "Single/Combination": "Single", "PMID": "41417226", "Cancer_Type": "Prostate", "Cancer_Type_Description": "DU145", "System": "PD-L1-targeting high-affinity NK (PD-L1 t-haNK) cells", "Dose": "0.5 µM, 48 h tumor-cell pretreatment", "Technique": "NK-cell cytotoxicity/lysis assay", "Controlled_Technique": "PD-L1 t-haNK-mediated lysis ↑ ~1.5-fold", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 / CD274", "Controlled_Terms_Function_enhanced_Number_increased": "No specific immune-cell decrease", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "No reported reduction in t-haNK viability", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "PD-L1 ↑, increasing the target available for PD-L1-directed killing", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/645", "Drug": "Tuvusertib (M1774)", "Drug_category": "Others/combination", "Drugbank_ID": "DB18790", "Target/s_or_mechanism_of_action": "ATR inhibitor", "KEGG_Drug__ID": "D12882", "Pubchem_ID": "90199447", "STR_LINK_(SMILES)": "CN1C=NC=C1C2=C(C=NC=C2NC(=O)C3=C4N=CC(=CN4N=C3N)F)F", "Single/Combination": "Single", "PMID": "41417226", "Cancer_Type": "Prostate", "Cancer_Type_Description": "22Rv1", "System": "Human NK cells", "Dose": "0.5 µM, 48 h pretreatment of tumor cells", "Technique": "flow cytometry; NK-cell lysis assay using xCELLigence RTCA", "Controlled_Technique": "TRAIL-R2", "Immune_System-Function_enhanced/numbers_increased": "TRAIL; TRAIL-R2 / DR5 / TNFRSF10B", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "TRAIL-R1, NKG2D ligand ULBP-1", "Immune_System_function_unaffected": "TRAIL", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1230", "Drug": "Vemurafenib (BRAF-I) +IFN a", "Drug_category": "Others/combination", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": "D09996", "Pubchem_ID": "42611257", "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Combination", "PMID": "26851802", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Colo38, M21, and SK-MEL-37 cells", "Dose": "vemurafenib (500 nM) and/or IFNα-2b (10 000 IU/mL)", "Technique": "Flow cytometry analysis of annexin V and PI staining", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "increased HLA-A, B, and C antigen, calnexin, and\n calreticulin expression, HLA-DR, DQ and DP antigens increased cleaved PARP ( inhibited the proliferation and induced apoptosis)", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; MHC class II; HLA-DR; HLA-A; Apoptosis; Cell proliferation; Calnexin; Calreticulin / CRT; PARP cleavage / PARP; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": "pERK", "Controlled_Terms_Function_inhibited_Number_decreased": "ERK / MAPK", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/422", "Drug": "Vemurafenib (BRAF-I) +IFN a", "Drug_category": "Others/combination", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": "D09996", "Pubchem_ID": "42611257", "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Combination", "PMID": "26851802", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "SK-Mel-37", "Dose": "vemurafenib (500 nM) and/or IFNα-2b (10 000 IU/mL)", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "PD-L1", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1163", "Drug": "Vemurafenib + Sodium butyrate", "Drug_category": "Others/combination", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": "D09996", "Pubchem_ID": "42611257, 5222465", "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1,\n CCCC(=O)[O-].[Na+]", "Single/Combination": "Combination", "PMID": "29308322", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Ma-Mel-86f", "Dose": "1 uM Vemurafenib+5 mM sodium butyrate", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NKG2D-L (MHC-1, MICA, UBLP2/5/6, CD112)", "Controlled_Terms_Function_enhanced_Number_increased": "CD112 / Nectin-2 / PVRL2; NKG2D / KLRK1; MICA; ; MICA/MICB", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD155", "Controlled_Terms_Unaffected": "CD155 / PVR", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1164", "Drug": "Vemurafenib + Sodium butyrate", "Drug_category": "Others/combination", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": "D09996", "Pubchem_ID": "42611257, 5222465", "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1,\n CCCC(=O)[O-].[Na+]", "Single/Combination": "Combination", "PMID": "29308322", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Ma-Mel-55", "Dose": "1 uM Vemurafenib+5 mM sodium butyrate", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NKG2D-L (MHC-1, MICA, UBLP3, UBLP2/5/6, CD112)", "Controlled_Terms_Function_enhanced_Number_increased": "CD112 / Nectin-2 / PVRL2; 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Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IFNy+ CD8+ PBMCS increased after short term treatment", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": "IFNy+ CD8+ TIL decreased/impaired during long term treatment resulting to double drugresistant melanoma cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD8; T cells; IFN-γ", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1281", "Drug": "Vemurafenib+trametinib", "Drug_category": "Others/combination", "Drugbank_ID": "DB08881, DB08911", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": "D09996, D10175", "Pubchem_ID": "42611257, 11707110", "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "30221038", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Ma-Mel-86c melanoma cells", "Dose": "vemurafenib, 0.5 uM+50 nM trametinib", "Technique": "Flow cytometry, ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IFNy+ CD8+ TIL increased after short term treatment", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": "IFNy+ CD8+ TIL decreased/impaired during long term treatment resulting to double drugresistant melanoma cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD8; T cells; IFN-γ", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/509", "Drug": "Venetoclax", "Drug_category": "Others/combination", "Drugbank_ID": "DB11581", "Target/s_or_mechanism_of_action": "D10679", "KEGG_Drug__ID": "49846579", "Pubchem_ID": "40300857", "STR_LINK_(SMILES)": "CC1(CCC(=C(C1)C2=CC=C(C=C2)Cl)CN3CCN(CC3)C4=CC(=C(C=C4)C(=O)NS(=O)(=O)C5=CC(=C(C=C5)NCC6CCOCC6)[N+](=O)[O-])OC7=CN=C8C(=C7)C=CN8)C", "Single/Combination": "Single", "PMID": "40300857", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "CRC cell", "System": "HT-29", "Dose": "1.25, 2.5 and 5 µM; 24 hours; time-course experiments at 5 µM", "Technique": "qRT-PCR, ELISA, Western blot", "Controlled_Technique": "CCL5, CXCL10 and IFN-β expression/secretion, STING, TBK1, and IRF3 phosphorylation", "Immune_System-Function_enhanced/numbers_increased": "IFN-β; CXCL10 / IP-10; CCL5 / RANTES; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/510", "Drug": "Venetoclax", "Drug_category": "Others/combination", "Drugbank_ID": "DB11581", "Target/s_or_mechanism_of_action": "D10679", "KEGG_Drug__ID": "49846579", "Pubchem_ID": "40300857", "STR_LINK_(SMILES)": "CC1(CCC(=C(C1)C2=CC=C(C=C2)Cl)CN3CCN(CC3)C4=CC(=C(C=C4)C(=O)NS(=O)(=O)C5=CC(=C(C=C5)NCC6CCOCC6)[N+](=O)[O-])OC7=CN=C8C(=C7)C=CN8)C", "Single/Combination": "Single", "PMID": "40300857", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "CRC cell", "System": "SW480", "Dose": "5 µM; 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24 h", "Technique": "RT-qPCR", "Controlled_Technique": "Increased IFN-β signaling", "Immune_System-Function_enhanced/numbers_increased": "IFN-β", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/964", "Drug": "Vinorelbine and cisplatin", "Drug_category": "Others/combination", "Drugbank_ID": "1. 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Vinorebine- [H][C@]89C=C(CC)CN(Cc1c([nH]c2ccccc12)[C@@](C(=O)OC)(c3cc4c(cc3OC)N(C)[C@@]5([H])[C@@](O)(C(=O)OC)[C@H](OC(C)=O)[C@]7(CC)C=CCN6CC[C@]45[C@@]67[H])C8)C9, 2. cisplatin-[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": "Combination", "PMID": "22316209", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC", "System": "NCI-H1703", "Dose": "cisplatin (0.5 μg/mL) + vinorelbine (0.04 μg/mL)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/395", "Drug": "Vinorelbine and cisplatin", "Drug_category": "Others/combination", "Drugbank_ID": "1. DB00361 (APRD00101), 2. DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "1. Tubulin beta chain 2. Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": "1. D08680, 2. D00275", "Pubchem_ID": null, "STR_LINK_(SMILES)": "1. Vinorebine- [H][C@]89C=C(CC)CN(Cc1c([nH]c2ccccc12)[C@@](C(=O)OC)(c3cc4c(cc3OC)N(C)[C@@]5([H])[C@@](O)(C(=O)OC)[C@H](OC(C)=O)[C@]7(CC)C=CCN6CC[C@]45[C@@]67[H])C8)C9, 2. cisplatin-[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": "Combination", "PMID": "22316209", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC", "System": "A549", "Dose": null, "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1431", "Drug": "Vorinostat (V) + mithramycin A (MA)", "Drug_category": "Others/combination", "Drugbank_ID": "vorinostat (V): DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM). Mithramycin (also known as Plicamycin) is an antineoplastic antibiotic produced by Streptomyces plicatus. Mithramycin A is a DNA/RNA polymerase inhibitor, DNA-binding transcriptional inhibitor, antibiotic, and observed to facilitate tumor necrosis factor (TNF)-α and Fas ligand-induced apoptosis.", "KEGG_Drug__ID": "vorinostat (V): D06320", "Pubchem_ID": "vorinostat (V): 5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1,\n C[C@@H]1[C@H]([C@@H](C[C@@H](O1)O[C@@H]2C[C@@H](O[C@@H]", "Single/Combination": "Combination", "PMID": "28536458", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin Cancer - Merkel Cell Carcinoma-Skin Cancer", "System": "MKL-2", "Dose": "vorinostat (V) 1.25 µM, 0.3 µM for mithramycin A", "Technique": "RT-qPCR,immunofluorescence ,confocal microscopy and Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunofluorescence assay; Microscopy; Confocal microscopy; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "HLA class-I APM components LMP2, LMP7, TAP1 and TAP2", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Antigen presentation; TAP1; TAP2; LMP2 / PSMB9; LMP7 / PSMB8", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1432", "Drug": "Vorinostat (V) + mithramycin A (MA)", "Drug_category": "Others/combination", "Drugbank_ID": "vorinostat (V): DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM). Mithramycin (also known as Plicamycin) is an antineoplastic antibiotic produced by Streptomyces plicatus. Mithramycin A is a DNA/RNA polymerase inhibitor, DNA-binding transcriptional inhibitor, antibiotic, and observed to facilitate tumor necrosis factor (TNF)-α and Fas ligand-induced apoptosis.", "KEGG_Drug__ID": "vorinostat (V): D06320", "Pubchem_ID": "vorinostat (V): 5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1,\n C[C@@H]1[C@H]([C@@H](C[C@@H](O1)O[C@@H]2C[C@@H](O[C@@H]", "Single/Combination": "Combination", "PMID": "28536458", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin Cancer - Merkel Cell Carcinoma-Skin Cancer", "System": "WaGa", "Dose": "vorinostat (V) 1.25 µM, 0.3 µM for mithramycin A", "Technique": "RT-qPCR,immunofluorescence ,confocal microscopy and Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunofluorescence assay; Microscopy; Confocal microscopy; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "HLA class-I APM components LMP2, LMP7, TAP1 and TAP2", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Antigen presentation; TAP1; TAP2; LMP2 / PSMB9; LMP7 / PSMB8", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1433", "Drug": "Vorinostat (V) + mithramycin A (MA)", "Drug_category": "Others/combination", "Drugbank_ID": "vorinostat (V): DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM). Mithramycin (also known as Plicamycin) is an antineoplastic antibiotic produced by Streptomyces plicatus. Mithramycin A is a DNA/RNA polymerase inhibitor, DNA-binding transcriptional inhibitor, antibiotic, and observed to facilitate tumor necrosis factor (TNF)-α and Fas ligand-induced apoptosis.", "KEGG_Drug__ID": "vorinostat (V): D06320", "Pubchem_ID": "vorinostat (V): 5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1,\n C[C@@H]1[C@H]([C@@H](C[C@@H](O1)O[C@@H]2C[C@@H](O[C@@H]", "Single/Combination": "Combination", "PMID": "28536458", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin Cancer - Merkel Cell Carcinoma-Skin Cancer", "System": "MKL-1", "Dose": "vorinostat (V) 1.25 µM, 0.3 µM for mithramycin A", "Technique": "RT-qPCR,immunofluorescence ,confocal microscopy and Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunofluorescence assay; Microscopy; Confocal microscopy; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "HLA class-I APM components LMP2, LMP7, TAP1 and TAP2", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Antigen presentation; TAP1; TAP2; LMP2 / PSMB9; LMP7 / PSMB8", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1435", "Drug": "Vorinostat (V) + mithramycin A (MA)", "Drug_category": "Others/combination", "Drugbank_ID": "vorinostat (V): DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM). Mithramycin (also known as Plicamycin) is an antineoplastic antibiotic produced by Streptomyces plicatus. Mithramycin A is a DNA/RNA polymerase inhibitor, DNA-binding transcriptional inhibitor, antibiotic, and observed to facilitate tumor necrosis factor (TNF)-α and Fas ligand-induced apoptosis.", "KEGG_Drug__ID": "vorinostat (V): D06320", "Pubchem_ID": "vorinostat (V): 5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1,\n C[C@@H]1[C@H]([C@@H](C[C@@H](O1)O[C@@H]2C[C@@H](O[C@@H]", "Single/Combination": "Combination", "PMID": "28536458", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin Cancer - Merkel Cell Carcinoma-Skin Cancer", "System": "BroLi", "Dose": "vorinostat (V) 1.25 µM, 0.3 µM for mithramycin A", "Technique": "RT-qPCR,immunofluorescence ,confocal microscopy and Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunofluorescence assay; Microscopy; Confocal microscopy; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "HLA class-I APM components LMP2, LMP7, TAP1 and TAP2", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Antigen presentation; TAP1; TAP2; LMP2 / PSMB9; LMP7 / PSMB8", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/102", "Drug": "Vorinostat + Avelumab ( anti-PD-1)", "Drug_category": "Others/combination", "Drugbank_ID": "DB02546, DB11945", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM).\n Avelumab binds PD-L1 through the FG loops 7 and blocks the interaction between PD-L1 and its receptors PD-1 and B7.1.", "KEGG_Drug__ID": "D06320, \n D10817", "Pubchem_ID": "5311, \n 347911260", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "30377559", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCL", "System": "NCI-H441+NK cells purified from two healthy donor PBMCs", "Dose": "vorinostat (3 µM) for 4 consecutive days, Avelumab - 2 ng/mL", "Technique": "111In-release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK lysis and ADCC-mediated lysis", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/114", "Drug": "Vorinostat + Avelumab ( anti-PD-1)", "Drug_category": "Others/combination", "Drugbank_ID": "DB02546, DB11945", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM).\n Avelumab binds PD-L1 through the FG loops 7 and blocks the interaction between PD-L1 and its receptors PD-1 and B7.1.", "KEGG_Drug__ID": "D06320, \n D10817", "Pubchem_ID": "5311, \n 347911260", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "30377559", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCL", "System": "NCI-H460 +NK cells purified from two healthy donor PBMCs", "Dose": "vorinostat (3 µM) for 4 consecutive days, Avelumab - 2 ng/mL", "Technique": "111In-release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK lysis and ADCC-mediated lysis", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/263", "Drug": "PI3K inhibitor (LY294002; )", "Drug_category": "PI3K inhibitor", "Drugbank_ID": "DB02656", "Target/s_or_mechanism_of_action": "Protein kinase inhibitors, the mode of action of LY294002 is through competition with ATP for binding the PI3K active site", "KEGG_Drug__ID": "C15195", "Pubchem_ID": "3973", "STR_LINK_(SMILES)": "O=C1C=C(OC2=C1C=CC=C2C1=CC=CC=C1)N1CCOCC1", "Single/Combination": "Single Drug", "PMID": "26637667", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC", "System": "CL25", "Dose": "1 µmol/L", "Technique": "Western Blotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 expression", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/380", "Drug": "Vorinostat + Avelumab ( anti-PD-1)", "Drug_category": "Others/combination", "Drugbank_ID": "DB02546, DB11945", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM).\n Avelumab binds PD-L1 through the FG loops 7 and blocks the interaction between PD-L1 and its receptors PD-1 and B7.1.", "KEGG_Drug__ID": "D06320, \n D10817", "Pubchem_ID": "5311, \n 347911260", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "30377559", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate", "System": "DU145 +NK cells purified from two healthy donor PBMCs", "Dose": "vorinostat (3 µM) for 4 consecutive days, Avelumab - 2 ng/mL", "Technique": "111In-release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK lysis and ADCC-mediated lysis", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/391", "Drug": "Vorinostat + Avelumab ( anti-PD-1)", "Drug_category": "Others/combination", "Drugbank_ID": "DB02546, DB11945", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM).\n Avelumab binds PD-L1 through the FG loops 7 and blocks the interaction between PD-L1 and its receptors PD-1 and B7.1.", "KEGG_Drug__ID": "D06320, \n D10817", "Pubchem_ID": "5311, \n 347911260", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "30377559", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate", "System": "PC-3 +NK cells purified from two healthy donor PBMCs", "Dose": "vorinostat (3 µM) for 4 consecutive days, Avelumab - 2 ng/mL", "Technique": "111In-release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK lysis and ADCC-mediated lysis", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; ADCC; Antibody-dependent cytotoxicity", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1577", "Drug": "Vorinostat combined with azacitidine", "Drug_category": "Others/combination", "Drugbank_ID": "DB02546, DB00928", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM). As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D06320, D03021", "Pubchem_ID": "5311, 9444", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1,\n NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Combination", "PMID": "29371976", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "4T1", "Dose": "vorinostat (Vor 1.5μM) ,azacitidine (Aza 5μM)", "Technique": "qReal-Time PCR", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in tumor cells,", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1579", "Drug": "Vorinostat combined with azacitidine", "Drug_category": "Others/combination", "Drugbank_ID": "DB02546, DB00928", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM). As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": "D06320, D03021", "Pubchem_ID": "5311, 9444", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1,\n NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Combination", "PMID": "29371976", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "EMT6", "Dose": "vorinostat (Vor 1.5μM) ,azacitidine (Aza 5μM)", "Technique": "qReal-Time PCR", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression in tumor cells,", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/72", "Drug": "Zebularine (Zeb) +Trichostatin A (TSA)", "Drug_category": "Others/combination", "Drugbank_ID": "DB03068, DB04297", "Target/s_or_mechanism_of_action": "A chemically stable, cytidine analog that displays anti-tumor properties. It acts as a transition state analog inhibitor of cytidine deaminase by binding to the active site as covalent hydrates. Also shown to inhibit DNA methylation and tumor growth both in vitro and in vivo.\n TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": "100016, 444732", "STR_LINK_(SMILES)": "OC[C@H]1O[C@H]([C@H](O)[C@@H]1O)N1C=CC=NC1=O,\n C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Combination", "PMID": "22419072", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "A549 cells", "Dose": "TSA (0.5 μM),zebularine (50-100 μM)", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD1d", "Controlled_Terms_Function_enhanced_Number_increased": "CD1d", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/688", "Drug": "Panobinostat (PAN/LBH589)+IFN-γ", "Drug_category": "Pan-histone deacetylase inhibitor", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "HDAC inhibitors", "KEGG_Drug__ID": "D10319", "Pubchem_ID": "6918837", "STR_LINK_(SMILES)": "CC1=C(C2=CC=CC=C2N1)CCNCC3=CC=C(C=C3)/C=C/C(=O)NO", "Single/Combination": "combination", "PMID": "31720815", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Breast cancer", "System": "4T1 and TS/A,", "Dose": "20 mg/kg/day", "Technique": "flow cytometry", "Controlled_Technique": "MHCII, MHC I, CD74,PD-L1 expression, STAT1, PD-L1, and\nCXCL10", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; MHC class II; PD-L1 / CD274; CXCL10 / IP-10; STAT1; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1268", "Drug": "Plerixafor (AMD3100)", "Drug_category": "Phenylmethylamines", "Drugbank_ID": "DB06809", "Target/s_or_mechanism_of_action": "Plerixafor inhibits the CXCR4 chemokine receptors on CD34+ cells and reversibly blocks binding of the ligand, stromal cell-derived factor-1-alpha (SDF-1α). By blocking the interaction between SDF-1α and CXCR4 with plerixafor, mobilization of progenitor cells is triggered.", "KEGG_Drug__ID": "D08971", "Pubchem_ID": "65015", "STR_LINK_(SMILES)": "C(N1CCCNCCNCCCNCC1)C1=CC=C(CN2CCCNCCNCCCNCC2)C=C1", "Single/Combination": "Single Drug", "PMID": "29100374", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma (RCC)", "System": "Teff: PB-Tregs pretreated with AMD3100 (1:1)", "Dose": "10 μM of AMD3100", "Technique": "Flow cytometry, ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "peripheral CD4+CD25− T effector (Teff) cells proliferation IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD25 / IL2RA; IFN-γ; Cell proliferation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1186", "Drug": "Domatinostat (4SC-202)", "Drug_category": "phenylpyrazoles", "Drugbank_ID": "DB13101", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": "15985904", "STR_LINK_(SMILES)": "CN1C=C(C=N1)C1=CC=C(C=C1)S(=O)(=O)N1C=CC(\\C=C\\C(=O)NC2=CC=CC=C2N)=C1", "Single/Combination": "Single Drug", "PMID": "31703604", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "A375", "Dose": "domatinostat (0.5 µM), IFN-γ (10 ng/mL)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "(HLA-ABC)", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1187", "Drug": "Domatinostat (4SC-202)", "Drug_category": "phenylpyrazoles", "Drugbank_ID": "DB13101", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": "15985904", "STR_LINK_(SMILES)": "CN1C=C(C=N1)C1=CC=C(C=C1)S(=O)(=O)N1C=CC(\\C=C\\C(=O)NC2=CC=CC=C2N)=C1", "Single/Combination": "Single Drug", "PMID": "31703604", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "HMCB", "Dose": "domatinostat (0.5 µM), IFN-γ (10 ng/mL)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "(HLA-ABC)", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1188", "Drug": "Domatinostat (4SC-202)", "Drug_category": "phenylpyrazoles", "Drugbank_ID": "DB13101", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": "15985904", "STR_LINK_(SMILES)": "CN1C=C(C=N1)C1=CC=C(C=C1)S(=O)(=O)N1C=CC(\\C=C\\C(=O)NC2=CC=CC=C2N)=C1", "Single/Combination": "Single Drug", "PMID": "31703604", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "MEWO", "Dose": "domatinostat (0.5 µM), IFN-γ (10 ng/mL)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "(HLA-ABC)", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1319", "Drug": "Domatinostat (4SC-202)", "Drug_category": "phenylpyrazoles", "Drugbank_ID": "DB13101", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": "15985904", "STR_LINK_(SMILES)": "CN1C=C(C=N1)C1=CC=C(C=C1)S(=O)(=O)N1C=CC(\\C=C\\C(=O)NC2=CC=CC=C2N)=C1", "Single/Combination": "Single Drug", "PMID": "31703604", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": "murine CT26", "Dose": "domatinostat (0.5 µM, 1 µM)", "Technique": "qPCR, Flow cytometry", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "MHC class I and II", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/261", "Drug": "PI3K inhibitor (LY294002; )", "Drug_category": "PI3K inhibitor", "Drugbank_ID": "DB02656", "Target/s_or_mechanism_of_action": "Protein kinase inhibitors, the mode of action of LY294002 is through competition with ATP for binding the PI3K active site", "KEGG_Drug__ID": "C15195", "Pubchem_ID": "3973", "STR_LINK_(SMILES)": "O=C1C=C(OC2=C1C=CC=C2C1=CC=CC=C1)N1CCOCC1", "Single/Combination": "Single Drug", "PMID": "26637667", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC", "System": "CL30", "Dose": "1 µmol/L", "Technique": "Western Blotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 expression", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/262", "Drug": "PI3K inhibitor (LY294002; )", "Drug_category": "PI3K inhibitor", "Drugbank_ID": "DB02656", "Target/s_or_mechanism_of_action": "Protein kinase inhibitors, the mode of action of LY294002 is through competition with ATP for binding the PI3K active site", "KEGG_Drug__ID": "C15195", "Pubchem_ID": "3973", "STR_LINK_(SMILES)": "O=C1C=C(OC2=C1C=CC=C2C1=CC=CC=C1)N1CCOCC1", "Single/Combination": "Single Drug", "PMID": "26637667", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC", "System": "IO33", "Dose": "1 µmol/L", "Technique": "Western Blotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 expression", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/579", "Drug": "Carboplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00958", "Target/s_or_mechanism_of_action": "Carboplatin undergoes activation inside cells and forms reactive platinum complexes that cause the intra- and inter-strand cross-linkage of DNA molecules within the cell.", "KEGG_Drug__ID": "D01363", "Pubchem_ID": "426756", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt]1(OC(=O)C2(CCC2)C(=O)O1)[N]([H])([H])[H]", "Single/Combination": "Single", "PMID": "32078695", "Cancer_Type": "Esophageal Cancer", "Cancer_Type_Description": "esophageal cancer cells (OE33 cells", "System": "OE33", "Dose": "0, 10 and 100 μM cisplatin", "Technique": "Flow cytometry", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "No significant differences were observed in CD1d expression in OE33 cells", "Immune_System_function_unaffected": "Expression / abundance phenotype; CD1d", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/703", "Drug": "Carboplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00958", "Target/s_or_mechanism_of_action": "Carboplatin undergoes activation inside cells and forms reactive platinum complexes that cause the intra- and inter-strand cross-linkage of DNA molecules within the cell.", "KEGG_Drug__ID": "D01363", "Pubchem_ID": "426756", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt]1(OC(=O)C2(CCC2)C(=O)O1)[N]([H])([H])[H]", "Single/Combination": "Single", "PMID": "32078695", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "upper gastrointestinal cancer", "System": "Invariant natural killer T (iNKT) cells+CD1d-transfected HeLa cells", "Dose": "10 or 50 μM", "Technique": "Flow cytometry", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "No significant decrease in IFN-γ expression by viable iNKT cells, No significant difference in granzyme B or perforin production by activated iNKT cells", "Immune_System_function_unaffected": "Expression / abundance phenotype; Granzyme B / GZMB; IFN-γ", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/86", "Drug": "Carboplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00958", "Target/s_or_mechanism_of_action": "Carboplatin undergoes activation inside cells and forms reactive platinum complexes that cause the intra- and inter-strand cross-linkage of DNA molecules within the cell.", "KEGG_Drug__ID": "D01363", "Pubchem_ID": "38904", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt]1(OC(=O)C2(CCC2)C(=O)O1)[N]([H])([H])[H]", "Single/Combination": "Single Drug", "PMID": "20683396", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": "MA-148", "Dose": "(5 microg/mL)", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Macrophage chemoattractant protein-1 (MCP-1)", "Controlled_Terms_Negative_Regulation": "CCL2 / MCP-1; Macrophages", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/87", "Drug": "Carboplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00958", "Target/s_or_mechanism_of_action": "Carboplatin undergoes activation inside cells and forms reactive platinum complexes that cause the intra- and inter-strand cross-linkage of DNA molecules within the cell.", "KEGG_Drug__ID": "D01363", "Pubchem_ID": "38904", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt]1(OC(=O)C2(CCC2)C(=O)O1)[N]([H])([H])[H]", "Single/Combination": "Single Drug", "PMID": "20683396", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": "SKOV-3", "Dose": "(5 microg/mL)", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Macrophage chemoattractant protein-1 (MCP-1)", "Controlled_Terms_Negative_Regulation": "CCL2 / MCP-1; Macrophages", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1190", "Drug": "Cisplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": "D00275", "Pubchem_ID": "5702198", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": "Single Drug", "PMID": "21765211", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Blm Melanoma Cells", "System": "BLM melanoma cells", "Dose": "10 μg/ml cisplatin", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L2 expression dephosphorylation of STAT6 in tumor cells", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L2 / PDCD1LG2; STAT6; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/817", "Drug": "Cisplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": "D00275", "Pubchem_ID": "5702198", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": "Single Drug", "PMID": "14617634", "Cancer_Type": "Brain cancer", "Cancer_Type_Description": "S-Type Neuroblastoma", "System": "SH-EP1", "Dose": "10 μg/ml", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Caspase-3 and caspase-9", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase-9; Caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "caspase-8", "Controlled_Terms_Unaffected": "Caspase-8; Caspase activation", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1530", "Drug": "Cisplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": "D00275", "Pubchem_ID": "5702198", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": "Single Drug", "PMID": "22396773", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "ZR-75-1", "Dose": "6 µM", "Technique": "immunoblotting, Flow cytometry, ELISA assay", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IFN-β MHC I", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; IFN-β;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/698", "Drug": "Cisplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515", "Target/s_or_mechanism_of_action": "DNA crosslinking and DNA damage", "KEGG_Drug__ID": "D00275", "Pubchem_ID": "2767", "STR_LINK_(SMILES)": "N.N.Cl[Pt]Cl", "Single/Combination": "Single", "PMID": "40380807", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "gastric cancer cell line", "System": "AGS", "Dose": "22.56μM", "Technique": "Flow cytometry; Western blot", "Controlled_Technique": "Increased cell-surface PD-L1 and MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; PD-L1 / CD274", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "Increased PD-L1 may promote inhibitory immune-checkpoint signaling", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 immune checkpoint pathway; Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/699", "Drug": "Cisplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515", "Target/s_or_mechanism_of_action": "DNA crosslinking and DNA damage", "KEGG_Drug__ID": "D00275", "Pubchem_ID": "2767", "STR_LINK_(SMILES)": "N.N.Cl[Pt]Cl", "Single/Combination": "Single", "PMID": "40380807", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "gastric cancer cell line", "System": "SNU-1", "Dose": "13.92μM", "Technique": "Flow cytometry; Western blot", "Controlled_Technique": "Increased cell-surface PD-L1 and MHC-I", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; PD-L1 / CD274", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": "Increased PD-L1 may promote inhibitory immune-checkpoint signaling", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 immune checkpoint pathway; Expression / abundance phenotype; PD-L1 / CD274", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/578", "Drug": "Cisplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515", "Target/s_or_mechanism_of_action": "DNA crosslinking and DNA damage", "KEGG_Drug__ID": "D00275", "Pubchem_ID": "84691", "STR_LINK_(SMILES)": "N.N.Cl[Pt]Cl", "Single/Combination": "Single", "PMID": "32078695", "Cancer_Type": "Esophageal Cancer", "Cancer_Type_Description": "esophageal cancer cells (OE33 cells", "System": "OE33", "Dose": "0, 10 and 100 μM cisplatin", "Technique": "Flow cytometry", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": "downregulation of CD1d in OE33 cells", "Immune_System-Function_inhibited/numbers_decreased": "Expression / abundance phenotype; CD1d", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/77", "Drug": "Cisplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": "D00275", "Pubchem_ID": "5702198", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": "Single Drug", "PMID": "26689911", "Cancer_Type": "Mesothelioma", "Cancer_Type_Description": "Malignant Mesothelioma (MM)", "System": "H2461", "Dose": "(0–100 μM)", "Technique": "qRT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "NLRP3", "Controlled_Terms_Negative_Regulation": "NLRP3 inflammasome", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/119", "Drug": "Cisplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": "D00275", "Pubchem_ID": "5702198", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": "Single Drug", "PMID": "23079474", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": "SK-OV-3", "Dose": "20 μM", "Technique": "Microarray analysis +RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "IRF-1 and IRF-7 are induced by CDDP in ovarian cancer cell lines", "Controlled_Terms_Negative_Regulation": "IRF-1; IRF-7", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/701", "Drug": "Cisplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515", "Target/s_or_mechanism_of_action": "DNA crosslinking and DNA damage", "KEGG_Drug__ID": "D00275", "Pubchem_ID": "84691", "STR_LINK_(SMILES)": "N.N.Cl[Pt]Cl", "Single/Combination": "Single", "PMID": "32078695", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "upper gastrointestinal cancer", "System": "Invariant natural killer T (iNKT) cells+CD1d-transfected HeLa cells", "Dose": "10 or 100 μM", "Technique": "Flow cytometry", "Controlled_Technique": "significant increase of granzyme B and perforin", "Immune_System-Function_enhanced/numbers_increased": "Granzyme B / GZMB; Perforin / PRF1", "Controlled_Terms_Function_enhanced_Number_increased": "inhibited IFN-γ production and CD107a externalization, PI9 expression decreased at high doses", "Immune_System-Function_inhibited/numbers_decreased": "Expression / abundance phenotype; CD107a / LAMP1; IFN-γ", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/340", "Drug": "Cisplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": "D00275", "Pubchem_ID": "5702198", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": "Single Drug", "PMID": "26689911", "Cancer_Type": "Mesothelioma", "Cancer_Type_Description": "Malignant Mesothelioma (MM)", "System": "Hmeso", "Dose": "(0–100 μM)", "Technique": "Western blot analysis or ELISA", "Controlled_Technique": "Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "IL-1β, IL-18, FGF2 and HMGB1 NLRP3 inflammasome, capsase-1", "Controlled_Terms_Negative_Regulation": "IL-1 family; IL-18; FGF2; NLRP3 inflammasome; HMGB1", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/341", "Drug": "Cisplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": "D00275", "Pubchem_ID": "5702198", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": "Single Drug", "PMID": "26689911", "Cancer_Type": "Mesothelioma", "Cancer_Type_Description": "Malignant Mesothelioma (MM)", "System": "H2373", "Dose": "(0–100 μM)", "Technique": "Western blot analysis or ELISA", "Controlled_Technique": "Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "IL-1β, IL-18, FGF2 and HMGB1 NLRP3 inflammasome, capsase-1", "Controlled_Terms_Negative_Regulation": "IL-1 family; IL-18; FGF2; NLRP3 inflammasome; HMGB1", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/772", "Drug": "Teniposide", "Drug_category": "Podophyllotoxins", "Drugbank_ID": "DB00444", "Target/s_or_mechanism_of_action": "Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA.", "KEGG_Drug__ID": "D02698", "Pubchem_ID": "452548", "STR_LINK_(SMILES)": "[H][C@]12COC(=O)[C@]1([H])[C@H](C1=CC(OC)=C(O)C(OC)=C1)C1=C(C=C3OCOC3=C1)[C@H]2O[C@]1([H])O[C@]2([H])CO[C@H](O[C@@]2([H])[C@H](O)[C@H]1O)C1=CC=CS1", "Single/Combination": "Single Drug", "PMID": "31408442", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "B16-OVA cells treated with teniposide or DMSO for 16 hours, then cocultures with BMDC and OT-I cells", "Dose": null, "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "T cell, T cells expressing the activation marker CD69 and effector molecule granzyme B (Gzm B) IL-2 and IFN-γ ( significantly increased in T cells)", "Controlled_Terms_Function_enhanced_Number_increased": "CD69; IL-2; IFN-γ; Granzyme B / GZMB; T 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This makes the strands unable to uncoil and separate.", "KEGG_Drug__ID": null, "Pubchem_ID": "Cisplatin-5702198 , Carboplatin-‎426756", "STR_LINK_(SMILES)": "Cisplatin-[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H] and Carboplatin-[H][N]([H])([H])[Pt]1(OC(=O)C2(CCC2)C(=O)O1)[N]([H])([H])[H]", "Single/Combination": null, "PMID": "7795278", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcomas", "System": "mouse sarcoma-180 cells + cisplatin (10 micrograms/ml) and carboplatin (50 micrograms/ml)-treated macrophages", "Dose": "cisplatin (10 micrograms/ml) and carboplatin (50 micrograms/ml)", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "interleukin-1 alpha and tumor necrosis factor-alpha Cytotoxicity", "Controlled_Terms_Function_enhanced_Number_increased": "IL-1 family; TNF-α / TNF; Cytotoxicity / cytolysis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/73", "Drug": "Cisplatin-based NAC", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": "D00275", "Pubchem_ID": "5702198", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": null, "PMID": "31404614", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC", "System": "Lewis lung carcinoma", "Dose": null, "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression on tumor", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/120", "Drug": "Cisplatin-based NAC", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": "D00275", "Pubchem_ID": "5702198", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": null, "PMID": "31404614", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC", "System": "LNM-R cells", "Dose": "dose-dependent manner( MAX 8 μM)", "Technique": "RT-PCR + Immunocytochemistry", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); 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Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunocytochemistry (ICC)", "Immune_System-Function_enhanced/numbers_increased": "Fas, FasL", "Controlled_Terms_Function_enhanced_Number_increased": "CD95 / Fas / FAS; Fas ligand / FasL / FASLG", "Immune_System-Function_inhibited/numbers_decreased": "FasL", "Controlled_Terms_Function_inhibited_Number_decreased": "Fas ligand / FasL / FASLG", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1303", "Drug": "Oxaliplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00526", "Target/s_or_mechanism_of_action": "Inhibiting DNA synthesis and transcription", "KEGG_Drug__ID": "D01790", "Pubchem_ID": "6857599", "STR_LINK_(SMILES)": "[H][N]1([H])[C@@H]2CCCC[C@H]2[N]([H])([H])[Pt]11OC(=O)C(=O)O1", "Single/Combination": "Single Drug", "PMID": "21151176", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Osteosarcoma", "System": "U2OS", "Dose": "(300 mM)", "Technique": "automated image acquisition and analysis + Flow cytometry", "Controlled_Technique": "Flow cytometry; 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Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "T cell CXCL10 (ICD marker) MHC-I and MHC-II expression on the tumor cell surface, β2m (B2m), an essential component of MHC-I,genes directing peptide cleavage (Erap1), peptide transporters (Tap1 and Tap2), and transporter-MHC interactions (Tapbp) Immunogenic cell death,apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; MHC class II; β2-microglobulin / B2M; CXCL10 / IP-10; Apoptosis; Immunogenic cell death; TAP1; TAP2; T cells; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1318", "Drug": "Teniposide", "Drug_category": "Podophyllotoxins", "Drugbank_ID": "DB00444", "Target/s_or_mechanism_of_action": "Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA.", "KEGG_Drug__ID": "D02698", "Pubchem_ID": "452548", "STR_LINK_(SMILES)": "[H][C@]12COC(=O)[C@]1([H])[C@H](C1=CC(OC)=C(O)C(OC)=C1)C1=C(C=C3OCOC3=C1)[C@H]2O[C@]1([H])O[C@]2([H])CO[C@H](O[C@@]2([H])[C@H](O)[C@H]1O)C1=CC=CS1", "Single/Combination": "Single Drug", "PMID": "31408442", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Adenocarcinoma", "System": "CT26", "Dose": "0-10 µM", "Technique": "HMGB1-Gluc reporter assay.Flow cytometry,qPCR", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "MHC-I and MHC-II expression on the tumor cell surface, β2m (B2m), an essential component of MHC-I,genes directing peptide cleavage (Erap1), peptide transporters (Tap1 and Tap2), and transporter-MHC interactions (Tapbp) Immunogenic cell death,apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; MHC class II; β2-microglobulin / B2M; Apoptosis; Immunogenic cell death; TAP1; TAP2; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1332", "Drug": "Teniposide", "Drug_category": "Podophyllotoxins", "Drugbank_ID": "DB00444", "Target/s_or_mechanism_of_action": "Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA.", "KEGG_Drug__ID": "D02698", "Pubchem_ID": "452548", "STR_LINK_(SMILES)": "[H][C@]12COC(=O)[C@]1([H])[C@H](C1=CC(OC)=C(O)C(OC)=C1)C1=C(C=C3OCOC3=C1)[C@H]2O[C@]1([H])O[C@]2([H])CO[C@H](O[C@@]2([H])[C@H](O)[C@H]1O)C1=CC=CS1", "Single/Combination": "Single Drug", "PMID": "31408442", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": "PDAC murine pancreatic cancer cells", "Dose": null, "Technique": "Flow cytometry,qPCR", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "MHC-I and MHC-II expression on the tumor cell surface, β2m (B2m), an essential component of MHC-I,genes directing peptide cleavage (Erap1), peptide transporters (Tap1 and Tap2), and transporter-MHC interactions (Tapbp)", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; MHC class II; β2-microglobulin / B2M; TAP1; TAP2; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1337", "Drug": "Teniposide", "Drug_category": "Podophyllotoxins", "Drugbank_ID": "DB00444", "Target/s_or_mechanism_of_action": "Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA.", "KEGG_Drug__ID": "D02698", "Pubchem_ID": "452548", "STR_LINK_(SMILES)": "[H][C@]12COC(=O)[C@]1([H])[C@H](C1=CC(OC)=C(O)C(OC)=C1)C1=C(C=C3OCOC3=C1)[C@H]2O[C@]1([H])O[C@]2([H])CO[C@H](O[C@@]2([H])[C@H](O)[C@H]1O)C1=CC=CS1", "Single/Combination": "Single Drug", "PMID": "31408442", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "OVA-expressing B16 mouse melanoma cells (B16-OVA) + cocultured with bone marrow–derived DCs (BMDCs) and OVA-specific CD8+ T cell hybridoma B3Z cells, B16", "Dose": null, "Technique": "HMGB1-Gluc reporter assay,qPCR, Flow cytometry, ELISA", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR); Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "T cell, T cells expressing the activation marker CD69 and effector molecule granzyme B (Gzm B) CXCL10 (ICD marker), IL-2 and IFN-γ ( significantly increased in T cells), IFN-β, CCL5, and CXCL10 MHC-I and MHC-II expression on the tumor cell surface, β2m (B2m), an essential component of MHC-I,genes directing peptide cleavage (Erap1), peptide transporters (Tap1 and Tap2), and transporter-MHC interactions (Tapbp), CD80, CD86, MHC-I, MHC-II, and CD40 on BMDCs (BMDC maturation, antigen presentation, and subsequent T cell activation) Immunogenic cell death", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; MHC class II; β2-microglobulin / B2M; CD40; CD80; CD86; CD69; IL-2; IFN-β; IFN-γ; CCL5 / RANTES; CXCL10 / IP-10; Immunogenic cell death; Antigen presentation; TAP1; TAP2; Granzyme B / GZMB; CD80/CD86 costimulation; T cells; Expression / abundance phenotype;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/100", "Drug": "Resveratrol", "Drug_category": "Polyphenolic phytoalexin", "Drugbank_ID": "DB02709", "Target/s_or_mechanism_of_action": "resveratrol suppresses NF-kappaB (NF-kappaB) activation in HSV infected cells. Reports have indicated that HSV activates NF-kappaB during productive infection and this may be an essential aspect of its replication scheme", "KEGG_Drug__ID": "C03582", "Pubchem_ID": "445154", "STR_LINK_(SMILES)": "OC1=CC=C(\\C=C\\C2=CC(O)=CC(O)=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "11406544", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Lymphoblastic Leukemias (ALLs)", "System": "SEM", "Dose": "50 mM resveratrol", "Technique": "RT-PCR, colorimetric\n assay using the caspase-9 activation kit", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Apoptosis/cell viability assay; Colorimetric/biochemical activity assay", "Immune_System-Function_enhanced/numbers_increased": "Caspase-9", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-9; Caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD95L", "Controlled_Terms_Unaffected": "Fas ligand / FasL / FASLG", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/101", "Drug": "Resveratrol", "Drug_category": "Polyphenolic phytoalexin", "Drugbank_ID": "DB02709", "Target/s_or_mechanism_of_action": "resveratrol suppresses NF-kappaB (NF-kappaB) activation in HSV infected cells. Reports have indicated that HSV activates NF-kappaB during productive infection and this may be an essential aspect of its replication scheme", "KEGG_Drug__ID": "C03582", "Pubchem_ID": "445154", "STR_LINK_(SMILES)": "OC1=CC=C(\\C=C\\C2=CC(O)=CC(O)=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "11406544", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Lymphoblastic Leukemias (ALLs)", "System": "RS4;11", "Dose": "50 mM resveratrol", "Technique": "RT-PCR, colorimetric\n assay using the caspase-9 activation kit", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Apoptosis/cell viability assay; Colorimetric/biochemical activity assay", "Immune_System-Function_enhanced/numbers_increased": "Caspase-9", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-9; Caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD95L", "Controlled_Terms_Unaffected": "Fas ligand / FasL / FASLG", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/103", "Drug": "Resveratrol", "Drug_category": "Polyphenolic phytoalexin", "Drugbank_ID": "DB02709", "Target/s_or_mechanism_of_action": "resveratrol suppresses NF-kappaB (NF-kappaB) activation in HSV infected cells. Reports have indicated that HSV activates NF-kappaB during productive infection and this may be an essential aspect of its replication scheme", "KEGG_Drug__ID": "C03582", "Pubchem_ID": "445154", "STR_LINK_(SMILES)": "OC1=CC=C(\\C=C\\C2=CC(O)=CC(O)=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "11406544", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Lymphoblastic Leukemias (ALLs)", "System": "REH", "Dose": "50 mM resveratrol", "Technique": "RT-PCR, colorimetric\n assay using the caspase-9 activation kit", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Apoptosis/cell viability assay; Colorimetric/biochemical activity assay", "Immune_System-Function_enhanced/numbers_increased": "Caspase-9", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-9; Caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD95L", "Controlled_Terms_Unaffected": "Fas ligand / FasL / FASLG", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/104", "Drug": "Resveratrol", "Drug_category": "Polyphenolic phytoalexin", "Drugbank_ID": "DB02709", "Target/s_or_mechanism_of_action": "resveratrol suppresses NF-kappaB (NF-kappaB) activation in HSV infected cells. Reports have indicated that HSV activates NF-kappaB during productive infection and this may be an essential aspect of its replication scheme", "KEGG_Drug__ID": "C03582", "Pubchem_ID": "445154", "STR_LINK_(SMILES)": "OC1=CC=C(\\C=C\\C2=CC(O)=CC(O)=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "11406544", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Lymphoblastic Leukemias (ALLs)", "System": "Nalm-6", "Dose": "50 mM resveratrol", "Technique": "RT-PCR, colorimetric\n assay using the caspase-9 activation kit", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Apoptosis/cell viability assay; Colorimetric/biochemical activity assay", "Immune_System-Function_enhanced/numbers_increased": "Caspase-9", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-9; Caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD95L", "Controlled_Terms_Unaffected": "Fas ligand / FasL / FASLG", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/105", "Drug": "Resveratrol", "Drug_category": "Polyphenolic phytoalexin", "Drugbank_ID": "DB02709", "Target/s_or_mechanism_of_action": "resveratrol suppresses NF-kappaB (NF-kappaB) activation in HSV infected cells. Reports have indicated that HSV activates NF-kappaB during productive infection and this may be an essential aspect of its replication scheme", "KEGG_Drug__ID": "C03582", "Pubchem_ID": "445154", "STR_LINK_(SMILES)": "OC1=CC=C(\\C=C\\C2=CC(O)=CC(O)=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "11406544", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Lymphoblastic Leukemias (ALLs)", "System": "MV4;11", "Dose": "50 mM resveratrol", "Technique": "RT-PCR, colorimetric\n assay using the caspase-9 activation kit", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Apoptosis/cell viability assay; Colorimetric/biochemical activity assay", "Immune_System-Function_enhanced/numbers_increased": "CD95L Caspase-9", "Controlled_Terms_Function_enhanced_Number_increased": "Fas ligand / FasL / FASLG; Caspase-9; Caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/106", "Drug": "Resveratrol", "Drug_category": "Polyphenolic phytoalexin", "Drugbank_ID": "DB02709", "Target/s_or_mechanism_of_action": "resveratrol suppresses NF-kappaB (NF-kappaB) activation in HSV infected cells. Reports have indicated that HSV activates NF-kappaB during productive infection and this may be an essential aspect of its replication scheme", "KEGG_Drug__ID": "C03582", "Pubchem_ID": "445154", "STR_LINK_(SMILES)": "OC1=CC=C(\\C=C\\C2=CC(O)=CC(O)=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "11406544", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Lymphoblastic Leukemias (ALLs)", "System": "Jurkat", "Dose": "50 mM resveratrol", "Technique": "RT-PCR, colorimetric\n assay using the caspase-9 activation kit", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Apoptosis/cell viability assay; Colorimetric/biochemical activity assay", "Immune_System-Function_enhanced/numbers_increased": "CD95L Caspase-9", "Controlled_Terms_Function_enhanced_Number_increased": "Fas ligand / FasL / FASLG; Caspase-9; Caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/107", "Drug": "Resveratrol", "Drug_category": "Polyphenolic phytoalexin", "Drugbank_ID": "DB02709", "Target/s_or_mechanism_of_action": "resveratrol suppresses NF-kappaB (NF-kappaB) activation in HSV infected cells. Reports have indicated that HSV activates NF-kappaB during productive infection and this may be an essential aspect of its replication scheme", "KEGG_Drug__ID": "C03582", "Pubchem_ID": "445154", "STR_LINK_(SMILES)": "OC1=CC=C(\\C=C\\C2=CC(O)=CC(O)=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "11406544", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Lymphoblastic Leukemias (ALLs)", "System": "CEM", "Dose": "50 mM resveratrol", "Technique": "RT-PCR, colorimetric\n assay using the caspase-9 activation kit", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Apoptosis/cell viability assay; Colorimetric/biochemical activity assay", "Immune_System-Function_enhanced/numbers_increased": "CD95L Caspase-9", "Controlled_Terms_Function_enhanced_Number_increased": "Fas ligand / FasL / FASLG; Caspase-9; Caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/99", "Drug": "Resveratrol", "Drug_category": "Polyphenolic phytoalexin", "Drugbank_ID": "DB02709", "Target/s_or_mechanism_of_action": "resveratrol suppresses NF-kappaB (NF-kappaB) activation in HSV infected cells. Reports have indicated that HSV activates NF-kappaB during productive infection and this may be an essential aspect of its replication scheme", "KEGG_Drug__ID": "C03582", "Pubchem_ID": "445154", "STR_LINK_(SMILES)": "OC1=CC=C(\\C=C\\C2=CC(O)=CC(O)=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "11406544", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Lymphoblastic Leukemias (ALLs)", "System": "HL60", "Dose": "50 mM resveratrol", "Technique": "RT-PCR, colorimetric\n assay using the caspase-9 activation kit", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Apoptosis/cell viability assay; Colorimetric/biochemical activity assay", "Immune_System-Function_enhanced/numbers_increased": "Caspase-9", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-9; Caspase activation", "Immune_System-Function_inhibited/numbers_decreased": "CD95L", "Controlled_Terms_Function_inhibited_Number_decreased": "Fas ligand / FasL / FASLG", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/904", "Drug": "AST 487", "Drug_category": "RET kinase inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31540894", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Medullary Carcinoma", "System": "TT cells", "Dose": "AST487(0-1000nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/971", "Drug": "AST 487", "Drug_category": "RET kinase inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31540894", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung - Human Lung Adenocarcinoma", "System": "LC-2/ad", "Dose": "AST487(0-100nM)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "HLA-A,B,C, HLA-A*02:01", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; HLA-A", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1481", "Drug": "AST 487", "Drug_category": "RET kinase inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "RET kinase inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31540894", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid - Human Papillary Thyroid Carcinoma", "System": "TPC1 cells", "Dose": "AST487(0-100nM)", "Technique": "Western BLot and Flow cytometry", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "HLA-A,B,C, HLA-A*02:01", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; HLA-A", "Immune_System-Function_inhibited/numbers_decreased": "pERK", "Controlled_Terms_Function_inhibited_Number_decreased": "ERK / MAPK", "Immune_System_function_unaffected": "IFNα, IFNγ, IL4, IL6 or TNFα secretion", "Controlled_Terms_Unaffected": "IL-4; IL-6; TNF-α / TNF; IFN-α; IFN-γ", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1073", "Drug": "All-trans-retinoic acid (ATRA), or Retinoic acid/ Tretinoin", "Drug_category": "Retinoids", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": "D00094", "Pubchem_ID": "5538", "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Single Drug", "PMID": "28515123", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Osteosarcoma", "System": "RAW264.7 cells treated with the supernatant of K7M2 WT cells", "Dose": "1 μmol/L ATRA for 48 hours", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "M1 polarization of macrophages CD86+ cells,(CCL3 and CCL5)", "Controlled_Terms_Function_enhanced_Number_increased": "CD86; CCL3 / MIP-1α; CCL5 / RANTES; Macrophages", "Immune_System-Function_inhibited/numbers_decreased": "M2 polarization CD206+", "Controlled_Terms_Function_inhibited_Number_decreased": "CD206 / MRC1; M2 macrophage polarization", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1336", "Drug": "All-trans-retinoic acid (ATRA), or Retinoic acid/ Tretinoin", "Drug_category": "Retinoids", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": "D00094", "Pubchem_ID": "5538", "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Single Drug", "PMID": "31296953", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Osteosarcoma", "System": "K7M2 WT cells", "Dose": null, "Technique": "Colony formation assay, tumor sphere-formation assay, Flow cytometry, real-time PCR", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "M2 polarization CD117+Stro-1+ cells ( M2 polarization-induced stemness of osteosarcoma cells), CD133, CXCR4 Nanog, and Oct4", "Controlled_Terms_Function_inhibited_Number_decreased": "CXCR4; M2 macrophage polarization; CD117 / KIT; STRO-1; CD133 / PROM1; NANOG; Stemness-associated phenotype; M2 polarization-associated stemness", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1430", "Drug": "ATRA (all-trans\n retinoic acid)", "Drug_category": "Retinoids", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": "D00094", "Pubchem_ID": "5538", "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Single Drug", "PMID": "16957513", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": "Colon cancer (SW480) cells", "Dose": "ATRA (all-trans\n retinoic acid) Range : 10–5, 10–6, 10–7 and 10–8mol/l,", "Technique": "Immunocytochemistry\n and Flow cytometry, RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunocytochemistry (ICC)", "Immune_System-Function_enhanced/numbers_increased": "Fas", "Controlled_Terms_Function_enhanced_Number_increased": "CD95 / Fas / FAS", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/744", "Drug": "Retinoic acid/ Tretinoin", "Drug_category": "Retinoids", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": "D00094", "Pubchem_ID": "5538", "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Single Drug", "PMID": "12115542", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "SCC‐4", "Dose": "10^6 M RA for 7 days", "Technique": "Cell migration assays, sandwich ELISA technique", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "monocyte migration, macrophages for secretion of angiogenic factors,IL-8 and VEGF-Pro angiogenic factors MCP-1 and TGF-β1-inducer of monocyte chemotaxis", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-8 / CXCL8; 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Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "CCL2, CXCL10, IL-1β, IL-6 and IL-8", "Controlled_Terms_Negative_Regulation": "IL-1 family; IL-6; IL-8 / CXCL8; CCL2 / MCP-1; CXCL10 / IP-10; IL-8/CXCL8", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1074", "Drug": "Paclitaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01229 (APRD00259, DB05261, DB05927, DB05526, DB05281)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": "D00491", "Pubchem_ID": "36314", "STR_LINK_(SMILES)": "[H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Single Drug", "PMID": "18074150", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Metastasizing Epithelioid Sarcoma (ES)", "System": "GRU", "Dose": "10 μg/ml", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD95 receptor expression CD95 activation resulted in apoptosis and cell death", "Controlled_Terms_Function_enhanced_Number_increased": "CD95 / Fas / FAS; Apoptosis; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1254", "Drug": "Paclitaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01229 (APRD00259, DB05261, DB05927, DB05526, DB05281)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": "D00491", "Pubchem_ID": "36314", "STR_LINK_(SMILES)": "[H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Single Drug", "PMID": "29138861", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "MDA-MB-231", "Dose": "paclitaxel (0.1-1 µM)", "Technique": "Flow cytometry + ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "HMGB1 and calreticulin in tumor microenvironment", "Controlled_Terms_Function_enhanced_Number_increased": "Calreticulin / CRT; HMGB1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1255", "Drug": "Paclitaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01229 (APRD00259, DB05261, DB05927, DB05526, DB05281)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": "D00491", "Pubchem_ID": "36314", "STR_LINK_(SMILES)": "[H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Single Drug", "PMID": "29138861", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "MCF-7,", "Dose": "paclitaxel (0.1-1 µM)", "Technique": "Flow cytometry + ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "HMGB1 and calreticulin in tumor microenvironment", "Controlled_Terms_Function_enhanced_Number_increased": "Calreticulin / CRT; HMGB1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1257", "Drug": "Paclitaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01229 (APRD00259, DB05261, DB05927, DB05526, DB05281)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": "D00491", "Pubchem_ID": "36314", "STR_LINK_(SMILES)": "[H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Single Drug", "PMID": "29138861", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "SK-BR-3", "Dose": "paclitaxel (0.1-1 µM)", "Technique": "Flow cytometry + ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "HMGB1 and calreticulin in tumor microenvironment", "Controlled_Terms_Function_enhanced_Number_increased": "Calreticulin / CRT; HMGB1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1273", "Drug": "Paclitaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01229 (APRD00259, DB05261, DB05927, DB05526, DB05281)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": "D00491", "Pubchem_ID": "36314", "STR_LINK_(SMILES)": "[H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Single Drug", "PMID": "21223350", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "T cells derived from tumour-bearing C57BL ⁄ 6 mice", "Dose": "0.1 micromole", "Technique": "Flow cytometry, ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "T reg IL-10 and TGF-b by Treg", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-10; Regulatory T cells / Tregs", "Immune_System_function_unaffected": "T-eff IL-2 and IFN-γ of Teff", "Controlled_Terms_Unaffected": "IL-2; IFN-γ", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1532", "Drug": "Paclitaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01229 (APRD00259, DB05261, DB05927, DB05526, DB05281)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": "D00491", "Pubchem_ID": "7847557", "STR_LINK_(SMILES)": "[H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Single Drug", "PMID": "22396773", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "ZR-75-1", "Dose": "3 µM", "Technique": "immunoblotting, Flow cytometry, ELISA assay", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IFN-β MHC I", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; IFN-β;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/581", "Drug": "paclitaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01229 (APRD00259, DB05261, DB05927, DB05526, DB05281)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": "D00491", "Pubchem_ID": "36314", "STR_LINK_(SMILES)": "[H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Single", "PMID": "32078695", "Cancer_Type": "Esophageal Cancer", "Cancer_Type_Description": "esophageal cancer cells (OE33 cells", "System": "OE33", "Dose": "0, 10 and 100 μM cisplatin", "Technique": "Flow cytometry", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": "No significant differences were observed in CD1d expression in OE33 cells", "Immune_System_function_unaffected": "Expression / abundance phenotype; CD1d", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/704", "Drug": "paclitaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01229 (APRD00259, DB05261, DB05927, DB05526, DB05281)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": "D00491", "Pubchem_ID": "36314", "STR_LINK_(SMILES)": "[H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Single", "PMID": "32078695", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "upper gastrointestinal cancer", "System": "Invariant natural killer T (iNKT) cells+CD1d-transfected HeLa cells", "Dose": "10 or 50 μM", "Technique": "Flow cytometry", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": "reduced CD107a expression", "Immune_System-Function_inhibited/numbers_decreased": "Expression / abundance phenotype; CD107a / LAMP1", "Controlled_Terms_Function_inhibited_Number_decreased": "No significant decrease in IFN-γ expression by viable iNKT cells, No significant difference in granzyme B or perforin production by activated iNKT cells", "Immune_System_function_unaffected": "Expression / abundance phenotype; Granzyme B / GZMB; IFN-γ", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/10", "Drug": "Paclitaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01229 (APRD00259, DB05261, DB05927, DB05526, DB05281)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": null, "Pubchem_ID": "36314", "STR_LINK_(SMILES)": "[H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Single Drug", "PMID": "22039576", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "BT474", "Dose": "10-25nm", "Technique": "qRT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); 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It works by inhibiting DNA topoisomerases, type I.", "KEGG_Drug__ID": "D08618", "Pubchem_ID": "60700", "STR_LINK_(SMILES)": "CC[C@@]1(O)C(=O)OCC2=C1C=C1N(CC3=CC4=C(C=CC(O)=C4CN(C)C)N=C13)C2=O", "Single/Combination": "Single Drug", "PMID": "22396773", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "MCF-7", "Dose": "TPT (40, 200, 20, and 40 nM, respectively) for 4 days", "Technique": "immunoblotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "MHC I", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/172", "Drug": "Topotecan", "Drug_category": "Topoisomerase I inhibitor", "Drugbank_ID": "DB01030", "Target/s_or_mechanism_of_action": "An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA topoisomerases, type I.", "KEGG_Drug__ID": "D08618", "Pubchem_ID": "60700", "STR_LINK_(SMILES)": "CC[C@@]1(O)C(=O)OCC2=C1C=C1N(CC3=CC4=C(C=CC(O)=C4CN(C)C)N=C13)C2=O", "Single/Combination": "Single Drug", "PMID": "22396773", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "T47D", "Dose": "TPT (40, 200, 20, and 40 nM, respectively) for 4 days", "Technique": "immunoblotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "MHC I", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/173", "Drug": "Topotecan", "Drug_category": "Topoisomerase I inhibitor", "Drugbank_ID": "DB01030", "Target/s_or_mechanism_of_action": "An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA topoisomerases, type I.", "KEGG_Drug__ID": "D08618", "Pubchem_ID": "60700", "STR_LINK_(SMILES)": "CC[C@@]1(O)C(=O)OCC2=C1C=C1N(CC3=CC4=C(C=CC(O)=C4CN(C)C)N=C13)C2=O", "Single/Combination": "Single Drug", "PMID": "22396773", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "MDA-MB-231", "Dose": "TPT (40, 200, 20, and 40 nM, respectively) for 4 days", "Technique": "immunoblotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "MHC I", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1197", "Drug": "Topotecan Hydrochloride,", "Drug_category": "Topoisomerase I inhibitor", "Drugbank_ID": "DB01030", "Target/s_or_mechanism_of_action": "An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA topoisomerases, type I.", "KEGG_Drug__ID": "D08618", "Pubchem_ID": "60700", "STR_LINK_(SMILES)": "CC[C@@]1(O)C(=O)OCC2=C1C=C1N(CC3=CC4=C(C=CC(O)=C4CN(C)C)N=C13)C2=O", "Single/Combination": "Single Drug", "PMID": "29267866", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "Melanoma cell line 2549, along with its autologous tumor-infiltrating lymphocytes (TILs)", "Dose": "1 µM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "T-cell activated caspase 3-apoptosis marker", "Controlled_Terms_Function_enhanced_Number_increased": "Caspase-3; Caspase activation; Apoptosis; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/574", "Drug": "Doxorubicin (DOX)+ indocyanine green +Ultrasound", "Drug_category": "topoisomerase inhibitor", "Drugbank_ID": "DB00997+DB09374", "Target/s_or_mechanism_of_action": "DOX inhibits topoisomerase II and intercalates DNA. ICG acts as a sonosensitizer under ultrasound exposure, promoting reactive oxygen species (ROS) generation and mitochondrial DNA oxidation/release, activating the cGAS–STING–TBK1–IRF3 pathway and type I interferon responses", "KEGG_Drug__ID": "D03899+D01342", "Pubchem_ID": "31703+11967809", "STR_LINK_(SMILES)": "COC1=CC=CC2=C1C(=O)C1=C(O)C3=C(C[C@](O)(C[C@@H]3O[C@H]3C[C@H](N)[C@H](O)[C@H](C)O3)C(=O)CO)C(O)=C1C2= and CC1(C)C(=CC=CC=CC=CC2=[N+](CCCCS([O-])(=O)=O)C3=CC=C4=CC=CC=C4C=C3C2(C)C)N(CCCCS(O)(=O)=O)C2=CC=C3C=CC=CC3=C12", "Single/Combination": "Combination", "PMID": "37391428", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal/colon cancer", "System": "CT26", "Dose": "CG: 3 μM; DOX: 0.5 μM; US: 5 min; BMDC co-culture for 24 h", "Technique": "IFN-β ELISA", "Controlled_Technique": "IFNβ (mainly from BMDCS) in the supernatant as a readout for STING activation; ICD markers such as CRT and HMGB1, with levels similar (for CRT) or higher (for HMGB1)", "Immune_System-Function_enhanced/numbers_increased": "HMGB1; Calreticulin / CRT; Immunogenic cell death; IFN-β", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1361", "Drug": "Acalabrutinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB11703", "Target/s_or_mechanism_of_action": "Acalabrutinib is a small molecule inhibitor of BTK. Both acalabrutinib and its active metabolite, ACP-5862, act to form a covalent bond with a cysteine residue (Cys481) in the BTK active site, leading to inhibition of BTK enzymatic activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "71226662", "STR_LINK_(SMILES)": "CC#CC(=O)N1CCC[C@H]1C1=NC(=C2N1C=CN=C2N)C1=CC=C(C=C1)C(=O)NC1=CC=CC=N1", "Single/Combination": "Single Drug", "PMID": "28714866", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Natural Killer (NK) Large Granular Lymphocyte (LGL) Leukemia", "System": "NKL", "Dose": "SAHA (1, 2, 5 and 10 µM) and cladribine (0.125 µM)", "Technique": "MTS assay, Flow cytometry, PCR microarray and Western blot analyses", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Cell viability/proliferation assay; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "cytotoxicity, apoptotic cell death,activation of both intrinsic mitochondrial and extrinsic death receptor pathways -AIFM1 (apoptosis inducing factor), CYCS (cytochrome complex) and APAF1 (apoptotic protease activating factor-1),pro-apoptotic regulators including BBC2, BAX, BAK1 and BCL2L11 ,FAS, FASLG, FADD, TNFSF10, TNFRSF1A, TNFRSF10B, initiator and effector CASP (caspases) ,CYCS, ABL1, BCL2L11, CASP4, CASP8, CD40L, CD70, FAS, FASLG, TNFSF10, NOL3 and RIPK2", "Controlled_Terms_Function_enhanced_Number_increased": "CD95 / Fas / FAS; Fas ligand / FasL / FASLG; TRAIL-R2 / DR5 / TNFRSF10B; Caspase-8; Apoptosis; Cytotoxicity / cytolysis; BAX; BAK; BIM / BCL2L11", "Immune_System-Function_inhibited/numbers_decreased": "anti-apoptotic genes- BCL2 and BCL2L1, ERK and STAT3 signaling pathways", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6/JAK/STAT3 signaling; STAT3; ERK / MAPK; BCL-2; BCL-xL / BCL2L1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/755", "Drug": "AG1478", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "AG1478 tyrosine kinase inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": "2051", "STR_LINK_(SMILES)": "COC1=C(C=C2C(=C1)C(=NC=N2)NC3=CC(=CC=C3)Cl)OC", "Single/Combination": "Single Drug", "PMID": "29056908", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung", "System": "D122-reactive CD8+ T cells were incubated with D122", "Dose": "(5 μM, 96 h)", "Technique": "ELISA,vitro lactate dehydrogenase assay", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells-mediated lysis. IFN-γ production by D122-specific CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; IFN-γ; Cytotoxicity / cytolysis; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1316", "Drug": "AG1478", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "AG1478 tyrosine kinase inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": "2051", "STR_LINK_(SMILES)": "COC1=C(C=C2C(=C1)C(=NC=N2)NC3=CC(=CC=C3)Cl)OC", "Single/Combination": "Single Drug", "PMID": "29056908", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Mama", "System": "F3II", "Dose": "AG1478 (5 μM)", "Technique": "Flow cytometry, qPCR", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "H-2K and H-2D β2-m, LMP subunits, PA28α, BLH, TAPs, ERAAP1, tapasin, calnexin, calreticulin, PDI, as well as ERp57", "Controlled_Terms_Function_enhanced_Number_increased": "Tapasin; Calnexin; Calreticulin / CRT; ERp57 / PDIA3", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1322", "Drug": "AG1478", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "AG1478 tyrosine kinase inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": "2051", "STR_LINK_(SMILES)": "COC1=C(C=C2C(=C1)C(=NC=N2)NC3=CC(=CC=C3)Cl)OC", "Single/Combination": "Single Drug", "PMID": "29056908", "Cancer_Type": "Epidermoid Carcinoma", "Cancer_Type_Description": "Epidermoid Carcinoma", "System": "A431", "Dose": "AG1478 (5 μM)", "Technique": "Flow cytometry, real-time quantitative PCR (qPCR)", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "HLA-ABC membrane expression, HLA-A, HLA-B, and HLA-C β2-m, LMP subunits, TAPs, as well as tapasin", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; HLA-A; HLA-B; HLA-C; Tapasin; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1329", "Drug": "AG1478", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "AG1478 tyrosine kinase inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": "2051", "STR_LINK_(SMILES)": "COC1=C(C=C2C(=C1)C(=NC=N2)NC3=CC(=CC=C3)Cl)OC", "Single/Combination": "Single Drug", "PMID": "29056908", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung", "System": "D122", "Dose": "AG1478 (5 μM)", "Technique": "Flow cytometry, qPCR", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "H-2K and H-2D β2-m, LMP subunits, PA28α, BLH, TAPs, ERAAP1, tapasin, calnexin, calreticulin, PDI, as well as ERp57", "Controlled_Terms_Function_enhanced_Number_increased": "Tapasin; Calnexin; Calreticulin / CRT; ERp57 / PDIA3", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1330", "Drug": "AG1478", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "AG1478 tyrosine kinase inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": "2051", "STR_LINK_(SMILES)": "COC1=C(C=C2C(=C1)C(=NC=N2)NC3=CC(=CC=C3)Cl)OC", "Single/Combination": "Single Drug", "PMID": "29056908", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Adenocarcinoma", "System": "H125", "Dose": "AG1478 (5 μM)", "Technique": "Flow cytometry, real-time quantitative PCR (qPCR)", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "HLA-ABC membrane expression, HLA-A, HLA-B, and HLA-C β2-m, LMP subunits, TAPs, as well as tapasin", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; HLA-A; HLA-B; HLA-C; Tapasin; Expression / abundance phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/351", "Drug": "Alectinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB11363", "Target/s_or_mechanism_of_action": "Alectinib is a second generation oral drug that selectively inhibits the activity of anaplastic lymphoma kinase (ALK) tyrosine kinase.", "KEGG_Drug__ID": "D10542", "Pubchem_ID": "49806720", "STR_LINK_(SMILES)": "CCC1=CC2=C(C=C1N1CCC(CC1)N1CCOCC1)C(C)(C)C1=C(C3=CC=C(C=C3N1)C#N)C2=O", "Single/Combination": "Single Drug", "PMID": "31540894", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Anaplastic Large Cell Lymphoma (ALCL)", "System": "Karpas 299", "Dose": "alectinib (0-100nM)", "Technique": "Western BLot and Flow cytometery", "Controlled_Technique": "Western blot/immunoblot analysis; Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "HLA-A,B,C", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; HLA-A", "Immune_System-Function_inhibited/numbers_decreased": "IL6 and TNFα pERK", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6; TNF-α / TNF; ERK / MAPK", "Immune_System_function_unaffected": "IFNα, IFNγ, IL4", "Controlled_Terms_Unaffected": "IL-4; IFN-α; IFN-γ", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/352", "Drug": "Alectinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB11363", "Target/s_or_mechanism_of_action": "Alectinib is a second generation oral drug that selectively inhibits the activity of anaplastic lymphoma kinase (ALK) tyrosine kinase.", "KEGG_Drug__ID": "D10542", "Pubchem_ID": "49806720", "STR_LINK_(SMILES)": "CCC1=CC2=C(C=C1N1CCC(CC1)N1CCOCC1)C(C)(C)C1=C(C3=CC=C(C=C3N1)C#N)C2=O", "Single/Combination": "Single Drug", "PMID": "31540894", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Anaplastic Large Cell Lymphoma (ALCL)", "System": "SUDHL-1", "Dose": "alectinib (0-100nM)", "Technique": "Western BLot and Flow cytometery", "Controlled_Technique": "Western blot/immunoblot analysis; Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "HLA-A,B,C", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; HLA-A", "Immune_System-Function_inhibited/numbers_decreased": "pERK", "Controlled_Terms_Function_inhibited_Number_decreased": "ERK / MAPK", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1300", "Drug": "Axitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB06626", "Target/s_or_mechanism_of_action": "Axitinib selectively blocks the tyrosine kinase receptors VEGFR-1 (vascular endothelial growth factor receptor), VEGFR-2, and VEGFR-3.", "KEGG_Drug__ID": "D03218", "Pubchem_ID": "6450551", "STR_LINK_(SMILES)": "CNC(=O)C1=C(SC2=CC=C3C(NN=C3\\C=C\\C3=CC=CC=N3)=C2)C=CC=C1", "Single/Combination": "Single Drug", "PMID": "24135499", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "B16F1 cells", "Dose": "(0, 1, 10, 100, 1000, 10 000 nmol/l) for 72 h", "Technique": "MTT assay, Annexin V/PI doublestaining assay", "Controlled_Technique": "Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "induced the apoptosis of B16F1 cells", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1231", "Drug": "Axitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB06626", "Target/s_or_mechanism_of_action": "Axitinib selectively blocks the tyrosine kinase receptors VEGFR-1 (vascular endothelial growth factor receptor), VEGFR-2, and VEGFR-3.", "KEGG_Drug__ID": "D03218", "Pubchem_ID": "6450551", "STR_LINK_(SMILES)": "CNC(=O)C1=C(SC2=CC=C3C(NN=C3\\C=C\\C3=CC=CC=N3)=C2)C=CC=C1", "Single/Combination": "Single Drug", "PMID": "24804814", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastric Cancer (GC)", "System": "BGC-823", "Dose": "4.27 µmol/L", "Technique": "Annexin V-FITC and PI staining by Flow cytometry", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "cell apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": "CD 34", "Controlled_Terms_Function_inhibited_Number_decreased": "CD34", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1232", "Drug": "Axitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB06626", "Target/s_or_mechanism_of_action": "Axitinib selectively blocks the tyrosine kinase receptors VEGFR-1 (vascular endothelial growth factor receptor), VEGFR-2, and VEGFR-3.", "KEGG_Drug__ID": "D03218", "Pubchem_ID": "6450551", "STR_LINK_(SMILES)": "CNC(=O)C1=C(SC2=CC=C3C(NN=C3\\C=C\\C3=CC=CC=N3)=C2)C=CC=C1", "Single/Combination": "Single Drug", "PMID": "24804814", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastric Cancer (GC)", "System": "HGC-27", "Dose": "12.5 µmol/L", "Technique": "Annexin V-FITC and PI staining by Flow cytometry", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "cell apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": "CD 34", "Controlled_Terms_Function_inhibited_Number_decreased": "CD34", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1548", "Drug": "Axitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB06626", "Target/s_or_mechanism_of_action": "Axitinib selectively blocks the tyrosine kinase receptors VEGFR-1 (vascular endothelial growth factor receptor), VEGFR-2, and VEGFR-3.", "KEGG_Drug__ID": "D03218", "Pubchem_ID": "6450551", "STR_LINK_(SMILES)": "CNC(=O)C1=C(SC2=CC=C3C(NN=C3\\C=C\\C3=CC=CC=N3)=C2)C=CC=C1", "Single/Combination": "Single Drug", "PMID": "26137411", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Subcutaneous And Intracranial Mouse Melanoma", "System": "Ly6G- (moMDSCs) and CD11b+Ly6CintLy6G+ (grMDSC) cells were sorted from the spleens of subcutaneous MO4-bearing mice on the 7th day of treatment with axitinib at 25 mg/kg", "Dose": null, "Technique": "suppression assay", "Controlled_Technique": "Immune suppression/blocking/depletion assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "suppressive capacity of CD11b+Ly6ChighLy6G- cells on CD4+ and CD8+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD8; CD11b / ITGAM; T cells; CD8+ T cells; T-cell suppressive function", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/757", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": "D10062", "Pubchem_ID": "25102847", "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "28274958", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": "PC3 human prostate cancer cells- PC3 cells were treated with 5 μM cabozantinib for 24 hours, followed by addition of neutrophils in a transwell migration assay for 4 hours. The neutrophils were obtained from a single patient donor with each condition being performed in 3 separate migration transwells", "Dose": "5 μM cabozantinib for 24 hours", "Technique": "transwell migration assay", "Controlled_Technique": "Cell co-culture/transwell assay", "Immune_System-Function_enhanced/numbers_increased": "neutrophil migration", "Controlled_Terms_Function_enhanced_Number_increased": "Neutrophils; Neutrophil migration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1267", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": "D10062", "Pubchem_ID": "25102847", "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "28274958", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": "SC1", "Dose": "30 μM", "Technique": "apoptosis analysis with Annexin V staining", "Controlled_Technique": "Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "modest apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1278", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": "D10062", "Pubchem_ID": "25102847", "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "28274958", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": "AC1", "Dose": "30 μM", "Technique": "apoptosis analysis with Annexin V staining", "Controlled_Technique": "Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "modest apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1289", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": "D10062", "Pubchem_ID": "25102847", "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "28274958", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": "AC3", "Dose": "30 μM", "Technique": "apoptosis analysis with Annexin V staining", "Controlled_Technique": "Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "modest apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1384", "Drug": "Erlotinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00530", "Target/s_or_mechanism_of_action": "Erlotinib inhibits the intracellular phosphorylation of tyrosine kinase associated with the epidermal growth factor receptor (EGFR).", "KEGG_Drug__ID": "D07907", "Pubchem_ID": "176870", "STR_LINK_(SMILES)": "COCCOC1=CC2=C(C=C1OCCOC)C(NC1=CC(=CC=C1)C#C)=NC=N2", "Single/Combination": "Single Drug", "PMID": "21499124", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "NCI-H23", "Dose": "10 μM", "Technique": "RT-PCR,Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "NKG2D ligand-surface expression of ULBP1", "Controlled_Terms_Function_enhanced_Number_increased": "NKG2D / KLRK1; ULBP1; Expression / abundance phenotype; NKG2D ligand", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/602", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": "D10062", "Pubchem_ID": "25102847", "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "25388653", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Adenocarcinoma", "System": "MC38-CEA cells treated with cabozantinib for 24 h and labeled with 111In, then coincubated with CTLs", "Dose": "2.5 μg/mL cabozantinib", "Technique": "Cytotoxic T lymphocyte killing assay", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay", "Immune_System-Function_enhanced/numbers_increased": "T cell-mediated lysis by cytotoxic T lymphocytes (CTLs)", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; T cells", 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"Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1061", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": "D10062", "Pubchem_ID": "25102847", "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "29152128", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": "Peripheral blood monocytes isolatedfrom patients - cultured with M-CSF", "Dose": null, "Technique": "FACS", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "M1 macrophage differentiation", "Controlled_Terms_Function_inhibited_Number_decreased": "Macrophages", "Immune_System_function_unaffected": "M2 macrophage", "Controlled_Terms_Unaffected": "Macrophages", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1062", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": "D10062", "Pubchem_ID": "25102847", "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "29152128", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": "Thioglycollate-induced, activated macrophages- cultured with or without lipopolysaccharide (LPS) or interleukin-4 (IL-4) or tumor lysate", "Dose": null, "Technique": "FACS", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "M1 macrophage", "Controlled_Terms_Function_inhibited_Number_decreased": "Macrophages", "Immune_System_function_unaffected": "M2 macrophage", "Controlled_Terms_Unaffected": "Macrophages", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/863", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": "D10062", "Pubchem_ID": "25102847", "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "25388653", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Adenocarcinoma", "System": "MC38-CEA cells", "Dose": "2.5 μg/mL cabozantinib", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC-I molecules on both the population level (H-2Db) and a per-cell basis (H-2Kb), increasing the potential for antigen presentation and T cell recognition of the tumor cells, ICAM-1, Fas, and 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"Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1553", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": "D10062", "Pubchem_ID": "25102847", "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "28274958", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": "SC1", "Dose": "30 μM cabozantinib", "Technique": "IHC", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "modest apoptosis", 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"COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "28274958", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": "AC1", "Dose": "30 μM cabozantinib", "Technique": "IHC", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "modest apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1555", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": "D10062", "Pubchem_ID": "25102847", "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "28274958", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": "AC3", "Dose": "30 μM cabozantinib", "Technique": "IHC", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "modest apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/353", "Drug": "Crizotinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08865", "Target/s_or_mechanism_of_action": "Crizotinib is a tyrosine kinase receptor inhibitor. More specifically, it inhibits anaplastic lymphoma kinase (ALK), hepatocyte growth factor receptor (HGFR, c-MET), and Recepteur d'Origine Nantais (RON). Abnormalities in the ALK gene caused by mutations or translocations may lead to expression of oncogenic fusion proteins. In patients with NSCLC, they have the EML4-ALK gene. Crizotinib inhibits ALK tyrosine kinase which ultimately results in decreased proliferation of cells that carry the genetic mutation and tumour survivability.", "KEGG_Drug__ID": "D09731", "Pubchem_ID": "11626560", "STR_LINK_(SMILES)": "C[C@@H]OC1=CC(=CN=C1N)C1=CN(N=C1)C1CCNCC1)C1=C(Cl)C=CC(F)=C1Cl", "Single/Combination": "Single Drug", "PMID": "31540894", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Anaplastic Large Cell Lymphoma (ALCL)", "System": "Karpas 299", "Dose": "Crizotinib(1-100nM)", "Technique": "Western BLot and Flow cytometery", "Controlled_Technique": "Western blot/immunoblot analysis; Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "HLA-A,B,C", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; HLA-A", "Immune_System-Function_inhibited/numbers_decreased": "pERK", "Controlled_Terms_Function_inhibited_Number_decreased": "ERK / MAPK", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/354", "Drug": "Crizotinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08865", "Target/s_or_mechanism_of_action": "Crizotinib is a tyrosine kinase receptor inhibitor. More specifically, it inhibits anaplastic lymphoma kinase (ALK), hepatocyte growth factor receptor (HGFR, c-MET), and Recepteur d'Origine Nantais (RON). Abnormalities in the ALK gene caused by mutations or translocations may lead to expression of oncogenic fusion proteins. In patients with NSCLC, they have the EML4-ALK gene. Crizotinib inhibits ALK tyrosine kinase which ultimately results in decreased proliferation of cells that carry the genetic mutation and tumour survivability.", "KEGG_Drug__ID": "D09731", "Pubchem_ID": "11626560", "STR_LINK_(SMILES)": "C[C@@H]OC1=CC(=CN=C1N)C1=CN(N=C1)C1CCNCC1)C1=C(Cl)C=CC(F)=C1Cl", "Single/Combination": "Single Drug", "PMID": "31540894", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Anaplastic Large Cell Lymphoma (ALCL)", "System": "SUDHL-1", "Dose": "Crizotinib(1-100nM)", "Technique": "Western BLot and Flow cytometery", "Controlled_Technique": "Western blot/immunoblot analysis; Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "HLA-A,B,C", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; HLA-A", "Immune_System-Function_inhibited/numbers_decreased": "pERK", "Controlled_Terms_Function_inhibited_Number_decreased": "ERK / MAPK", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1220", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": "D03658", "Pubchem_ID": "3062316", "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "19295545", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "PBMCs from CLL patients", "Dose": "1 μM lenalidomide", "Technique": "apoptosis was analyzed by staining with annexin V, Flow cytometry, CFSE Staining", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "NKT-like cells (CD3+CD8+CD56+), proliferation of NK cells, CD4 T cells IL-2 by CD4 T cells NKp30 on NK cells apoptosis of leukemia cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD3; CD4; CD8; CD56 / NCAM1; NKp30 / NCR3; IL-2; Apoptosis; Cell proliferation; T cells; CD8+ T cells; CD4+ T cells; NKT cells; NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1571", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": "D03658", "Pubchem_ID": "3062316", "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "22419518", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": "primary CLL cells", "Dose": "lenalidomide (0.5 μM)", "Technique": "Flow cytometery, real-time reverse-transcribed polymerase chain reaction,laser scanning confocal microscopy", "Controlled_Technique": "Microscopy; Confocal microscopy; Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD23 and CD38 activation markers on CLL cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD23 / FCER2; CD38", "Immune_System-Function_inhibited/numbers_decreased": "CD20 expression on CLL cells (CD20 internalization)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD20 / MS4A1; Expression / abundance phenotype", "Immune_System_function_unaffected": "CD19, CD5, and CD52", "Controlled_Terms_Unaffected": "CD52; CD19", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1367", "Drug": "Erlotinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00530", "Target/s_or_mechanism_of_action": "Erlotinib inhibits the intracellular phosphorylation of tyrosine kinase associated with the epidermal growth factor receptor (EGFR).", "KEGG_Drug__ID": "D07907", "Pubchem_ID": "176870", "STR_LINK_(SMILES)": "COCCOC1=CC2=C(C=C1OCCOC)C(NC1=CC(=CC=C1)C#C)=NC=N2", "Single/Combination": "Single Drug", "PMID": "31291990", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "PMA/ionomycin stimulation of CD4 T cells and CD 8 cells from the lungs of tumor bearing CCSP-rtTA; TetO-EGFRL858R mice treated with erlotinib", "Dose": "25 mg/kg, 5 days a week", "Technique": "Bio-Plex Cytokine assay", "Controlled_Technique": "Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "IFN-γ, TNF-α and IL-2", "Controlled_Terms_Function_enhanced_Number_increased": "IL-2; TNF-α / TNF; IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/125", "Drug": "Erlotinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00530", "Target/s_or_mechanism_of_action": "Erlotinib inhibits the intracellular phosphorylation of tyrosine kinase associated with the epidermal growth factor receptor (EGFR).", "KEGG_Drug__ID": "D07907", "Pubchem_ID": "176870", "STR_LINK_(SMILES)": "COCCOC1=CC2=C(C=C1OCCOC)C(NC1=CC(=CC=C1)C#C)=NC=N2", "Single/Combination": "Single Drug", "PMID": "21499124", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "A549+cocultured with NK-92 cells", "Dose": "10 μM", "Technique": "using the DELFIA EuTDA cytotoxicity Reagents.", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "cytolytic activity of NK cells,", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", 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"DB00317", "Target/s_or_mechanism_of_action": "Gefitinib is an inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase that binds to the adenosine triphosphate (ATP)-binding site of the enzyme.", "KEGG_Drug__ID": "D01977", "Pubchem_ID": "123631", "STR_LINK_(SMILES)": "COC1=C(OCCCN2CCOCC2)C=C2C(NC3=CC(Cl)=C(F)C=C3)=NC=NC2=C1", "Single/Combination": "Single Drug", "PMID": "27698894", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": "PC-9 cells", "Dose": "0.1 μM", "Technique": "Flow cytometry, western blot,", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 expression, pEGFR and its downstream pathway - in the pAKT, pERK and pSTAT3 expression", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; ERK / MAPK; PD-L1 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"Drugbank_ID": "DB00317", "Target/s_or_mechanism_of_action": "Gefitinib is an inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase that binds to the adenosine triphosphate (ATP)-binding site of the enzyme.", "KEGG_Drug__ID": "D01977", "Pubchem_ID": "123631", "STR_LINK_(SMILES)": "COC1=C(OCCCN2CCOCC2)C=C2C(NC3=CC(Cl)=C(F)C=C3)=NC=NC2=C1", "Single/Combination": "Single Drug", "PMID": "32195020", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": "CAL-27", "Dose": "gefitinib and stimulated with 1 μg/mL LPS for 24 h", "Technique": "ELISA,western blotting", "Controlled_Technique": "Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, 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Cell viability/proliferation assay; Cell proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "T cell proliferation IFNγ secretion", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; Cell proliferation; T cells; T-cell proliferation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1214", "Drug": "Ibrutinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB09053", "Target/s_or_mechanism_of_action": "Ibrutinib is an inhibitor of Bruton’s tyrosine kinase (BTK).", "KEGG_Drug__ID": "D10223", "Pubchem_ID": "24821094", "STR_LINK_(SMILES)": "NC1=NC=NC2=C1C(=NN2[C@@H]1CCCN(C1)C(=O)C=C)C1=CC=C(OC2=CC=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "31921116", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Natural Killer (NK) Large Granular Lymphocyte (LGL) Leukemia", "System": "Leukaemic NK cells from six chronic NK-LGL patients (CD3−CD56+ NK cells > 80%)", "Dose": "SAHA (1, 2, 5 and 10 µM) and cladribine (0.125 µM)", "Technique": "MTS assay, Flow cytometry", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "cytotoxicity, apoptotic cell death", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1381", "Drug": "Ibrutinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB09053", "Target/s_or_mechanism_of_action": "Ibrutinib is an inhibitor of Bruton’s tyrosine kinase (BTK).", "KEGG_Drug__ID": "D10223", "Pubchem_ID": "24821094", "STR_LINK_(SMILES)": "NC1=NC=NC2=C1C(=NN2[C@@H]1CCCN(C1)C(=O)C=C)C1=CC=C(OC2=CC=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "27602755", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "Raji cells", "Dose": "(1 µM)", "Technique": "Time course RT-PCR,Flow cytometry", "Controlled_Technique": "Flow cytometry; 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Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/672", "Drug": "Ibrutinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB09053", "Target/s_or_mechanism_of_action": "Irreversible covalent BTK inhibition at Cys481", "KEGG_Drug__ID": "D10223", "Pubchem_ID": "24821094", "STR_LINK_(SMILES)": "NC1=NC=NC2=C1C(=NN2[C@@H]1CCCN(C1)C(=O)C=C)C1=CC=C(OC2=CC=CC=C2)C=C1", "Single/Combination": "single", "PMID": "41019037", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "melanoma", "System": "B16F10", "Dose": "0–10 μM, 24 h in vitro", "Technique": "Flow cytometry", "Controlled_Technique": "MHC-I expression", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1604", "Drug": "Ibrutinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB09053", "Target/s_or_mechanism_of_action": "Ibrutinib is an inhibitor of Bruton’s tyrosine kinase (BTK).", "KEGG_Drug__ID": "D10223", "Pubchem_ID": "24821094", "STR_LINK_(SMILES)": "NC1=NC=NC2=C1C(=NN2[C@@H]1CCCN(C1)C(=O)C=C)C1=CC=C(OC2=CC=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "28424405", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma", "System": "THP-1 differentiated macrophages (2.5 × 105))", "Dose": "ibrutinib (0.2, 0.5, 1, 2, 5 μM) for 1 hour", "Technique": "ELISA, real time PCR", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CXCL12, CXCL13, CCL19, VEGF NF-κB, STAT3, and AP-1", "Controlled_Terms_Function_inhibited_Number_decreased": "CXCL13; VEGF; IL-6/JAK/STAT3 signaling; STAT3; NF-κB; CXCL12 / SDF-1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/50", "Drug": "Ibrutinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB09053", "Target/s_or_mechanism_of_action": "Ibrutinib is an inhibitor of Bruton’s tyrosine kinase (BTK).", "KEGG_Drug__ID": "D10223", "Pubchem_ID": "24821094", "STR_LINK_(SMILES)": "NC1=NC=NC2=C1C(=NN2[C@@H]1CCCN(C1)C(=O)C=C)C1=CC=C(OC2=CC=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "27602755", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "U937", "Dose": "(1 µM)", "Technique": "Time course RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); 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Polymerase chain reaction (PCR/qPCR); Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "TNF-related costimulatory molecules - 4-1BB ligand (4-1BBL/TNFSF9) p21/WAF/CDKN1A cell cycle inhibitor", "Controlled_Terms_Function_enhanced_Number_increased": "4-1BB / CD137; 4-1BB ligand / TNFSF9; TNF-α / TNF; p21 / CDKN1A; CD80/CD86 costimulation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/210", "Drug": "Ibrutinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB09053", "Target/s_or_mechanism_of_action": "Ibrutinib is an inhibitor of Bruton’s tyrosine kinase (BTK).", "KEGG_Drug__ID": "D10223", "Pubchem_ID": "24821094", "STR_LINK_(SMILES)": "NC1=NC=NC2=C1C(=NN2[C@@H]1CCCN(C1)C(=O)C=C)C1=CC=C(OC2=CC=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "28714866", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "Jurkat", "Dose": "CHAP31-100 nmol/L, (20 and 100 ng/mL, respectively)", "Technique": "Western blotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "TRAIL-induced apoptosis-phosphatidylserine externalization, processing of caspase-3 to its catalytically active large subunits (p19/p17) and cleavage of PARP", "Controlled_Terms_Function_enhanced_Number_increased": "TRAIL; Caspase-3; Caspase activation; Apoptosis; PARP cleavage / PARP", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/211", "Drug": "Ibrutinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB09053", "Target/s_or_mechanism_of_action": "Ibrutinib is an inhibitor of Bruton’s tyrosine kinase (BTK).", "KEGG_Drug__ID": "D10223", "Pubchem_ID": "24821094", "STR_LINK_(SMILES)": "NC1=NC=NC2=C1C(=NN2[C@@H]1CCCN(C1)C(=O)C=C)C1=CC=C(OC2=CC=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "28714866", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": "K562 cells", "Dose": "CHAP31- (25 nmol/L), (20 and 100 ng/mL, respectively)", "Technique": "Western blotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "TRAIL-induced apoptosis-phosphatidylserine externalization, processing of caspase-3 to its catalytically active large subunits (p19/p17) and cleavage of PARP", "Controlled_Terms_Function_enhanced_Number_increased": "TRAIL; 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Microscopy; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 expression BCL2, p-EGFR,apoptosis", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; Apoptosis; BCL-2; EGFR; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/366", "Drug": "Icotinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB11737", "Target/s_or_mechanism_of_action": "Icotinib is a potent and specific epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI)", "KEGG_Drug__ID": "D11251", "Pubchem_ID": "22024915", "STR_LINK_(SMILES)": "C#CC1=CC=CC(NC2=NC=NC3=CC4=C(OCCOCCOCCO4)C=C23)=C1", "Single/Combination": "Single Drug", "PMID": "30538492", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": "Huh7", "Dose": "0.5 and 5 µM", "Technique": "western blot,fluorescence microscopy,situ TUNEL assay.", "Controlled_Technique": "Western blot/immunoblot analysis; Microscopy; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 expression BCL2, p-EGFR,apoptosis", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; Apoptosis; BCL-2; EGFR; PD-L1 immune checkpoint pathway; Expression / abundance phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/580", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": "D01441", "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "15286804", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastrointestinal Stromal Tumor (GIST)", "System": "CD3–/CD56+ NK cells from GIST patients treated with drug + NK cell-–sensitive K562 targets and against a GIST cell line", "Dose": "(400 mg/day)", "Technique": "51Cr release assay", "Controlled_Technique": "Cytotoxicity/release assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell lysis", "Controlled_Terms_Function_enhanced_Number_increased": "Cytotoxicity / cytolysis; NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/722", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": "D01441", "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "15286804", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastrointestinal Stromal Tumor (GIST)", "System": "Blood NK cells purified from GIST patients treated with drug + MD-DCs in the presence of LPS", "Dose": "(400 mg/day)", "Technique": "Cytotoxicity assays", "Controlled_Technique": "Cytotoxicity/release assay; Cellular cytotoxicity/function assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell IFN-γ production IFN-gamma production", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1424", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": "D01441", "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "27470968", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastrointestinal Stromal Tumor (GIST)", "System": "GIST-T1", "Dose": "(Im; 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It is an inhibitor of the JAK1 and JAK2 protein kinases and works by competitively inhibiting the ATP-binding catalytic site on JAK1 and JAK2", "KEGG_Drug__ID": "D09959", "Pubchem_ID": "25126798", "STR_LINK_(SMILES)": "N#CC[C@H](C1CCCC1)N1C=C(C=N1)C1=C2C=CNC2=NC=N1", "Single/Combination": "Single Drug", "PMID": "25149535", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": "1087-mel melanoma cells", "Dose": "(0.5 μM, 1 μM, 5 μM and 10 μM) and 48 hours", "Technique": "Flow cytometry using Annexin-V/7-AAD staining, western blotting", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Cell viability/proliferation assay; Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "inhibits P-STAT3 expression but does not induce apoptosis", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6/JAK/STAT3 signaling; STAT3; Apoptosis; Expression / abundance phenotype; STAT3 phosphorylation", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/867", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", 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"CANIMM/978", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "30123861", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatoma", "System": "SkHep1", "Dose": "7.5-60 μM", "Technique": "Apo-one Homogeneous Caspase-3/7 Assay (Promega)", "Controlled_Technique": "Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, 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"Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "31078430", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": "human peripheral blood mononuclear cell (PBMC)-derived CAR (huCAR) T cells", "Dose": "10 μM sorafenib", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "IL-2, IFN-γ, TNF-α", "Controlled_Terms_Function_enhanced_Number_increased": "IL-2; TNF-α / TNF; IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD107a", "Controlled_Terms_Unaffected": "CD107a / LAMP1; Degranulation", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/908", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "31078430", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": "coculture of mCAR T cells with LPS-activated Bone marrow-derived macrophages (BMDMs)", "Dose": "1–5 μM) sorafenib", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "ncreased the IFN-γ production of mCAR T cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/909", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "27540594", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": "Pretreatment samples of PBMCs from HCC patients were stimulated with anti-CD3/CD28", "Dose": "10 μM", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD4+ and CD8+ T cells IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; IFN-γ; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "Foxp3+ Tregs and CTLA-4+ Tregs VEGFR2 expression on both CD4+PD-1+ and CD8+PD-1+ T 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"CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "31391334", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": "PBMCs from patients with HCC were stimulated with anti–CD3/CD28", "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD4+Ki67+IFN-γ+ T cells,CD8+Ki67+ T cells IFN-γ granzyme B", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; IFN-γ; Granzyme B / GZMB; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/911", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "31078430", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": "mouse CAR T cells", "Dose": "10 μM sorafenib", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "IL-2, IFN-γ, TNF-α CD107a", "Controlled_Terms_Function_inhibited_Number_decreased": "CD107a / LAMP1; IL-2; TNF-α / TNF; IFN-γ; Degranulation", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/913", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": "D08524", "Pubchem_ID": "216239", "STR_LINK_(SMILES)": 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Cyclin D2; Cyclin D3", "Immune_System_function_unaffected": "Mcl-1, Bcl-2, Bcl-xL, Bax, Puma and Noxa", "Controlled_Terms_Unaffected": "BCL-2; BCL-xL / BCL2L1; MCL-1; BAX; PUMA / BBC3; NOXA / PMAIP1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1514", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": "D06402", "Pubchem_ID": "5329102", "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "19244102", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma (RCC)", "System": "786-O", "Dose": "0-10 μM", "Technique": "Flow Cytometry,MTS assay,Western blot analyses", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "p-Stat3 inhibition,cleaved PARP, Cyclin E, Cyclin D1 and Survivin", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6/JAK/STAT3 signaling; STAT3; PARP cleavage / PARP; Survivin / BIRC5; Cyclin D1 / CCND1; Cyclin E; STAT3 phosphorylation", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1515", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": "D06402", "Pubchem_ID": "5329102", "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "19244102", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma (RCC)", "System": "RCC4", "Dose": "0-10 μM", "Technique": "Flow Cytometry,MTS assay,Western blot analyses", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "p-Stat3 inhibition,cleaved PARP, Cyclin E, Cyclin D1 and Survivin", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6/JAK/STAT3 signaling; STAT3; PARP cleavage / PARP; Survivin / BIRC5; Cyclin D1 / CCND1; Cyclin E; STAT3 phosphorylation", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1516", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": "D06402", "Pubchem_ID": "5329102", "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "19244102", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma (RCC)", "System": "murine Renca", "Dose": "0-10 μM", "Technique": "Flow Cytometry,MTS assay,Western blot analyses", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "cleaved PARP, Cyclin E, Cyclin D1 and Survivin", "Controlled_Terms_Function_inhibited_Number_decreased": "PARP cleavage / PARP; Survivin / BIRC5; Cyclin D1 / CCND1; Cyclin E", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/464", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits VEGFR1/2/3, PDGFRα/β, KIT, FLT3, CSF1R, RET; activates IFNγ/STAT1 → ↑MHC-I", "KEGG_Drug__ID": "D08591", "Pubchem_ID": "5329102", "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "single", "PMID": "41019037", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast cancer", "System": "4T1", "Dose": "0–10 μM, 24 h in vitro", "Technique": "Flow cytometry", "Controlled_Technique": "MHC-I expression", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/670", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits VEGFR1/2/3, PDGFRα/β, KIT, FLT3, CSF1R, RET; activates IFNγ/STAT1 → ↑MHC-I", "KEGG_Drug__ID": "D08591", "Pubchem_ID": "5329102", "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "single", "PMID": "41019037", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "melanoma", "System": "B16F10", "Dose": "0–10 μM, 24 h in vitro", "Technique": "Flow cytometry", "Controlled_Technique": "MHC-I expression", "Immune_System-Function_enhanced/numbers_increased": "MHC class I; Expression / abundance phenotype", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/1535", "Drug": "Vinblastine", "Drug_category": "Vinca alkaloids", "Drugbank_ID": "DB00570", "Target/s_or_mechanism_of_action": "inhibition of mitosis at metaphase through its interaction with tubulin. Vinblastine binds to the microtubular proteins of the mitotic spindle, leading to crystallization of the microtubule and mitotic arrest or cell death.", "KEGG_Drug__ID": "D08675", "Pubchem_ID": "13342", "STR_LINK_(SMILES)": "[H][C@@]12N(C)C3=CC(OC)=C(C=C3[C@@]11CCN3CC=C[C@@](CC)([C@@H](OC(C)=O)[C@]2(O)C(=O)OC)[C@@]13[H])[C@]1(C[C@@]2([H])CN(C[C@](O)(CC)C2)CCC2=C1NC1=C2C=CC=C1)C(=O)OC", "Single/Combination": "Single Drug", "PMID": "22396773", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": "ZR-75-1", "Dose": "6 nM", "Technique": "immunoblotting, Flow cytometry, ELISA assay", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IFN-β MHC I", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; IFN-β;", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "cell_line", "ID": "CANIMM/609", "Drug": "vinorelbine", "Drug_category": "Vinca alkaloids", "Drugbank_ID": "DB00361", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": "D08680", "Pubchem_ID": "5311497", "STR_LINK_(SMILES)": "CCC1=C[C@H]2C[C@@](C3=C(CN(C2)C1)C4=CC=CC=C4N3)(C5=C(C=C6C(=C5)[C@]78CCN9[C@H]7[C@@](C=CC9)([C@H]([C@@]([C@@H]8N6C)(C(=O)OC)O)OC(=O)C)CC)OC)C(=O)OC", "Single/Combination": "single", "PMID": "40076874", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-small-cell lung cancer (NSCLC)", "System": "Monocytes, M1 macrophages and M2 macrophages", "Dose": "50 nM and 100 nM vinorelbine for 48 h", "Technique": "Flow cytometry;", "Controlled_Technique": "CD80", "Immune_System-Function_enhanced/numbers_increased": "CD80", "Controlled_Terms_Function_enhanced_Number_increased": "CD206 and CD163", "Immune_System-Function_inhibited/numbers_decreased": "CD206 / MRC1; 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4 mg/kg)", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "CCL2 (MCP-1), CCL7 (MCP-3), and CCL8 (MCP-2)-cancer stem-like cell (CSC) phenotype and contributing to tumor relapse", "Controlled_Terms_Negative_Regulation": "CCL2 / MCP-1; CCL7 / MCP-3; CCL8 / MCP-2", "KEGG_Drug_ID": "D03899", "Drug_Pubchem": "31703", "Animal_Strain_used": "NSG", "Cell_line_used_to_induce_tumor_in_mice": "MDA-MB-231", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2126", "Drug": "Doxorubicin", "Drug_category": "Anthracyclines", "Drugbank_ID": "DB00997", "Target/s_or_mechanism_of_action": "DNA intercalation; 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Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "B cells, CD4+ T cells, CD8+ T cells, NK cells, dendritic cells, monocytes/macrophages or MDSC", "Controlled_Terms_Unaffected": "CD4; CD8; Myeloid-derived suppressor cells / MDSCs; Macrophages; Monocytes; Dendritic cells; NK cells; B cells; T cells; CD8+ T cells; CD4+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Foxp3+ Treg TGFβ", "Controlled_Terms_Negative_Regulation": "TGF-β; FOXP3; Regulatory T cells / Tregs", "KEGG_Drug_ID": "C06854", "Drug_Pubchem": "5360373", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26 tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1716", "Drug": "PLX4720", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Single Drug", "PMID": "22934253", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "a chow diet containing 417 mg/kg PLX4720", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "T cells, B cells, NK cells, MDSCs or macrophages", "Controlled_Terms_Unaffected": "Myeloid-derived suppressor cells / MDSCs; Macrophages; NK cells; B cells; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "B16F10 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1717", "Drug": "PLX4720", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Single Drug", "PMID": "22934253", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "a chow diet containing 417 mg/kg PLX4720", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD45+ leukocytes, CD8+ and CD4+ T cells in the melanomas ,frequency of NK-cells, myeloid derived suppressor cells (MDSCs), macrophages", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD8; CD45; Myeloid-derived suppressor cells / MDSCs; Macrophages; T cells; CD4+ T cells", "Immune_System_function_unaffected": "B220+CD19+ B-lymphocytes", "Controlled_Terms_Unaffected": "CD19; B cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "Tyr::CreERT2PTENF−/−BRAFF-V600E/+", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1724", "Drug": "PLX4720", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Single Drug", "PMID": "23454771", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "20 mg/kg i.p.)", "Technique": "SDS-PAGE", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "CCR2+ tumor-infiltrating\n leukocytes (TILs), NK cells (NK1.1+ TCRβ–), CD8+ T cells (CD8+ TCRβ+), CD8/Treg ratio DNAM-1 ligand, CD155;\n the nonclassical MHC, CD1d; and PD-L1,Fas and DR5", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD155 / PVR; PD-L1 / CD274; Regulatory T cells / Tregs; NK cells; T cells; CD8+ T cells; Tumor-infiltrating lymphocytes / TILs; Immune checkpoint pathway; CCR2; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "Tregs (CD4+ Foxp3+), pERK, CCL2", "Controlled_Terms_Function_inhibited_Number_decreased": "CCL2 / MCP-1; CD4; FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": "total T cells (NK1.1– TCRβ+), CD4+ T cells\n (CD4+ TCRβ+), CD11b+ Gr-1+ myeloid cells", "Controlled_Terms_Unaffected": "CD4; CD11b / ITGAM; T cells; CD4+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1754", "Drug": "PLX4720", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Single Drug", "PMID": "24736544", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "(417mg PLX4720/kg) for another 21 days", "Technique": "Flow Cytometry, Immunohistochemical Staining", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD4 and CD8 T lymphocytes infiltrating PLX4720-treated melanomas, maturation status of both TAMs and TIDCs CD4 T cells produced IFNγ (i.e., TH1 cells) CD40L on intratumoral CD4 T cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; CD40L / CD154; Tumor-associated macrophages / TAMs; Dendritic cells; T cells; Th1 / type 1 T-cell response; CD8+ T cells; CD4+ T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "intratumoral CD11b+/Gr-1+ cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM", "Immune_System_function_unaffected": "CD4 T cell production of IL-2 and TNFα.", "Controlled_Terms_Unaffected": "IL-2; TNF-α / TNF; CD4; T cells; CD4+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-1+ CD4 T cells", "Controlled_Terms_Negative_Regulation": "CD4; PD-1 / PDCD1; T cells; CD4+ T cells", "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "Braf/Pten", "Cell_line_used_to_induce_tumor_in_mice": "1μl 4-hydroxytamoxifen (4-HT) (8mg/ml in ethanol) topically on the back skin and examined every week for melanoma growth", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1755", "Drug": "PLX4720", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Single Drug", "PMID": "24736544", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "417mg/kg PLX4720", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD4+ and CD8+ T cells, FoxP3− CD4+ T cells, TH1 cells, CD40L+ CD4+ T cells, PD-1+ CD4+ T cells IFN-y", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; CD40L / CD154; PD-1 / PDCD1; FOXP3; T cells; Th1 / type 1 T-cell response; CD8+ T cells; CD4+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "FoxP3+ Treg CD4+ T cells and CD11b+/Gr-1+", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD11b / ITGAM; FOXP3; Regulatory T cells / Tregs; T cells; CD4+ T cells", "Immune_System_function_unaffected": "IL-2 and TNFα.", "Controlled_Terms_Unaffected": "IL-2; TNF-α / TNF", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "BrafV600E/Pten", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1766", "Drug": "PLX4720", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Single Drug", "PMID": "24994118", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer", "System": null, "Dose": "PLX4720-impregnated chow (417 mg/kg", "Technique": "Immunohistochemical Analysis", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cell infiltration was observed in tumors, infiltrating B220+ B cells, marker of monocytes and macrophages, F4/80 Caspase 3 cleavage- marker of apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Macrophages; Monocytes; B cells; T cells; CD8+ T cells; Apoptosis / caspase activation; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "B6129SF1/J", "Cell_line_used_to_induce_tumor_in_mice": "TBP-3743", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1767", "Drug": "PLX4720", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Single Drug", "PMID": "24994118", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer - (Anaplastic)", "System": null, "Dose": "PLX4720-impregnated\n chow (417 mg/kg),", "Technique": "Immunohistochemial Analysis", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "B6129SF1/J syngeneic", "Cell_line_used_to_induce_tumor_in_mice": "105 TBP-3743 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1774", "Drug": "PLX4720", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Single Drug", "PMID": "25183499", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "(417 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8 T cells by proportion of CD45+ cells, but not by absolute number, CD4 T cells by the proportion of CD45+ cells but not the absolute number", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD45; T cells; CD8+ T cells; CD4+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "Foxp3+ Tregs in the tumor microenvironment, myeloid-derived suppressor cells (MDSC)-CD11b+Gr1+ cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; FOXP3; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": "CD4 T-cell expression of transcription factors T-bet, GATA3, and RORγt", "Controlled_Terms_Unaffected": "CD4; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "Tyr::CreER+/−BrafCA/+Ptenlox/lox(Braf/Pten) - bred onto a B6 background", "Cell_line_used_to_induce_tumor_in_mice": "intradermal injection of 4-hydroxy-tamoxifen (10μl of a 20 μM solution in DMSO)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1834", "Drug": "BRAFi PLX4720", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Single Drug", "PMID": "26943572", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer", "System": null, "Dose": "PLX4720-impregnated chow (417 mg/kg)", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "B6129SF1/J", "Cell_line_used_to_induce_tumor_in_mice": "105 genetically engineered murine ATC; TBP 3743\n BRAFV600E/WT P53-/- cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1868", "Drug": "PLX4720", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Single Drug", "PMID": "28123875", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "BRAFi [B] PLX4720 was provided in chow; MEKi [M] trametinib was dosed by daily oral gavage at 15 µg (on average 0.75 mg/kg); PI3Ki [P] BKM120 daily oral gavage at 400 µg (on average 20 mg/kg)", "Technique": "Flow Cytometry, Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "intratumoral IFNγ positive CD8+ T cells The infiltrating CD8+ T cells expressed high levels of PD-1 in about 50% of the cells , a marker shown to be associated with tumor-antigen-specific T cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; PD-1 / PDCD1; T cells; CD8+ T cells; Antigen-specific recognition; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "D4M.3A mouse melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1942", "Drug": "PLX4720", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Single Drug", "PMID": "30327563", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid - Anaplastic Thyroid Cancer", "System": null, "Dose": "PLX4720PLX4720-impregnated chow (417 mg/kg body weight), (n=\n 14, 7 for each timepoint at 1 week and 2 weeks)", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ cytotoxic T cells, granzyme B , and FoxP3+ T cells, NK cells, F4/80+CD206− cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD206 / MRC1; FOXP3; NK cells; T cells; Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": "monocytic MDSCs(CD11b+ Ly6G−Ly6C+)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs", "Immune_System_function_unaffected": "F4/80+CD206+IA/IE+ and F4/\n 80+CD206+IA/IE− cells (M2-polarised subsets) IFNγ", "Controlled_Terms_Unaffected": "IFN-γ; CD206 / MRC1; M2 macrophage phenotype", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "B6129SF1/J", "Cell_line_used_to_induce_tumor_in_mice": "TBP-3743 cells(105)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1964", "Drug": "Trametinib", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Single Drug", "PMID": "30771521", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": null, "Dose": "trametinib for three days prior to initiation of combination or Single treatment+ trametinib (0.25, 0.5, and 1 mg/kg) continued for three weeks", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PMN-MDSCs, CD45+/CD11b+/Ly6Ghigh/Ly6Clow", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; CD45; Myeloid-derived suppressor cells / MDSCs; PMN-MDSCs / granulocytic MDSCs", "Immune_System_function_unaffected": "percentage of CD4+ and CD8+ cells, monocytic-MDSCs CD45+/CD11b+/Ly6G-/Ly6Chigh,", "Controlled_Terms_Unaffected": "CD4; CD8; CD11b / ITGAM; CD45; Myeloid-derived suppressor cells / MDSCs", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09996", "Drug_Pubchem": "42611257", "Animal_Strain_used": "PKL (Lung tumors were induced by Ad-Cre in the transgenic mouse model)", "Cell_line_used_to_induce_tumor_in_mice": "3 × 105 PKL5–2 cells into the right flank of mice", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2007", "Drug": "PLX4720", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Single Drug", "PMID": "31702822", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "\"3 × 105 D4M cells injected subcutaneously (s.c.)+ after 8 days BRAFi containg Chow(417 mg PLX4720/kg) +2 mg/kg of\n the TLR7A at Day 19 (middle of sensitive phase)\"", "Technique": "Flow cytometry, qRT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD45+ immune cells, In BRAFi-sensitive tumors, more T\n and NK cells when compared to untreated tumors increased mRNA levels for chemokines CCL2, CCL3, CCL4, CXCL9, CXCL10 and cytokines IL-\n 12a, IL-12b, IL-15, IL-18 in BRAFi-sensitive tumors. IL-10 and TGF-β1 were also highly expressed in BRAFisensitive\n tumors, NK cells, CD4+ T cells and\n CD8+ T cells produced more IFN-γ in BRAFi-sensitive tumors, TNF-α+ cells CD4+ T cells and\n CD8+ T cells from BRAFi-sensitive tumors, granzyme B-positive\n cells CD69 in BRAFi-sensitive\n tumors on T cells, the inhibitory ligands PD-L1 as well as PD-L2 were\n expressed at higher levels in BRAFi-sensitive\n tumors gp100 and trp-2 in BRAFi-sensitive tumors, NKG2D+ cells were significantly higher on\n both NK and T cells in BRAFi-sensitive mice", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-10; IL-12; IL-18; TNF-α / TNF; TGF-β; CCL2 / MCP-1; CCL3 / MIP-1α; CCL4 / MIP-1β; CXCL9 / MIG; CXCL10 / IP-10; CD4; CD8; CD69; CD45; PD-L1 / CD274; PD-L2 / PDCD1LG2; NK cells; T cells; CD8+ T cells; CD4+ T cells; Granzyme B / GZMB; NKG2D ligand / receptor pathway; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": "infiltrating NK cells were decreased in the\n BRAFi resistant tumors mRNA levels for CCL2, CCL3, CCL4, CXCL9 and\n CXCL10 and cytokines IL-\n 12a, IL-12b, IL-15, IL-18 in in BRAFi resistant tumors. IL-10 and TGF-β1 were also highly expressed in in BRAFi resistant tumors PD-1 Decreased in BRAFisensitive\n tumors gp100 and trp-2 in BRAFi resistant tumors, NKG2D+ cells were significantly higher on\n both NK and T cells in BRAFi-resistant mice", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-10; IL-12; IL-18; TGF-β; CCL2 / MCP-1; CCL3 / MIP-1α; CCL4 / MIP-1β; CXCL9 / MIG; CXCL10 / IP-10; PD-1 / PDCD1; NK cells; T cells; NKG2D ligand / receptor pathway; Immune-cell infiltration", "Immune_System_function_unaffected": "TNF-α secretion did not change in NK cells TIM-3", "Controlled_Terms_Unaffected": "TNF-α / TNF; NK cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "BRAFV600E/PTEN D4M-3A (RRID:CVCL_0P27)25 murine\n melanoma cell line", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2045", "Drug": "Abemaciclib", "Drug_category": "CDK4 protein kinase inhibitor", "Drugbank_ID": "DB12001", "Target/s_or_mechanism_of_action": "Abemaciclib selectively inhibits CDK4 and CDK6 with low nanomolar potency, inhibits Rb phosphorylation resulting in a G1 arrest and inhibition of proliferation, and its activity is specific for Rb-proficient cells", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN1CCN(CC2=CC=C(NC3=NC=C(F)C(=N3)C3=CC(F)=C4N=C(C)N(C(C)C)C4=C3)N=C2)CC1", "Single/Combination": "Single Drug", "PMID": "32929370", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": null, "Dose": "Abemaciclib (CDK4/6i)-(50 mg/kg)", "Technique": "Immunohistochemistry (IHC) and\n Immunofluorescence (IF)", "Controlled_Technique": "Immunohistochemistry (IHC); Immunofluorescence assay; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "CD45+ cells, CD8+ cells, CD19+ cells and PD-L1+ cells in ID8 tumors, IFN-y+ CD107 a+, CD8+ cells and IFN-y+ CD107 a+, CD4+foxp3- T cell, IFN-γ producing B cells, CD40+CD80+ CD86+ DCs, MHCII+ cells T bet CD69", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; CD69; CD80; CD86; CD40; CD45; CD19; PD-L1 / CD274; MHC class II; FOXP3; Dendritic cells; B cells; T cells; IFN-γ-producing cells; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": "CD11B+Gr-1+ myeloid-derived suppressor cell\n (MDSC), IL-10 producing B cells, CD206+ cells", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-10; CD11b / ITGAM; CD206 / MRC1; Myeloid-derived suppressor cells / MDSCs; B cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10688", "Drug_Pubchem": "46220502", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "ID8 (ID8-luc) cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1988", "Drug": "AZD5069 (αCXCR2)", "Drug_category": "CXCR2 antagonist", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(CO)O)OC1=NC(=NC(=C1)NS(=O)(=O)N2CCC2)SCC3=C(C(=CC=C3)F)F", "Single/Combination": "Single Drug", "PMID": "31433989", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": null, "Dose": "αCXCR2 (AZD5069) 100mg/kg daily for a period of 3 weeks + neutralizing antibody for TNFα", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "p16 levels", "Controlled_Terms_Function_inhibited_Number_decreased": "p16 levels", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "56645576", "Animal_Strain_used": "C57BL/6N", "Cell_line_used_to_induce_tumor_in_mice": "2.5x106 Pten−/−-TRAMP-C1 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1989", "Drug": "AZD5069 (αCXCR2)", "Drug_category": "CXCR2 antagonist", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(CO)O)OC1=NC(=NC(=C1)NS(=O)(=O)N2CCC2)SCC3=C(C(=CC=C3)F)F", "Single/Combination": "Single Drug", "PMID": "31433989", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate 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"Controlled_Terms_Function_enhanced_Number_increased": "TNF-α / TNF; CD4; CD8; CD11c / ITGAX; CD206 / MRC1; Regulatory T cells / Tregs; Tumor-associated macrophages / TAMs; T cells; CD8+ T cells; Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": "F4/80+CD11c+/−CD206+ cells arginase and CD206 levels Ki-67 staining ,", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11c / ITGAX; CD206 / MRC1; Cell proliferation / Ki-67", "Immune_System_function_unaffected": "CD45+CD11b+LY6G−F4/80+macrophages", "Controlled_Terms_Unaffected": "CD11b / ITGAM; CD45; Macrophages", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "56645576", "Animal_Strain_used": "Ptenpc−/−", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1991", "Drug": "AZD5069 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"Immune_System-Function_inhibited/numbers_decreased": "F4/80+CD11c+/−CD206+ cells arginase and CD206 levels Ki-67 staining ,", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11c / ITGAX; CD206 / MRC1; Cell proliferation / Ki-67", "Immune_System_function_unaffected": "CD45+CD11b+LY6G−F4/80+macrophages", "Controlled_Terms_Unaffected": "CD11b / ITGAM; CD45; Macrophages", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "56645576", "Animal_Strain_used": "Ptenpc−/−; Trp53pc−/−", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1892", "Drug": "NU7441", "Drug_category": "DNA-dependent protein kinase (DNA-PK) Inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "NU7441 (KU-57788) is a highly potent and selective DNA-PK inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1COCCN1C2=CC(=O)C3=C(O2)C(=CC=C3)C4=CC=CC5=C4SC6=CC=CC=C56", "Single/Combination": "Single Drug", "PMID": "28775208", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "NU7026 (6 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "11327430", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "B16-F1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2032", "Drug": "VPA (valpromide)", "Drug_category": "Fatty acid derivatives", "Drugbank_ID": "DB00313", "Target/s_or_mechanism_of_action": "Valproic acid exhibits its pharmacologic effects in a couple of ways, such as by acting on GABA (γ aminobutyric acid) levels in the CNS, blocking voltage-gated ion channels, and inhibiting histone deacetylase", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCC(CCC)C(O)=O", "Single/Combination": "Single Drug", "PMID": "32158627", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "VPA (500 mg/kg) untill day 15", "Technique": "Flow Cytometery", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cells (CD3ɛ−NK1.1+) and CD8+ T-cells\n (CD3ɛ+CD4−CD8α+) in tumors, CD69hi cells in CD8+ T -cells (CD3ɛ+CD8α+CD4−) and NK cells (CD3ɛ−NK1.1+) CCR2 on monocytic (M)-MDSCs", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; Myeloid-derived suppressor cells / MDSCs; NK cells; T cells; CCR2", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs (CD11b+Gr-1+),PMN-MDSCs (CD11b+Ly6int), M-MDSCs (CD11b+Ly-6Chi)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; PMN-MDSCs / granulocytic MDSCs", "Immune_System_function_unaffected": "TAMs (CD11b+Ly-6C−Ly-6G−F4/80+),Tregs (CD4+CD8α−CD25+)", "Controlled_Terms_Unaffected": "CD4; CD25 / IL2RA; CD11b / ITGAM; Regulatory T cells / Tregs; Tumor-associated macrophages / TAMs", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00399", "Drug_Pubchem": "3121", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "B16-F10", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2033", "Drug": "VPA (valpromide)", "Drug_category": "Fatty acid derivatives", "Drugbank_ID": "DB00313", "Target/s_or_mechanism_of_action": "Valproic acid exhibits its pharmacologic effects in a couple of ways, such as by acting on GABA (γ aminobutyric acid) levels in the CNS, blocking voltage-gated ion channels, and inhibiting histone deacetylase", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCC(CCC)C(O)=O", "Single/Combination": "Single Drug", "PMID": "32158627", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "VPA (500 mg/kg) untill day 13", "Technique": "Flow Cytometery", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cells (CD3ɛ−NK1.1+) and CD8+ T-cells\n (CD3ɛ+CD4−CD8α+) in tumors, CD69hi cells in CD8+ T -cells (CD3ɛ+CD8α+CD4−) and NK cells (CD3ɛ−NK1.1+) CCR2 on monocytic (M)-MDSCs", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; Myeloid-derived suppressor cells / MDSCs; NK cells; T cells; CCR2", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs (CD11b+Gr-1+),", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": "TAMs (CD11b+Ly-6C−Ly-6G−F4/80+),Tregs (CD4+CD8α−CD25+)", "Controlled_Terms_Unaffected": "CD4; CD25 / IL2RA; CD11b / ITGAM; Regulatory T cells / Tregs; Tumor-associated macrophages / TAMs", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00399", "Drug_Pubchem": "3121", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "EL4", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2034", "Drug": "VPA (valpromide)", "Drug_category": "Fatty acid 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"Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00399", "Drug_Pubchem": "3121", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "EL4", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2035", "Drug": "VPA (valpromide)", "Drug_category": "Fatty acid derivatives", "Drugbank_ID": "DB00313", "Target/s_or_mechanism_of_action": "Valproic acid exhibits its pharmacologic effects in a couple of ways, such as by acting on GABA (γ aminobutyric acid) levels in the CNS, blocking voltage-gated ion channels, and inhibiting histone deacetylase", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCC(CCC)C(O)=O", "Single/Combination": "Single Drug", "PMID": "32158627", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "VPA(500 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00399", "Drug_Pubchem": "3121", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "B16-F10", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1703", "Drug": "Entinostat", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "22303460", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma", "System": null, "Dose": "entinostat (5 mg/kg, daily, 5 d/wk by oral gavage)", "Technique": "Flow Cytometry,Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Foxp3 levels in Tregs, Tregs infiltrating the tumors", "Controlled_Terms_Function_inhibited_Number_decreased": "FOXP3; Regulatory T cells / Tregs; Immune-cell infiltration", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "BALB/c mouse", "Cell_line_used_to_induce_tumor_in_mice": "RENCA", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1705", "Drug": "Entinostat", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "22303460", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer -Castration Resistant Prostate Cancer", "System": null, "Dose": "entinostat (5 days/wk, 5 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Foxp3 level in Tregs of tumor-bearing mice", "Controlled_Terms_Function_inhibited_Number_decreased": "FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "male FVB", "Cell_line_used_to_induce_tumor_in_mice": "CR Myc-CaP tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1740", "Drug": "Panobinostat (LBH589)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "23963286", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "25mg/kg LBH589", "Technique": "Survival Analysis", "Controlled_Technique": "Survival analysis (Kaplan–Meier)", "Immune_System-Function_enhanced/numbers_increased": "adaptive immune system", "Controlled_Terms_Function_enhanced_Number_increased": "adaptive immune system", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10019", "Drug_Pubchem": "6918837", "Animal_Strain_used": "C57BL6 or immunodeficient B6.129S7-Rag1tm1Mom/J", "Cell_line_used_to_induce_tumor_in_mice": "B16", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1946", "Drug": "Vorinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "30377559", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": null, "Dose": "vorinostat (150 mg/kg, p.o.).", "Technique": "Immunofluorescence, Fluorescent Image Intensity", "Controlled_Technique": "Immunofluorescence assay; Immunostaining/image analysis; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06320", "Drug_Pubchem": "5311", "Animal_Strain_used": "Female nu/nu", "Cell_line_used_to_induce_tumor_in_mice": "NCI-H460 (lung)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1743", "Drug": "Entinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "24203492", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Fibrosarcoma Lung Metastasis", "System": null, "Dose": "752 ng entinostat via intraperitoneal administration (in 0.1 mL PBS), or 8 × 106 IL-2-activated NK cells (in 0.2 mL PBS) by tail-vein injection", "Technique": "In Vivo Bioluminescent Imaging", "Controlled_Technique": "Bioluminescence/luciferase assay", "Immune_System-Function_enhanced/numbers_increased": "NK cell significantly lower tumor burden", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; Tumor growth / burden outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "NOD.Cg-Rag1tm1MomPrf1tm1Sdz/SzJ", "Cell_line_used_to_induce_tumor_in_mice": "HT1080.eGFP-FFLuc tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1792", "Drug": "Trichostatin A (TSA)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Single Drug", "PMID": "25745993", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma", "System": null, "Dose": "1μM/kg TSA", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD4+ CD62L− activated T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "444732", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "EL4 lymphoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1793", "Drug": "Trichostatin A (TSA)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Single Drug", "PMID": "25745993", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "1 μm/kg or 3 μm/kg TSA was injected i.p. every 2 days", "Technique": "Flow Cytometry, Immunohistochemistry,Real-Time Pcr", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR); Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD4+ CD62L− activated T cells,effector memory T cells interleukin-2 (IL-2), interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α) and granulocyte-macrophage colony stimulating factor (GM-CSF)", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-2; TNF-α / TNF; GM-CSF / CSF2; CD4; Macrophages; Neutrophils / granulocytes; T cells", "Immune_System-Function_inhibited/numbers_decreased": "FasL-mediated AICD of tumor-infiltrating CD4+ T", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; Immune-cell infiltration", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "444732", "Animal_Strain_used": "C57BL/6 and nude ,Rag1−/−,β2m−/− , CIITA−/−,gld/gld", "Cell_line_used_to_induce_tumor_in_mice": "B16F0 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1810", "Drug": "Nexturastat A", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCCN(CC1=CC=C(C=C1)C(=O)NO)C(=O)NC2=CC=CC=C2", "Single/Combination": "Single Drug", "PMID": "25957812", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "25 mg/kg", "Technique": "Blocking Antibodies", "Controlled_Technique": "Immune suppression/blocking/depletion assay", "Immune_System-Function_enhanced/numbers_increased": "delayed tumor growth-Anti‐tumor activity in vivo is dependent on intact immunity", "Controlled_Terms_Function_enhanced_Number_increased": "Tumor growth / burden outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "71462653", "Animal_Strain_used": "C57BL/6 /Nexturastat A", "Cell_line_used_to_induce_tumor_in_mice": "B16–F10", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1811", "Drug": "Tubastatin A", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "HDAC6 inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCC2=C(C1)C3=CC=CC=C3N2CC4=CC=C(C=C4)C(=O)NO", "Single/Combination": "Single Drug", "PMID": "25957812", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "25 mg/kg", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "delayed tumor growth", "Controlled_Terms_Function_enhanced_Number_increased": "Tumor growth / burden outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "49850262", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "B16–F10", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1817", "Drug": "LBH589 (Panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "26176219", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Wilms Tumor ( Embryonic Kidney Cancer)", "System": null, "Dose": "LBH589 10mg/kg and 20mg/kg dose three times per wee", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10019", "Drug_Pubchem": "6918837", "Animal_Strain_used": "nude", "Cell_line_used_to_induce_tumor_in_mice": "SK-NEP-1 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1821", "Drug": "LBH589 (panobinostat)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "LBH589 (15mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1, PD-L2 expression in melanoma cell", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; PD-L2 / PDCD1LG2; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10019", "Drug_Pubchem": "6918837", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "B16F10", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1837", "Drug": "Romidepsin", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Single Drug", "PMID": "26964571", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": null, "Dose": "(2mg/kg on days 14,16,18)", "Technique": "RT-PCR, Flow cytometry,Microarray studies", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "T cell, CD8 T cell infiltration of tumor T cell chemokines-Ccl5 and Cxcl9/10", "Controlled_Terms_Function_enhanced_Number_increased": "CCL5 / RANTES; CXCL9 / MIG; CD8; T cells; CD8+ T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06637", "Drug_Pubchem": "57515973", "Animal_Strain_used": "129S4/SvJaeJ", "Cell_line_used_to_induce_tumor_in_mice": "LKR cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1882", "Drug": "Ricolinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB12376", "Target/s_or_mechanism_of_action": "Ricolinostat (ACY-1215) is an orally available selective HDAC6 inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "28408401", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": null, "Dose": "50 mg/kg daily", "Technique": "Flow cytometry, Single cell RNA sequencing", "Controlled_Technique": "Flow cytometry; Gene expression/sequencing analysis; Single-cell RNA sequencing", "Immune_System-Function_enhanced/numbers_increased": "tumor-infiltrating CD8+ T cells IFN-γ activation marker CD69-on tumor-infiltrating CD8+ T cells, Cd69, Cd44, Cd247, and Zap70- -on tumor-infiltrating T cells, MHC class II as well as co-stimulatory molecule CD86on TAMs", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; CD69; MHC class II; Tumor-associated macrophages / TAMs; T cells; CD8+ T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "CD4+Foxp3+ Treg cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10661", "Drug_Pubchem": "53340666", "Animal_Strain_used": "Genetically engineered harboring Kras+/LSL-G12DTrp53L/L (KP) or EGFRLSL-T790M/L858R (TL)", "Cell_line_used_to_induce_tumor_in_mice": "For lung tumor induction, mice received 1 × 106 CFU Cre-encoding adenovirus intranasally at 5–6 weeks of age", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1902", "Drug": "Trichostatin A (TSA)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Single Drug", "PMID": "28871002", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "TSA (30 mg/kg) was administered every day for 18 days via an intraperitoneal (i.p.) route", "Technique": "Blocking Antibodies To Deplete NK Cells, Flow Cytometry", "Controlled_Technique": "Flow cytometry; Immune suppression/blocking/depletion assay", "Immune_System-Function_enhanced/numbers_increased": "NK cells, infiltrated NK cells in the tumor reduced the Hepa1-6 tumor size", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "444732", "Animal_Strain_used": "BALB/c nude", "Cell_line_used_to_induce_tumor_in_mice": "Hepa1-6 carcinoma", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1945", "Drug": "Entinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "30377559", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": null, "Dose": "entinostat (20 mg/kg, p.o.)", "Technique": "Immunofluorescence, Fluorescent Image Intensity", "Controlled_Technique": "Immunofluorescence assay; Immunostaining/image analysis; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "Female nu/nu", "Cell_line_used_to_induce_tumor_in_mice": "NCI-H460 (lung)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2167", "Drug": "NextA", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Promotes M1 macrophage polarization and decreases M2 macrophages", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "38414061", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Murine melanoma", "System": null, "Dose": "20 mg/kg every other day", "Technique": "In vivo melanoma model; 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Immunostaining/image analysis; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "Female nu/nu", "Cell_line_used_to_induce_tumor_in_mice": "PC-3 (prostate)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1949", "Drug": "Vorinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "30377559", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": null, "Dose": "vorinostat (150 mg/kg, p.o.).", "Technique": "Immunofluorescence, Fluorescent Image Intensity", "Controlled_Technique": "Immunofluorescence assay; Immunostaining/image analysis; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06320", "Drug_Pubchem": "5311", "Animal_Strain_used": "Female nu/nu", "Cell_line_used_to_induce_tumor_in_mice": "DU145 (prostate)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1950", "Drug": "Vorinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "30377559", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": null, "Dose": "vorinostat (150 mg/kg, p.o.).", "Technique": "Immunofluorescence, Fluorescent Image Intensity", "Controlled_Technique": "Immunofluorescence assay; Immunostaining/image analysis; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "PD-L1 expression", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06320", "Drug_Pubchem": "5311", "Animal_Strain_used": "Female nu/nu", "Cell_line_used_to_induce_tumor_in_mice": "PC-3 (prostate)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1951", "Drug": "Entinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "30423192", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": null, "Dose": "14 days of treatment with entinostat 20 mg/kg", "Technique": "NanoString® assay,Flow cytometry", "Controlled_Technique": "Flow cytometry; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "intratumoral accumulation of cytotoxic CD8+ T cells interferon gamma (IFNγ) granzyme B, CXCL10, PD-L1, MHCI alpha chains as well as CIITA, MHCII expression on tumor/stromal cells reduce ovarian tumor size and prolong survival", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CXCL10 / IP-10; CD8; PD-L1 / CD274; MHC class II; MHC class I; CIITA; T cells; CD8+ T cells; Granzyme B / GZMB; Immune checkpoint pathway; Survival outcome", "Immune_System-Function_inhibited/numbers_decreased": "FoxP3 expression, LAG3 and BTLA", "Controlled_Terms_Function_inhibited_Number_decreased": "LAG-3; BTLA; FOXP3", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "Immunocompetent C57BL/6 , Rag1 knockout", "Cell_line_used_to_induce_tumor_in_mice": "ID8 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1952", "Drug": "Vorinostat (SAHA)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "30537988", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastric Cancer (GC)", "System": null, "Dose": "daily dose of 20 mg/kg", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "infiltrating CD8+ T cells slower tumor growth", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; 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CD8; PD-L1 / CD274; MHC class II; MHC class I; CIITA; T cells; CD8+ T cells; Granzyme B / GZMB; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "TS/A tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2018", "Drug": "Panobinostat (LBH589)", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Single Drug", "PMID": "31720815", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": null, "Technique": "Flow cytometry,RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "MHCII-expressing on tumor cells", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class II", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10019", "Drug_Pubchem": "6918837", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "TS/A tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2055", "Drug": "Domatinostat (4SC-202)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB17521", "Target/s_or_mechanism_of_action": "Class I HDAC inhibition; 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DNA damage → cGAS-STING → IFNβ/JAK-STAT signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "38182579", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Triple-negative breast cancer", "System": null, "Dose": "50 mg/kg", "Technique": "Immunofluorescence ,western blotting; RT-qPCR", "Controlled_Technique": "Immunofluorescence assay; Western blot/immunoblot analysis; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "IFNβ, CCL5, CXCL10, activation of the cGAS–STING signaling pathway", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-β; CCL5 / RANTES; CXCL10 / IP-10; cGAS–STING signaling", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 ↑", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "Female BALB/c nude", "Cell_line_used_to_induce_tumor_in_mice": "MDA-MB-231", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2068", "Drug": "B302", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "PARP1/PARP2 + HDAC inhibition; DNA damage → cGAS-STING → IFNβ/JAK-STAT signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "38182579", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Triple-negative breast cancer", "System": null, "Dose": "50 mg/kg", "Technique": "Immunofluorescence ,western blotting; RT-qPCR", "Controlled_Technique": "Immunofluorescence assay; Western blot/immunoblot analysis; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "IFNβ, CCL5, CXCL10, activation of the cGAS–STING signaling pathway", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-β; CCL5 / RANTES; CXCL10 / IP-10; cGAS–STING signaling", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 ↑", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "Female BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2069", "Drug": "Entinostat (ENT/MS-275)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "HDAC inhibitors", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3", "Single/Combination": "Single", "PMID": "31720815", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast cancer", "System": null, "Dose": "20 mg/kg/day", "Technique": "Nanostring, RT-qPCR, flow cytometry, TCR repertoire sequencing, T-cell restimulation", "Controlled_Technique": "Gene expression/sequencing analysis; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC-II , MHC-I , CD74 , class II transcriptional activator (CIITA), granzyme B (GZMB), perforin (PRF-1), interferon-γ\n(IFNG), and l-selectin (SELL),CXCL10, CXCL13, CD8/Treg ratio", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CXCL10 / IP-10; CXCL13; CD8; Regulatory T cells / Tregs; Granzyme B / GZMB; Perforin / PRF1; MHC class I; MHC class II; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "Treg cells, FOXP3 expression", "Controlled_Terms_Function_inhibited_Number_decreased": "FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1, PD-L2, inhibitory immune-ligand expression", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L2", "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "BALB/c mice", "Cell_line_used_to_induce_tumor_in_mice": "TS/A", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2070", "Drug": "Panobinostat (PAN/LBH589)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "HDAC inhibitors", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=C(C2=CC=CC=C2N1)CCNCC3=CC=C(C=C3)/C=C/C(=O)NO", "Single/Combination": "Single", "PMID": "31720815", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast cancer", "System": null, "Dose": "20 mg/kg/day", "Technique": "Nanostring, RT-qPCR, flow cytometry, TCR repertoire sequencing, T-cell restimulation", "Controlled_Technique": "Gene expression/sequencing analysis; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC-II , MHC-I , CD74 , class II transcriptional activator (CIITA), granzyme B (GZMB), perforin (PRF-1), interferon-γ\n(IFNG), and l-selectin (SELL),CXCL10, CXCL13, CD8/Treg ratio", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CXCL10 / IP-10; CXCL13; CD8; Regulatory T cells / Tregs; Granzyme B / GZMB; Perforin / PRF1; MHC class I; MHC class II; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "Treg cells, FOXP3 expression", "Controlled_Terms_Function_inhibited_Number_decreased": "FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1, PD-L2, inhibitory immune-ligand expression", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L2", "KEGG_Drug_ID": "D10319", "Drug_Pubchem": "6918837", "Animal_Strain_used": "BALB/c mice", "Cell_line_used_to_induce_tumor_in_mice": "TS/A", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2071", "Drug": "Panobinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Pan-HDAC inhibition → epigenetic modulation, apoptosis and growth inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=C(C2=CC=CC=C2N1)CCNCC3=CC=C(C=C3)/C=C/C(=O)NO", "Single/Combination": "Single", "PMID": "34531855", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast cancer", "System": null, "Dose": "Panobinostat (10 mg/kg) three times a week", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK-cell numbers, CD69+ NK cells, CD107A+ NK cells, activating receptors NKG2D and CD226 NK", "Controlled_Terms_Function_enhanced_Number_increased": "CD69; CD107a; NK cells", "Immune_System-Function_inhibited/numbers_decreased": "inhibitory receptors PD-1, NKG2A and Ly49I/C", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-1 / PDCD1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10319", "Drug_Pubchem": "6918837", "Animal_Strain_used": "C57BL/6 mice", "Cell_line_used_to_induce_tumor_in_mice": "RMA-S (4 X 105 cells/mice)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2072", "Drug": "B102", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "PARP1/PARP2 + HDAC inhibition; DNA damage → cGAS-STING → type-I IFN signaling; promotes antigen presentation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "38182579", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Triple-negative breast cancer", "System": null, "Dose": "15 mg/kg", "Technique": "Immunofluorescence ,western blotting; RT-qPCR", "Controlled_Technique": "Immunofluorescence assay; Western blot/immunoblot analysis; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "Type-I IFN signaling", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 ↑", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "Female BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2090", "Drug": "HBI-8000 (chidamide/tucidinostat)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB06334", "Target/s_or_mechanism_of_action": "Inhibits class I HDACs, particularly HDAC1/2/3; modulates tumor immune microenvironment and immune-related gene expression", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC(=CN=C1)/C=C/C(=O)NCC2=CC=C(C=C2)C(=O)NC3=C(C=C(C=C3)F)N", "Single/Combination": "Single", "PMID": "34461854", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Murine colon carcinoma", "System": null, "Dose": "50 mg/kg orally, daily", "Technique": "Syngeneic tumor model; NanoString nCounter PanCancer Immune Profiling", "Controlled_Technique": "Gene expression/sequencing analysis; Immune-cell profiling/phenotyping", "Immune_System-Function_enhanced/numbers_increased": "dendritic-cell score, macrophage score, NK-cell score, cytotoxic-cell score, CD45-cell score, antigen-presentation/MHC expression, immune effector genes", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD45; Macrophages; NK cells; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10993", "Drug_Pubchem": "12136798", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2116", "Drug": "FK228 (Romidepsin)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "HDAC inhibitor; reported to directly inhibit HDAC1, HDAC2, HDAC4 and HDAC6. In this study, FK228 induces ER-stress-associated necroptosis in tumor cells, producing immunogenic cell death and remodeling the tumor immune microenvironment.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C/C=C\\1/C(=O)N[C@H](C(=O)O[C@H]\\2CC(=O)N[C@@H](C(=O)N[C@H](CSSCC/C=C2)C(=O)N1)C(C)C)C(C)C", "Single/Combination": "Single", "PMID": "40940553", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": null, "System": null, "Dose": "FK228 (0.5 mg/kg) via the tail vein every 2 days (5 times\nin total) and FK228 treated dead CT26 cells", "Technique": "In-vivo vaccination assay, immunohistochemistry/immunofluorescence, flow cytometry, single-cell RNA sequencing (scRNA-seq), pySCENIC transcription-factor analysis.", "Controlled_Technique": "In-vivo/in-vitro immunological assay; Immunohistochemistry (IHC); Immunofluorescence assay; Flow cytometry; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "CD8⁺ T-cell infiltration increased,CD8⁺ T-cell activation increased, GZMB- and IFN-γ-expressing CD8⁺ T cells increased, NK-cell infiltration increased, macrophages shifted toward a pro-inflammatory phenotype, neutrophils increased in the combination-treatment tumor microenvironment.", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; Macrophages; NK cells; T cells; Neutrophils / granulocytes; Granzyme B / GZMB; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression increased on cancer cells and macrophages; PD-1 expression increased on total T cells and CD8⁺ T cells following FK228 treatment. Tregs also increased", "Controlled_Terms_Negative_Regulation": "CD8; PD-L1 / CD274; PD-1 / PDCD1; Regulatory T cells / Tregs; Macrophages; T cells", "KEGG_Drug_ID": "D06637", "Drug_Pubchem": "5352062", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2174", "Drug": "Entinostat (MS-275)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "HDAC1/HDAC3 inhibition; increases MHC-I and immunogenicity", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3", "Single/Combination": "Single", "PMID": "39438988", "Cancer_Type": "Brain Cancer", "Cancer_Type_Description": "9464D murine neuroblastoma", "System": null, "Dose": "5 mg/kg/day i.p. ×14 days", "Technique": "Flow cytometry, IHC, immunofluorescence, cytokine/chemokine analysis", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC); Immunofluorescence assay; Cytokine/chemokine analysis", "Immune_System-Function_enhanced/numbers_increased": "MHC-I, CD8⁺ T cells, CD4⁺ T cells, NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; NK cells; T cells; MHC class I; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "Female C57BL/6 mice, 6–8 weeks", "Cell_line_used_to_induce_tumor_in_mice": "9464D", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2117", "Drug": "FK228 (Romidepsin)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "HDAC inhibitor; reported to directly inhibit HDAC1, HDAC2, HDAC4 and HDAC6. In this study, FK228 induces ER-stress-associated necroptosis in tumor cells, producing immunogenic cell death and remodeling the tumor immune microenvironment.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C/C=C\\1/C(=O)N[C@H](C(=O)O[C@H]\\2CC(=O)N[C@@H](C(=O)N[C@H](CSSCC/C=C2)C(=O)N1)C(C)C)C(C)C", "Single/Combination": "Single", "PMID": "40940553", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": null, "System": null, "Dose": "FK228 (0.5 mg/kg) via the tail vein every 2 days (5 times\nin total) and FK228 treated dead 4T1 cells", "Technique": "In-vivo vaccination assay, immunohistochemistry/immunofluorescence, flow cytometry, single-cell RNA sequencing (scRNA-seq), pySCENIC transcription-factor analysis.", "Controlled_Technique": "In-vivo/in-vitro immunological assay; Immunohistochemistry (IHC); Immunofluorescence assay; Flow cytometry; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "CD8⁺ T-cell infiltration increased,CD8⁺ T-cell activation increased, GZMB- and IFN-γ-expressing CD8⁺ T cells increased, NK-cell infiltration increased, macrophages shifted toward a pro-inflammatory phenotype, neutrophils increased in the combination-treatment tumor microenvironment.", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; Macrophages; NK cells; T cells; Neutrophils / granulocytes; Granzyme B / GZMB; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression increased on cancer cells and macrophages; PD-1 expression increased on total T cells and CD8⁺ T cells following FK228 treatment. Tregs also increased", "Controlled_Terms_Negative_Regulation": "CD8; PD-L1 / CD274; PD-1 / PDCD1; Regulatory T cells / Tregs; Macrophages; T cells", "KEGG_Drug_ID": "D06637", "Drug_Pubchem": "5352062", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2118", "Drug": "Domatinostat (4SC-202)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB17521", "Target/s_or_mechanism_of_action": "Class I HDAC inhibition; epigenetic modulation; increases antigen processing/presentation, MHC-I/MHC-II expression and T-cell-mediated antitumor immunity", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C=C(C=N1)C2=CC=C(C=C2)S(=O)(=O)N3C=CC(=C3)/C=C/C(=O)NC4=CC=CC=C4N", "Single/Combination": "Single", "PMID": "31703604", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": null, "System": null, "Dose": "20 mg/kg twice daily", "Technique": "Flow cytometry; tumor immune-cell profiling", "Controlled_Technique": "Flow cytometry; Immune-cell profiling/phenotyping", "Immune_System-Function_enhanced/numbers_increased": "Intratumoral CTLs increased approximately 8-fold; CD4+ T cells increased approximately 3-fold; CTL/Treg ratio increased; antigen-processing machinery genes increased; MHC-I/MHC-II increased; IFNG increased; IFN-gamma response increased", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; Regulatory T cells / Tregs; T cells; MHC class I; MHC class II; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "Intratumoral MDSCs slightly decreased", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": "Tumor-infiltrating B cells; NK cells; peripheral-blood immune-cell populations largely unaffected", "Controlled_Terms_Unaffected": "NK cells; B cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Regulatory T cells increased; PD-1/LAG3-positive CTLs increased, representing inhibitory feedback", "Controlled_Terms_Negative_Regulation": "PD-1 / PDCD1; LAG-3; Regulatory T cells / Tregs; T cells", "KEGG_Drug_ID": null, "Drug_Pubchem": "15985904", "Animal_Strain_used": "BALB/c mice", "Cell_line_used_to_induce_tumor_in_mice": "CT26 murine colorectal carcinoma", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2123", "Drug": "OBP-801", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB12279", "Target/s_or_mechanism_of_action": "Potent class-I HDAC inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C)[C@H]1NC(=O)[C@H]2CSSCC/C=C/[C@H](CC(=O)N[C@H](C)C(=O)N2)OC(=O)C[C@@H]1O", "Single/Combination": "Single", "PMID": "39682244", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Clear cell renal cell carcinoma", "System": null, "Dose": "10 mg/kg IV, days 1,4,7,11 in tumor-growth experiment; days 1,4,7 in TIL experiment", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "MHC-I presentation; LMP2/PSMB9; CD45⁺CD3e⁺ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD3; CD45; T cells; MHC class I; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD8a⁺CD8b⁺ T-cell", "Controlled_Terms_Unaffected": "CD8; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "11178958", "Animal_Strain_used": "BALB/c mice", "Cell_line_used_to_induce_tumor_in_mice": "RENCA", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2129", "Drug": "Citarinostat (ACY241)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB15449", "Target/s_or_mechanism_of_action": "Selective HDAC6 inhibition; increases α-tubulin acetylation and modulates tumor immunity", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "35223194", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC / lung adenocarcinoma", "System": null, "Dose": "25 mg/kg i.p., 3×/week; efficacy studies up to 6 weeks", "Technique": "Flow cytometery, transcriptomics", "Controlled_Technique": "Flow cytometry; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "CD4+Foxp3− T cells, CD8+ T cells, NK cells, CD69/Ki-67, memory T cells, CD107a/granzyme B, tumor-associated macrophages (TAMs; CD11b+CD11c-Gr1-) have high expression of MHC-I/MHC-II, CD80, CD86, CD40", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD11b / ITGAM; CD11c / ITGAX; CD40; CD69; CD80; CD86; CD107a; FOXP3; Macrophages; Tumor-associated macrophages / TAMs; NK cells; T cells; Granzyme B / GZMB; MHC class I; MHC class II; Cell proliferation / Ki-67; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "CD4+ CD25hiFoxp3+ regulatory T cells,  lung tumor-infiltrating CD8 + T cells expressed lower levels of the inhibitory receptors BTLA, PD-1, and CTLA-4, TAMs (tumour associated macroohages) have reduced PD-L1/PD-L2, CTLA4, VSIR, TIGIT, LGALS9, ARG1", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD8; CD25 / IL2RA; PD-L1 / CD274; PD-L2; PD-1 / PDCD1; CTLA-4; TIGIT; BTLA; VSIR; LGALS9; FOXP3; Regulatory T cells / Tregs; T cells; Arginase-1 / ARG1", "Immune_System_function_unaffected": "tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSC), and dendritic cells (DC)", "Controlled_Terms_Unaffected": "Myeloid-derived suppressor cells / MDSCs; Macrophages; Tumor-associated macrophages / TAMs; Dendritic cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10918", "Drug_Pubchem": "53340426", "Animal_Strain_used": "Kras+/LSL-G12D; Trp53L/L (KP) mice", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2130", "Drug": "Entinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "HDAC inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3", "Single/Combination": "Single", "PMID": "35764364", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "MHC-I/APM-deficient murine lung cancer", "System": null, "Dose": "6 mg/kg/day, oral diet", "Technique": "flow cytometry, immune profiling, RNA-seq", "Controlled_Technique": "Flow cytometry; Immune-cell profiling/phenotyping; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "MHC-I/APM-related immune recognition", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "Female C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "CMT.64", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2131", "Drug": "Entinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "HDAC1/HDAC3 inhibition; systemic immune modulation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3", "Single/Combination": "Single", "PMID": "42515717", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Syngeneic murine NSCLC", "System": null, "Dose": "7.5 mg/kg orally, 5×/week; 8 doses over 10 days", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD4⁺ T cells, CD8⁺ T cells, systemic T-cell populations expanded", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD4⁺ IFN-γ production unchanged after gp33/gp66 stimulation", "Controlled_Terms_Unaffected": "IFN-γ; CD4", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "C57BL/6 mice", "Cell_line_used_to_induce_tumor_in_mice": "KPN1.1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2142", "Drug": "Entinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Inhibits HDACs; promotes MHC-I/APM expression and immune-response gene programs", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3", "Single/Combination": "Single", "PMID": "35764364", "Cancer_Type": "Lung Cancer; Hpv16-Expressing Tumors", "Cancer_Type_Description": "MHC-I-deficient, HPV16 E6/E7+ lung tumor model", "System": null, "Dose": "6 mg/kg/day, oral diet for 10 days", "Technique": "Flow cytometry; RNA-seq; pathway analysis", "Controlled_Technique": "Flow cytometry; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "MHC-I/APM-related immune recognition", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "Female C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "TC-1/a9", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2150", "Drug": "CN133", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "NR", "Target/s_or_mechanism_of_action": "Potent class-I HDAC inhibitor; inhibits HDAC1, HDAC2 and HDAC3", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN(Cc1ccc(/C=C/C(=O)NO)cc1)CC12CC3CC(CC(C3)C1)C2", "Single/Combination": "Single", "PMID": "37880708", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Subcutaneous prostate-cancer allograft", "System": null, "Dose": "1 mg/kg, intraperitoneally, twice/week", "Technique": "flow cytometry, RNA-seq/microarray, RT-qPCR", "Controlled_Technique": "Flow cytometry; Gene expression/sequencing analysis; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD4⁺ T cells, CD8⁺ T cells, CD8⁺ T-cell granzyme B, perforin", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; T cells; Granzyme B / GZMB; Perforin / PRF1", "Immune_System-Function_inhibited/numbers_decreased": "PMN-MDSCs (CD11b⁺Ly6G⁺), Arg-1, iNOS, HGF, CCL5, IL-6 and CCL12", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6; CCL5 / RANTES; CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs; PMN-MDSCs / G-MDSCs; Arginase-1 / ARG1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "NR", "Drug_Pubchem": "NR", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "RM1 prostate cancer cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2155", "Drug": "Entinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "HDAC inhibition and epigenetic modulation of immune-response pathways", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3", "Single/Combination": "Single", "PMID": "35764364", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "MHC-I-deficient, IFN-γ-resistant sarcoma", "System": null, "Dose": "6 mg/kg/day, oral diet", "Technique": "Tumor growth; immune profiling by flow cytometry", "Controlled_Technique": "Tumor growth/survival analysis; Flow cytometry; Immune-cell profiling/phenotyping", "Immune_System-Function_enhanced/numbers_increased": "MHC-I/APM-related immune recognition", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "Female C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "RVP3", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1644", "Drug": "CC-4047/ACTIMID/ Pomalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB08910", "Target/s_or_mechanism_of_action": "Promalidomide is an immunomodulatory agent with antineoplastic activity. It is shown to inhibit the proliferation and induce apoptosis of various tumour cells.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC2=C1C(=O)N(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "11994441", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal -Ectopic Colorectal Cancer", "System": null, "Dose": null, "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "IFN-y, IL-2", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-2", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08976", "Drug_Pubchem": "134780", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1669", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "19965642", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": null, "Dose": "(gavage, 300 mg/kg, twice daily for 7 days)", "Technique": "ELISA, Flow cytometery", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); 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Immune suppression/blocking/depletion assay", "Immune_System-Function_enhanced/numbers_increased": "NK cells, including IFN-γ-secreting and IL-4-secreting NK cells, decreased on ex vivo stimulation, CD25+Foxp3+CD4+ regulatory T (Treg) cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-4; CD4; CD25 / IL2RA; FOXP3; Regulatory T cells / Tregs; NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": "216326", "Animal_Strain_used": "C57BL/KaLwRij", "Cell_line_used_to_induce_tumor_in_mice": "5TGM1 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1842", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "27287425", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": null, "Dose": "1 mg/kg for 5 consecutive days", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": "216326", "Animal_Strain_used": "C57/BL6", "Cell_line_used_to_induce_tumor_in_mice": "EL4 T-cell lymphoma", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1934", "Drug": "Pomalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB08910", "Target/s_or_mechanism_of_action": "Promalidomide is an immunomodulatory agent with antineoplastic activity. 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CD8⁺/CD4⁺ ratio", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD3", "Immune_System-Function_inhibited/numbers_decreased": "Inducible PD-L1; PD-1/PD-L1-mediated suppression", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; PD-1 / PDCD1", "Immune_System_function_unaffected": "Constitutive PD-L1 largely unaffected", "Controlled_Terms_Unaffected": "PD-L1 / CD274", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08976", "Drug_Pubchem": "134780", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2098", "Drug": "Pomalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB08910", "Target/s_or_mechanism_of_action": "Binds cereblon (CRBN); modulates ubiquitin-ligase substrate specificity and immunomodulates T-cell and NK-cell activity", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1CC(=O)NC(=O)C1N2C(=O)C3=C(C2=O)C(=CC=C3)N", "Single/Combination": "Single", "PMID": "19009291", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "CT26 syngeneic murine colorectal carcinoma model", "System": null, "Dose": "50 mg/kg intraperitoneally once daily for 6 days in mice", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "40% reduction in CD4+CD25+CTLA-4+FOXP3+ Tregs in draining lymph nodes versus control", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; 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These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "23531921", "Cancer_Type": "Brain Cancer", "Cancer_Type_Description": "Neuroblastoma", "System": null, "Dose": "30 mg/kg QD per mouse", "Technique": "Western Blot Analyses,H & E Staining", "Controlled_Technique": "Western blot/immunoblot analysis; Hematoxylin and eosin (H&E)/histology; Hematoxylin and eosin (H&E)/histology", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "tyrosine phosphorylated STAT3 as well as of STAT3 downstream targets (CyclinD1,-3, Bcl-2 and Survivin)", "Controlled_Terms_Function_inhibited_Number_decreased": "STAT3 signaling", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "16659841", "Animal_Strain_used": "athymic nude", "Cell_line_used_to_induce_tumor_in_mice": "SY5Y", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1727", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "23531921", "Cancer_Type": "Rhabdomyosarcoma", "Cancer_Type_Description": "Rhabdomyosarcoma", "System": null, "Dose": "30 mg/kg BID per mouse", "Technique": "Western Blot Analyses,H & E Staining", "Controlled_Technique": "Western blot/immunoblot analysis; Hematoxylin and eosin (H&E)/histology; Hematoxylin and eosin (H&E)/histology", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "tyrosine phosphorylated STAT3 as well as of STAT3 downstream targets (CyclinD1,-3, Bcl-2 and Survivin)", "Controlled_Terms_Function_inhibited_Number_decreased": "STAT3 signaling", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "16659841", "Animal_Strain_used": "SCID/Beige", "Cell_line_used_to_induce_tumor_in_mice": "Rh18", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1728", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "23531921", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Ewing Sarcoma", "System": null, "Dose": "30 mg/kg BID per mouse", "Technique": "Western Blot Analyses,H & E Staining", "Controlled_Technique": "Western blot/immunoblot analysis; Hematoxylin and eosin (H&E)/histology; Hematoxylin and eosin (H&E)/histology", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "tyrosine phosphorylated STAT3 as well as of STAT3 downstream targets (CyclinD1,-3, Bcl-2 and Survivin)", "Controlled_Terms_Function_inhibited_Number_decreased": "STAT3 signaling", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "16659841", "Animal_Strain_used": "SCID/Beige", "Cell_line_used_to_induce_tumor_in_mice": "TC32", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1772", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "25149535", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "AZD1480 at 30 mg/kg or with vehicle by oral gavage twice a day for 7 days", "Technique": "Western Blot Analysis", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "CD4+ and CD8+ T cells, tumor-infiltrating CD4+ and CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; T cells; CD8+ T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "monocytic MDSCs (moMDSC; CD11b+Ly6C+Ly6G−) and granulocytic MDSCs (grMDSC; CD11b+Ly6ClowLy6G+,tumor-infiltrating DCs, moMDSCs and grMDSCs within the tumor microenvironment complete inhibition of P-STAT3 expression", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; PMN-MDSCs / granulocytic MDSCs; Dendritic cells; STAT3 signaling; Immune-cell infiltration", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "16659841", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "AZD1480", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1830", "Drug": "AZD1480", "Drug_category": "JAK2 inhibitor", "Drugbank_ID": "DB12588", "Target/s_or_mechanism_of_action": "AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines. These biological responses to AZD1480 are associated with concomitant inhibition of phosphorylation of JAK2, STAT3 and MAPK signaling proteins.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C[C@H](NC1=NC=C(Cl)C(NC2=NNC(C)=C2)=N1)C1=NC=C(F)C=N1", "Single/Combination": "Single Drug", "PMID": "26660519", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Carcinoma Cells", "System": null, "Dose": "30 mg/kg AZD1480.", "Technique": "Immunoblot And Electro Chemiluminescent Elisa Analysis", "Controlled_Technique": "Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "pSTAT3Y705 levels", "Controlled_Terms_Function_inhibited_Number_decreased": "STAT3", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "16659841", "Animal_Strain_used": "MISIIR-TAg", "Cell_line_used_to_induce_tumor_in_mice": "spontaneous development", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1776", "Drug": "PD184352 (\n CI-1040)", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB12429", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "FC1=C(F)C(NC2=CC=C(I)C=C2Cl)=C(C=C1)C(=O)NOCC1CC1", "Single/Combination": "Single Drug", "PMID": "25256614", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "25 mg/kg/day PD184352", "Technique": "Immunohistochemistry,Quantitative real time PCR analysis", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "pan macrophage marker CD68in tumors, monocyte and macrophage marker F4/80 M1 macrophage marker CD86, the M2 marker CD163 and TNFα in tumors", "Controlled_Terms_Function_enhanced_Number_increased": "TNF-α / TNF; CD86; CD163; Macrophages; Monocytes; M1 macrophage phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "6918454", "Animal_Strain_used": "C57J/B6", "Cell_line_used_to_induce_tumor_in_mice": "BRafV600E-4434", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1864", "Drug": "Trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "27803104", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Mammary Tumor", "System": null, "Dose": "1.0 mg/kg trametinib", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD11b+MHC-II−Ly6ChiLy6G− monocytic-MDSCs (M-MDSCs)-M-MDSCs expressed high levels of Arginase and Nos2 and were capable of suppressing the proliferation of activated T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; MHC class II; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; T cells; Cell proliferation / Ki-67", "Immune_System_function_unaffected": "CD8+ or CD4+ T cells at tumor beds, PD-1+ intratumoral CD8+ or CD4+ T cells, Foxp3+ Tregs and differentiated (MHC-II+) macrophages, CD11b+MHC-II−Ly6ClowLy6G+ polymorphonuclear-MDSCs (PMN-MDSCs)", "Controlled_Terms_Unaffected": "CD4; CD8; CD11b / ITGAM; PD-1 / PDCD1; MHC class II; FOXP3; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; PMN-MDSCs / granulocytic MDSCs; Macrophages; T cells; CD4+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "WT C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Brpkp110 tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1898", "Drug": "MEK inhibitor selumetinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Single Drug", "PMID": "28807001", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "25 mg/kg, twice daily", "Technique": "Immunohistochemical Staining,Flow Cytometry Analysis", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD4+ T-cells, intratumoral MHC-II+ Ly6C+ intermediary differentiating monocytes", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; MHC class II; Monocytes; T cells", "Immune_System-Function_inhibited/numbers_decreased": "tumor-infiltrating gMDSC/neutrophil p-ERK levels", "Controlled_Terms_Function_inhibited_Number_decreased": "PMN-MDSCs / granulocytic MDSCs; Neutrophils / granulocytes; MAPK signaling; Immune-cell infiltration", "Immune_System_function_unaffected": "CD8+ T-cells or CD4+ Foxp3+", "Controlled_Terms_Unaffected": "CD4; CD8; FOXP3; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09666", "Drug_Pubchem": "10127622", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1904", "Drug": "Trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "28928458", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "trametinib (1 mg/kg/daily)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD8+, CD4+ FOXP3−, and CD4+ FOXP3+ cells reduced IFNγ production of CD8+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "IFN-γ; CD4; CD8; FOXP3; T cells; CD8+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "AT3ova", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1905", "Drug": "Trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": "28928458", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "trametinib (1 mg/kg/daily)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD8+ T cells and both populations of CD4+ T cells; helper (FOXP3−) and T regulatory cells CD8+ and CD4+ T-cell cytokine production (IFNγ)", "Controlled_Terms_Function_inhibited_Number_decreased": "IFN-γ; CD4; CD8; FOXP3; Regulatory T cells / Tregs; T cells; CD8+ T cells; CD4+ T cells", "Immune_System_function_unaffected": "innate immune subsets such as NK cells and NK T cells revealed no changes in frequency (CD3+ NK1.1+, CD3− NK1.1+), maturation (CD11b+ CD27−), or effector function (Granzyme B+)", "Controlled_Terms_Unaffected": "CD3; CD11b / ITGAM; NK cells; T cells; Granzyme B / GZMB", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "AT3ova", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1972", "Drug": "Selumetinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Single Drug", "PMID": "30995478", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": null, "Dose": "Pulsative selumetinib (0-1uM)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "pERK expression in CD4+ and CD8+ T cells T-bet in both CD4+ and CD8+ T cells from lung tumors CTLA-4 and PD-1 expression on CD8+ T cells, PD-1 and CTLA -4 expression on CD4+ cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; PD-1 / PDCD1; CTLA-4; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09666", "Drug_Pubchem": "10127622", "Animal_Strain_used": "HKP1 lung-cancer-bearing", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2039", "Drug": "MEKi GDC-0623", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB11982", "Target/s_or_mechanism_of_action": "Not Available", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "OCCONC(=O)C1=C(NC2=C(F)C=C(I)C=C2)N2C=NC=C2C=C1", "Single/Combination": "Single Drug", "PMID": "32358491", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Murine Colon Carcinoma", "System": null, "Dose": null, "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "M2 CD206+ phenotype", "Controlled_Terms_Function_inhibited_Number_decreased": "CD206 / MRC1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "42642654", "Animal_Strain_used": "C57BL/6-Ly5.1", "Cell_line_used_to_induce_tumor_in_mice": "MC-38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2042", "Drug": "MEKi GDC-0623", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB11982", "Target/s_or_mechanism_of_action": "Not Available", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "OCCONC(=O)C1=C(NC2=C(F)C=C(I)C=C2)N2C=NC=C2C=C1", "Single/Combination": "Single Drug", "PMID": "32358491", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Tumor", "System": null, "Dose": null, "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "M2 CD206+ phenotype,MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD206 / MRC1; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "42642654", "Animal_Strain_used": "C57BL/6-Ly5.1", "Cell_line_used_to_induce_tumor_in_mice": "PDA30364", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2051", "Drug": "Trametinib", "Drug_category": "MEK inhibitor", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Single Drug", "PMID": null, "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung", "System": null, "Dose": "1.0 mg/kg trametinib", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "monocytic-MDSCs (M-MDSCs)", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "WT C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Lewis Lung Carcinoma cells (LLC1)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2073", "Drug": "Cobimetinib", "Drug_category": "MEK inhibitor/ MEK inhibitors", "Drugbank_ID": "DB05239", "Target/s_or_mechanism_of_action": "MEK1/MEK2 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1CCN[C@@H](C1)C2(CN(C2)C(=O)C3=C(C(=C(C=C3)F)F)NC4=C(C=C(C=C4)I)F)O", "Single/Combination": "Single", "PMID": "42183887", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "4T1, murine TNBC xenograft", "System": null, "Dose": "10 mg/kg orally, once daily (QD), 22 days", "Technique": "IHC, flow cytometry of splenocytes, immunofluorescence", "Controlled_Technique": "Immunohistochemistry (IHC); Flow cytometry; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "activated caspase-8, Bax, Bak, CRT, and HMGB1, CD8+ T cells increased; naïve CD8+ T cells increased; effector CD4+ T cells increased; intratumoral CD4+ and CD8+ T cells increased; CD8+Granzyme-B+ cells increased; CD80+CD86+ (mature) and MHC-IIhigh (antigen-presenting) DCs", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD80; CD86; T cells; Granzyme B / GZMB; Calreticulin / CRT; HMGB1; Apoptosis / caspase activation; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "inactivated ERK,  Foxp3+ Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "FOXP3; Regulatory T cells / Tregs; MAPK signaling", "Immune_System_function_unaffected": "Total body weight did not show progressive loss; splenocyte/T-cell effects differed in non-tumor-bearing mice", "Controlled_Terms_Unaffected": "T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10405", "Drug_Pubchem": "16222096", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2099", "Drug": "Cobimetinib", "Drug_category": "MEK inhibitor/ MEK inhibitors", "Drugbank_ID": "DB05239", "Target/s_or_mechanism_of_action": "Inhibits MEK1/2 → suppresses MAPK/ERK signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC1)C(=O)C2=C(C=C(C=C2F)F)NC3=C(C=C(C=C3)F)I", "Single/Combination": "Single", "PMID": "34389557", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": null, "Dose": "Cobimetinib 7.5 mg/kg M/W/F", "Technique": "flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells and T regulatory cells, IFNγ and GZMB in MEK1-KO tumors, CD4+ central memory and effector memory cells, CD8+ central memory and effector memory cells, proliferating CD8+ T cells and CD4+ T cells, CD86+ CD19+ and MHCII+ CD19+ cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; CD19; CD86; Regulatory T cells / Tregs; T cells; Granzyme B / GZMB; MHC class I; MHC class II; Cell proliferation / Ki-67; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD4+ T cells", "Controlled_Terms_Unaffected": "CD4; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10405", "Drug_Pubchem": "16222096", "Animal_Strain_used": "Balb/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2100", "Drug": "Cobimetinib", "Drug_category": "MEK inhibitor/ MEK inhibitors", "Drugbank_ID": "DB05239", "Target/s_or_mechanism_of_action": "Inhibits MEK1/2 → suppresses MAPK/ERK signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC1)C(=O)C2=C(C=C(C=C2F)F)NC3=C(C=C(C=C3)F)I", "Single/Combination": "Single", "PMID": "34389557", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": null, "Dose": "Cobimetinib 7.5 mg/kg M/W/F", "Technique": "flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells and T regulatory cells, IFNγ and GZMB in MEK1-KO tumors, CD4+ central memory and effector memory cells, CD8+ central memory and effector memory cells, proliferating CD8+ T cells and CD4+ T cells, CD86+ CD19+ and MHCII+ CD19+ cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; CD19; CD86; Regulatory T cells / Tregs; T cells; Granzyme B / GZMB; MHC class I; MHC class II; Cell proliferation / Ki-67; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD4+ T cells", "Controlled_Terms_Unaffected": "CD4; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10405", "Drug_Pubchem": "16222096", "Animal_Strain_used": "Balb/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26 MEK1-KO cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2169", "Drug": "PD0325901", "Drug_category": "MEK inhibitor/ MEK inhibitors", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "MEK1/2 inhibition; reduces ERK1/2 phosphorylation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "32661093", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "BRAF V600E-mutant, PTEN-loss melanoma", "System": null, "Dose": "7 ppm in chow", "Technique": "Flow cytometry; Western blot", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "Increased tumor immunogenicity and CD8⁺ T-cell infiltration", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "No significant changes reported in CD4⁺ T cells, FOXP3⁺ regulatory T cells or NK cells in the reported comparison", "Controlled_Terms_Unaffected": "CD4; FOXP3; Regulatory T cells / Tregs; NK cells; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57BL/6; NSG", "Cell_line_used_to_induce_tumor_in_mice": "D4M3.A", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2101", "Drug": "Cobimetinib + anti-PD-1 + anti-4-1BB", "Drug_category": "MEK inhibitor/ MEK inhibitors; Monoclonal Antbody", "Drugbank_ID": "DB05239", "Target/s_or_mechanism_of_action": "Inhibits MEK1/2 → suppresses MAPK/ERK signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC1)C(=O)C2=C(C=C(C=C2F)F)NC3=C(C=C(C=C3)F)I", "Single/Combination": "Single", "PMID": "34389557", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": null, "Dose": "Cobimetinib 7.5 mg/kg M/W/F + anti-PD-1 0.25 mg/mouse + anti-4-1BB 0.025 mg/mouse", "Technique": "flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "IFNγ, GZMB, TNFα, and CD69; increase in CD8+ T cells;percentage of both GZMB+ CD8+ T and Ki67+ CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; TNF-α / TNF; CD8; CD69; T cells; Granzyme B / GZMB; Cell proliferation / Ki-67", "Immune_System-Function_inhibited/numbers_decreased": "significant decrease in PD-1+ Lag3+ double positive CD8+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD8; PD-1 / PDCD1; LAG-3; T cells", "Immune_System_function_unaffected": "percentage of CD4+ T cells", "Controlled_Terms_Unaffected": "CD4; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10405", "Drug_Pubchem": "16222096", "Animal_Strain_used": "Balb/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2006", "Drug": "Cobimetinib", "Drug_category": "MEK inhibitors", "Drugbank_ID": "DB05239", "Target/s_or_mechanism_of_action": "MEK inhibitor Cobimetinib specifically binds to and inhibits the catalytic activity of MEK1, resulting in inhibition of extracellular signal-related kinase 2 (ERK2) phosphorylation and activation and decreased tumor cell proliferation. Cobimetinib and vemurafenib target two different kinases in the RAS/RAF/MEK/ERK pathway.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "OC1(CN(C1)C(=O)C1=C(NC2=C(F)C=C(I)C=C2)C(F)=C(F)C=C1)[C@@H]1CCCCN1", "Single/Combination": "Single Drug", "PMID": "31671149", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "7.5 mg/kg of cobimetinib(MEKi) three times weekly via intraperitoneal injection", "Technique": "Flow Cytometry, Quantitative Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ and CD4+ T cells increased in MEK treated tumors", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; T cells; CD4+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "B 10 cells , T2-MZP Bregs, Tim1+ Bregs in the tumor draining nodes of the\n cobimetinib-treated mice", "Controlled_Terms_Function_inhibited_Number_decreased": "B10 cells; T2-MZP B regulatory cells (Bregs); TIM-1-positive B regulatory cells (Bregs)", "Immune_System_function_unaffected": "anti-tumor IgG", "Controlled_Terms_Unaffected": "Antitumor immunoglobulin G (IgG)", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10405", "Drug_Pubchem": "16222096", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "1x105\n CT26 colon cancer cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1689", "Drug": "Trastuzumab (4D5)", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "21321106", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Adenocarcinoma", "System": null, "Dose": "1 mg/kg 4D5", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IFN-y, RANTES IL-8", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-8 / CXCL8; CCL5 / RANTES", "Immune_System-Function_inhibited/numbers_decreased": "MIP-1α was minimal", "Controlled_Terms_Function_inhibited_Number_decreased": "CCL3 / MIP-1α", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03257", "Drug_Pubchem": "46507516", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "1 × 106 CT-26HER2/neu cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1691", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "21387286", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "human PBMCs (5.0 × 106 cells/mouse, i.p.) injections + trastuzumab (0.005 mg/g, intraperitoneally [i.p.])", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "human lymphocytes were invaded intercellular and stroma in tumor tissue.", "Controlled_Terms_Function_enhanced_Number_increased": "lymphocytes", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03257", "Drug_Pubchem": "46507516", "Animal_Strain_used": "NOD/SCID", "Cell_line_used_to_induce_tumor_in_mice": "HCC1569 cells (5.0 × 106)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1692", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "21387286", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "human PBMCsKLRG1(−) (5.0 × 106 cells/mouse, i.p.) injections + trastuzumab (0.005 mg/g, intraperitoneally [i.p.])", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "human lymphocytes were invaded intercellular and stroma in tumor tissue.", "Controlled_Terms_Function_enhanced_Number_increased": "lymphocytes", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03257", "Drug_Pubchem": "46507516", "Animal_Strain_used": "NOD/SCID", "Cell_line_used_to_induce_tumor_in_mice": "HCC1569 cells (5.0 × 106)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1693", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "21387286", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "human PBMCsKLRG1(−) (5.0 × 106 cells/mouse, i.p.) injections", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03257", "Drug_Pubchem": "46507516", "Animal_Strain_used": "NOD/SCID", "Cell_line_used_to_induce_tumor_in_mice": "HCC1569 cells (5.0 × 106)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1694", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "21387286", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "trastuzumab (0.005 mg/g, intraperitoneally [i.p.])", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03257", "Drug_Pubchem": "46507516", "Animal_Strain_used": "NOD/SCID", "Cell_line_used_to_induce_tumor_in_mice": "HCC1569 cells (5.0 × 106)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1711", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", 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null, "Dose": "(5 mg/kg i.p. twice weekly × 3 weeks)", "Technique": "ELISA,Immunoblot Assays", "Controlled_Technique": "Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "tumor cells with higher autonomous expression of TGF-β TGF-β–dependent activation of AKT and EMT", "Controlled_Terms_Negative_Regulation": "TGF-β; AKT signaling; Epithelial-mesenchymal transition", "KEGG_Drug_ID": "D03455", "Drug_Pubchem": "46507042", "Animal_Strain_used": "Athymic (nu/nu)", "Cell_line_used_to_induce_tumor_in_mice": "1CC8", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1714", "Drug": "Anti-CTLA-4", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "22934253", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "Mice were injected intraperitoneal with the anti-CTLA-4 mAbs dissolved in HBSS. Dosing per injection was 200 μg for the hamster-derived anti-CTLA-4 mAb clone 9H10 (BioXcell, BE0131) and 100 μg for the mouse-derived anti-CTLA-4 mAb clone 9D9 (BioXcell, BE0164)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD45+ leukocytes, CD8+ T cells, CD4+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD45; T cells; CD8+ T cells; CD4+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "regulatory T cells", "Controlled_Terms_Unaffected": "Regulatory T cells / Tregs; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "Tyr::CreERT2PTENF−/−BRAFF-V600E/+", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1753", "Drug": "Anti-CD40 antibody (FGK45)", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "24736544", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "(250μg/mouse) every three days from weeks 6-8", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "maturation status of both TAMs and TIDCs", "Controlled_Terms_Function_enhanced_Number_increased": "Tumor-associated macrophages / TAMs; 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CD45; Myeloid-derived suppressor cells / MDSCs; PMN-MDSCs / granulocytic MDSCs", "Immune_System_function_unaffected": "percentage of CD4+ and CD8+ cells, monocytic-MDSCs CD45+/CD11b+/Ly6G-/Ly6Chigh,", "Controlled_Terms_Unaffected": "CD4; CD8; CD11b / ITGAM; CD45; Myeloid-derived suppressor cells / MDSCs", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "PKL (Lung tumors were induced by Ad-Cre in the transgenic mouse model)", "Cell_line_used_to_induce_tumor_in_mice": "3 × 105 PKL5–2 cells into the right flank of mice", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1970", "Drug": "Anti-PD-1", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "30992475", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Murine Melanoma", "System": null, "Dose": "15 mg/kg anti-PD-1", "Technique": "QRT-PCR, immunoblot", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "IFNγ in the TME", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 and PD-L2 in tumor cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-L2 / PDCD1LG2; Immune checkpoint pathway", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "SM1 murine melanoma tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1997", "Drug": "Anti -PD-1", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31661001", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": null, "Dose": "murine anti-PD-1 [RMP1–14] (5 mg/kg, twice week for 2 weeks)", "Technique": "Immunostaining, Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC); 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The third cycle (C3) and fourth cycle (C4) were as same as C2.", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8 T cells and CD45-PD-L1 + cells in tumor", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD45; PD-L1 / CD274; T cells; CD8+ T cells; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": "CD4 T-cells and B cells in spleen, CD45+ cells in tumor", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD45; B cells; T cells", "Immune_System_function_unaffected": "CD8 T-cells , NK cells, MDSCs and Tregs in spleen; NK cells in tumor IL-10, IL-6 and TGF-β", "Controlled_Terms_Unaffected": "IL-6; IL-10; TGF-β; CD8; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; NK cells; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00584", "Drug_Pubchem": "3385", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1890", "Drug": "Fluorouracil", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O", "Single/Combination": "Single Drug", "PMID": "28637493", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Oral Squamous Cell Carcinoma (OSCC).", "System": null, "Dose": "20 mg/kg every 4 days for 3 weeks", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "pro-IL-1β in OSCC tissues NLRP3 in OSCC tissues", "Controlled_Terms_Negative_Regulation": "IL-1 family", "KEGG_Drug_ID": "D00584", "Drug_Pubchem": "3385", "Animal_Strain_used": "BALB/c nude", "Cell_line_used_to_induce_tumor_in_mice": "WSU-HN6 or CAL27 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1926", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "29622799", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "20 μg DAC for 5 consecutive days", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD4+ T lymphocytes and CD8+ T lymphocytes in the TME IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; T cells; CD8+ T cells; CD4+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03665", "Drug_Pubchem": "451668", "Animal_Strain_used": "BALB/c mouse", "Cell_line_used_to_induce_tumor_in_mice": "CT26 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1927", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "29622799", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "20 μg DAC for 5 consecutive days + PD-1 blockade -500 μg", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "T lymphocytes", "Controlled_Terms_Function_enhanced_Number_increased": "T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03665", "Drug_Pubchem": "451668", "Animal_Strain_used": "BALB/c mouse", "Cell_line_used_to_induce_tumor_in_mice": "CT26 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1955", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single Drug", "PMID": "30657234", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Ductal Adenocarcinoma", "System": null, "Dose": "50 mg/kg GEM", "Technique": "Flow Cytometry, Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD4+ cells and CD8+ cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8", "Immune_System-Function_inhibited/numbers_decreased": "CD11b+Gr‐1+ myeloid cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02368", "Drug_Pubchem": "60750", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "PAN02 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1992", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single Drug", "PMID": "31488209", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "60 mg/kg", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD11b+Gr1+ in spleen and lungs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02372", "Drug_Pubchem": "60750", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2020", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single Drug", "PMID": "31776206", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Murine Mammary Cancer", "System": null, "Dose": "GEM (60 mg/kg body weight) four times on days 10, 14,\n 18, and 22 or a single treatment on day 22", "Technique": "Flow cytometry, ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "monocytic MDSC (CD11b+Ly6G-Ly6Chigh) GM-CSF,sICAM-1 PD-L1 and IDO1", "Controlled_Terms_Function_enhanced_Number_increased": "GM-CSF / CSF2; CD11b / ITGAM; PD-L1 / CD274; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; Immune checkpoint pathway; IDO1", "Immune_System-Function_inhibited/numbers_decreased": "IFN-g–producing CD4 and\n CD8 T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD8; T cells; CD8+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02368", "Drug_Pubchem": "60750", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "one million E0771 tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2025", "Drug": "5-fluorouracil", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O", "Single/Combination": "Single Drug", "PMID": "32079180", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "50 mg/kg", "Technique": "Immunoblotting,Immunohistochemistry", "Controlled_Technique": "Western blot/immunoblot analysis; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "tumor programmed cell death 1 ligand 1 (PD-L1) level", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00584", "Drug_Pubchem": "3385", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2026", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "32079180", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "20 μg", "Technique": "Immunoblotting,immunohistochemistry,qRT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "Ifng, Ifngr1, (Tnfaip3, Ifit3b, Il1a, Isg15, Il1rn, Mx2), chemokine-associated genes (Ccl6, Ccl2, Cx3cl1, Cxcl1, Cxcl10, Cxcl2, Ccl7, Cxcl9), Cd274 (Pdl1) and Pdcd1lg2 (Pdl2),immune response genes (Sbno2, Icam1, Pf4, Lilrb4a, Spib, Rsad2) tumor programmed cell death 1 ligand 1 (PD-L1) level, phosphorylation of STAT1 and its downstream transcription factor IRF1", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-1 family; CCL2 / MCP-1; CCL7 / MCP-3; CXCL9 / MIG; CXCL10 / IP-10; CXCL1; PD-L1 / CD274; PD-L2 / PDCD1LG2; Immune checkpoint pathway; STAT1; ICAM-1 / CD54", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03665", "Drug_Pubchem": "451668", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2053", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single Drug", "PMID": null, "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": null, "Dose": "120 mg/kg", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "MDSC", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02368", "Drug_Pubchem": "60750", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Panc02 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2132", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Ribonucleotide reductase inhibition; DNA synthesis inhibition; induces ICD", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single", "PMID": "38988937", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung cancer", "System": null, "Dose": "25 mg/kg", "Technique": "Flow cytometery", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+IFN-γ+ T cells, activated DCs,memory T cells (CD3+CD4+CD62L−)", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD3; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD3+CD4+ or CD3+CD8+ T cells", "Controlled_Terms_Unaffected": "CD4; CD8; CD3; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02368", "Drug_Pubchem": "60750", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "LLC", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1646", "Drug": "All-trans-retinoic acid (ATRA), or Retinoic acid/ Tretinoin", "Drug_category": "others/combination", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Combination", "PMID": "12907617", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Fibrosarcoma", "System": null, "Dose": "ATRA pellets (21-day release, 5 mg)", "Technique": "ELISPOT assay", "Controlled_Technique": "ELISpot/FluoroSpot assay", "Immune_System-Function_enhanced/numbers_increased": "antigenspecific IFN-γ -producing T cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00094", "Drug_Pubchem": "5538", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "C3", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1648", "Drug": "All-trans-retinoic acid (ATRA), or Retinoic acid/ Tretinoin", "Drug_category": "others/combination", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Combination", "PMID": "12907617", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma", "System": null, "Dose": "ATRA pellets (21-day release, 5 mg)", "Technique": "ELISPOT assay, Flow cytometry", "Controlled_Technique": "Flow cytometry; ELISpot/FluoroSpot assay", "Immune_System-Function_enhanced/numbers_increased": "antigenspecific T cells", "Controlled_Terms_Function_enhanced_Number_increased": "T cells", "Immune_System-Function_inhibited/numbers_decreased": "Gr-1+CD11b+ ImCs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00094", "Drug_Pubchem": "5538", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "MethA sarcoma", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1649", "Drug": "Gemcitabine plus anti-CD40 antibody, FGK45 alone", "Drug_category": "others/combination", "Drugbank_ID": "DB00515 (APRD00359), DB00441", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation, Inhibition of DNA polymerase", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H], NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Combination", "PMID": "12907622", "Cancer_Type": "Mesothelioma", "Cancer_Type_Description": "Mesothelioma", "System": null, "Dose": "120 μg/gram gemcitabine i.p. q3dx5 and/or 100 μg of FGK45 i.p. three times over 6 days", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD4 and CD8 cells infilteration of tumor", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00275,D02368", "Drug_Pubchem": "5702198, 60750", "Animal_Strain_used": "BALB/c (H-2d)", "Cell_line_used_to_induce_tumor_in_mice": "AB1-HA tumor", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1662", "Drug": "CHAP31++tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "16818655", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": null, "Dose": "ibrutinib", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "No significant change in circulating T cell numbers before and after ibrutinib treatment", "Controlled_Terms_Unaffected": "T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": ". Wild type B6", "Cell_line_used_to_induce_tumor_in_mice": "CLL cells ( splenocytes from leukemic Eμ-TCL1\n transgenic mice)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1663", "Drug": "Trichostatin A +tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)", "Drug_category": "others/combination", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Combination", "PMID": "16818655", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": null, "Dose": "RK20449 (30mg/kg) for 7 days", "Technique": "Quantitative RT-PCR, Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD206+ cells,proliferating BrdU+ cells, and CD31+ endothelial cells AAM genes Il4, Il10, Il13, Arg1, and Ym1, but minimal effects on the CAM genes Il1β, Tnfα, and Nos2 inhibition of Hck", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-1 family; IL-4; IL-10; IL-13; TNF-α / TNF; CD31 / PECAM-1; CD206 / MRC1; Arginase-1 / ARG1; Cell proliferation / Ki-67", "Immune_System_function_unaffected": "CD45+ cells or F4/80+ macrophages", "Controlled_Terms_Unaffected": "CD45; Macrophages", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "444732", "Animal_Strain_used": "HckKO", "Cell_line_used_to_induce_tumor_in_mice": "MC38 CRC cell line", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1664", "Drug": "IL-2 with the HDAC inhibitor MS-275(Entinostat)", "Drug_category": "others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "17671140", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal - Metastatic Renal Cell Cancer", "System": null, "Dose": "150,000 IU of IL-2 twice daily by i.p. injections (twice weekly), 5 mg/kg of MS-275 daily by oral gavage (5 d/wk),", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD4+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; T cells; CD4+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "regulatory T cells (CD4+ Foxp3+)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; FOXP3; Regulatory T cells / Tregs; T cells", "Immune_System_function_unaffected": "CD8+, natural killer, and natural killer T cells", "Controlled_Terms_Unaffected": "CD8; NKT cells; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "RENCA luciferase-expressing cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1677", "Drug": "Carboplatin +paclitaxel", "Drug_category": "others/combination", "Drugbank_ID": "DB00958, DB01229", "Target/s_or_mechanism_of_action": "1. Carboplatin undergoes activation inside cells and forms reactive platinum complexes that cause the intra- and inter-strand cross-linkage of DNA molecules within the cell. 2.Pacilitaxel-Inhibition of tubulin depolymerization", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "carboplatin-[H][N]([H])([H])[Pt]1(OC(=O)C2(CCC2)C(=O)O1)[N]([H])([H])[H], pacilitaxel- [H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Combination", "PMID": "20683396", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": null, "Dose": "(10 mg/kg) and carboplatin (32.5 mg/kg)", "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "1. D01363, 2. D00491", "Drug_Pubchem": "38904, 36314", "Animal_Strain_used": "Female athymic nude (nu/nu)", "Cell_line_used_to_induce_tumor_in_mice": "MA-148 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1680", "Drug": "Oxaliplatin + interleukin 12", "Drug_category": "others/combination", "Drugbank_ID": "DB00526", "Target/s_or_mechanism_of_action": "Inhibiting DNA synthesis and transcription", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "[H][N]1([H])[C@@H]2CCCC[C@H]2[N]([H])([H])[Pt]11OC(=O)C(=O)O1", "Single/Combination": "Combination", "PMID": "20855451", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal - Metastatic Colorectal Cancer", "System": null, "Dose": "5 mg/kg", "Technique": "ELISA, Flow cytometery", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+/T regulatory cell ratio IFNg", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; Regulatory T cells / Tregs", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01790", "Drug_Pubchem": "6857599", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MC38Luc1 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1681", "Drug": "IL-12 +cyclophosphamide", "Drug_category": "others/combination", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Combination", "PMID": "21148040", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Carcinoma", "System": null, "Dose": "125 mg/kg", "Technique": "Immunohistochemisrry ,Flow Cytometry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "infiltration by CD8+ T cells and tumor Ag-specific CD8+ T cells ,Ly6Chigh myeloid cells-Ly6C(high)Ly6G(low) inflammatory monocytes and Ly6G(high)Ly6C(+) neutrophils(inflammatory myeloid cells (IMC)) IL-1, IL-6, IL-12, CCL5, and CCL3", "Controlled_Terms_Function_enhanced_Number_increased": "IL-1 family; IL-6; IL-12; CCL3 / MIP-1α; CCL5 / RANTES; CD8; Monocytes; Neutrophils / granulocytes; T cells; CD8+ T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "CD4+ Foxp3+ T cells ,Mo-MDSC\n infiltration", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; FOXP3; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; T cells; Immune-cell infiltration", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": "2907", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1686", "Drug": "IL-12+ Trastuzumab (4D5)", "Drug_category": "others/combination", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "21321106", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Adenocarcinoma", "System": null, "Dose": "1 μg murine IL-12, 1 mg/kg 4D5", "Technique": "ELISA, Flow cytometery", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD69+ cells IFN-y, RANTES CD335", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CCL5 / RANTES; CD69", "Immune_System-Function_inhibited/numbers_decreased": "IL-8 MIP-1α was minimal", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-8 / CXCL8; CCL3 / MIP-1α", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03257", "Drug_Pubchem": "46507516", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "1 × 106 CT-26HER2/neu cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1687", "Drug": "IL-12+ Trastuzumab+ anti-asialo GM1 Ab", "Drug_category": "others/combination", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "21321106", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Adenocarcinoma", "System": null, "Dose": "1 μg murine IL-12, 1 mg/kg 4D5 +anti-asialo GM1 Ab", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "IFN-y", "Controlled_Terms_Function_inhibited_Number_decreased": "IFN-γ", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03257", "Drug_Pubchem": "46507516", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "1 × 106 CT-26HER2/neu cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1688", "Drug": "IL12", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "21321106", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Adenocarcinoma", "System": null, "Dose": "1 μg murine IL-12", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IFN-y, RANTES IL-8", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-8 / CXCL8; CCL5 / RANTES", "Immune_System-Function_inhibited/numbers_decreased": "MIP-1α was minimal", "Controlled_Terms_Function_inhibited_Number_decreased": "CCL3 / MIP-1α", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "1 × 106 CT-26HER2/neu cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1697", "Drug": "Imatinib and CTLA-4", "Drug_category": "others/combination", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Combination", "PMID": "21873989", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastrointestinal Stromal Tumor (GIST)", "System": null, "Dose": "1.12 mg i.p. twice daily based on an established dose of 45 mg kg−1+CTLA-4 blocking antibodies (BioXCell) for induction by injecting 200 µg clone 9H10 i.p. on day 3, 100 ug clone 9H10 i.p. on days 6, 9, and 12, followed by 100 µg of clone 9D9 every 3 d thereafter for long term studies.", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "IFN-γ producing CD8+ T cells. IFN-γ producing CD8+ T cells.", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; T cells; CD8+ T cells; IFN-γ-producing cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": "5291", "Animal_Strain_used": "(KitV558Δ/+)", "Cell_line_used_to_induce_tumor_in_mice": "spontaneous", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1698", "Drug": "Cyclophosphamide (CY) 1 d + IL-12/GM-CSF therapy", "Drug_category": "others/combination", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Combination", "PMID": "21908736", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Spontaneous Mammary Tumors", "System": null, "Dose": "200 mg/kg", "Technique": "Flow Cytometry, Real Time Pcr", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD8(+) CTL IFNγ and Granzyme B", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; Cytotoxic T lymphocytes / CTLs; Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": "CD4+ Foxp3+", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; FOXP3", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": "2907", "Animal_Strain_used": "FVBneuN", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1699", "Drug": "SGI-1776(inhibitor of PIM kinase activity) and sunitinib", "Drug_category": "others/combination", "Drugbank_ID": "DB12494, DB01268", "Target/s_or_mechanism_of_action": "SGI-1776 has been used in trials studying the treatment of Prostate Cancer, Non-Hodgkins Lymphoma, and Relapsed/Refractory Leukemias, Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCC(CNC2=NN3C(C=C2)=NC=C3C2=CC=CC(OC(F)(F)F)=C2)CC1, CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Combination", "PMID": "22015557", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma (RCC)", "System": null, "Dose": "sunitinib (40 mg kg–1 PO), SGI-1776 (200 mg kg–1 free base PO)", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Bad phosphorylation(induces apoptosis), c-Myc levels and decreases tumour cell proliferation", "Controlled_Terms_Function_inhibited_Number_decreased": "Apoptosis / caspase activation; Cell proliferation / Ki-67", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "24795070, 5329102", "Animal_Strain_used": "nude (BALB/c background)", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1700", "Drug": "SGI-1776(inhibitor of PIM kinase activity) and sunitinib", "Drug_category": "others/combination", "Drugbank_ID": "DB12494, DB01268", "Target/s_or_mechanism_of_action": "SGI-1776 has been used in trials studying the treatment of Prostate Cancer, Non-Hodgkins Lymphoma, and Relapsed/Refractory Leukemias, Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCC(CNC2=NN3C(C=C2)=NC=C3C2=CC=CC(OC(F)(F)F)=C2)CC1, CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Combination", "PMID": "22015557", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma (RCC)", "System": null, "Dose": "sunitinib (40 mg kg–1 PO), SGI-1776 (200 mg kg–1 free base PO)", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Bad phosphorylation(induces apoptosis), c-Myc levels and decreases tumour cell proliferation", "Controlled_Terms_Function_inhibited_Number_decreased": "Apoptosis / caspase activation; Cell proliferation / Ki-67", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "24795070, 5329102", "Animal_Strain_used": "nude (BALB/c background)", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1704", "Drug": "IL-2 and entinostat", "Drug_category": "others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "22303460", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma", "System": null, "Dose": "IL-2 (Prometheus, 150,000 IU, twice a day, 2 d/wk, i.p.), entinostat (5 mg/kg, daily, 5 d/wk by oral gavage)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "IFN-γ induction-by CD8", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "BALB/c mouse", "Cell_line_used_to_induce_tumor_in_mice": "RENCA", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1706", "Drug": "Entinostat + survivin peptide vaccine SVN53-67/M57-KLH (SurVaxM)", "Drug_category": "others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "22303460", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer -Castration Resistant Prostate Cancer", "System": null, "Dose": "entinostat (5 days/wk, 5 mg/kg), SurVaxM (1 dose/wk)", "Technique": "Flow Cytometry,Mhc Class I Tetramer Binding Assay", "Controlled_Technique": "Flow cytometry; MHC class I tetramer-binding assay", "Immune_System-Function_enhanced/numbers_increased": "CD8+IFN-γ+ cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8", "Immune_System-Function_inhibited/numbers_decreased": "Foxp3 level in Tregs of tumor-bearing mice", "Controlled_Terms_Function_inhibited_Number_decreased": "FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "male FVB", "Cell_line_used_to_induce_tumor_in_mice": "CR Myc-CaP tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1707", "Drug": "Decitabine + Vorinostat", "Drug_category": "others/combination", "Drugbank_ID": "DB01262, DB02546", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses.\n Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1\n ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "22461695", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Carcinoma", "System": null, "Dose": "Decitabine (0.1 mg/kg body weight), Vorinostat (25 mg/kg body weight)", "Technique": "Flow cytometry, RT PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "tumor-infiltrating CD8+ T cell and CD8− lung cells expressed FasL FasL, FasL-mediated tumor suppression", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; CD8+ T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03665, D06320", "Drug_Pubchem": "451668, 5311", "Animal_Strain_used": "BALB/c and Fasgld", "Cell_line_used_to_induce_tumor_in_mice": "CT26 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1756", "Drug": "PLX4720+agonistic anti CD40", "Drug_category": "others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "24736544", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "417mg/kg PLX4720+agonistic anti-CD40 Ab (250μg/mouse)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "FoxP3+ Treg CD4+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; FOXP3; Regulatory T cells / Tregs; T cells; CD4+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD4+ and CD8+ T cells, CD11b+/Gr-1+", "Controlled_Terms_Unaffected": "CD4; CD8; CD11b / ITGAM; T cells; CD8+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "BrafV600E/Pten", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1709", "Drug": "Combined vaccine + axitinib therapy", "Drug_category": "others/combination", "Drugbank_ID": "DB06626", "Target/s_or_mechanism_of_action": "Axitinib selectively blocks the tyrosine kinase receptors VEGFR-1 (vascular endothelial growth factor receptor), VEGFR-2, and VEGFR-3.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=C(SC2=CC=C3C(NN=C3\\C=C\\C3=CC=CC=N3)=C2)C=CC=C1", "Single/Combination": "Combination", "PMID": "22504156", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "s.c. vaccine (syngenic DC.IL12 pulsed with the OVA257–264 and OVA323–339 peptides on days 7 and 14), axitinib alone (0.5 mg/day provided via oral gavage on days 7–13) or the combination of vaccine + axitinib", "Technique": "Flow Cytometry, Rt-Pcr And Fluorescence Microscopy", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Microscopy", "Immune_System-Function_enhanced/numbers_increased": "bulk CD8+ T cells IFN-γ,CXCR3,CXCL12 CD31+ vascular endothelial cells in treated melanomas appeared activated based on their enhanced expression of VCAM-1 Tbet", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CXCL12 / SDF-1; CD8; CD31 / PECAM-1; T cells; CD8+ T cells; VCAM-1; CXCR3", "Immune_System-Function_inhibited/numbers_decreased": "MDSC and Treg populations", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03218", "Drug_Pubchem": "6450551", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MO5 (B16.OVA) tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1710", "Drug": "Vaccine -syngenic DC.IL12 pulsed with the OVA257–264 and OVA323–339 peptides", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "22504156", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "s.c. vaccine (syngenic DC.IL12 pulsed with the OVA257–264 and OVA323–339 peptides on days 7 and 14)", "Technique": "Flow Cytometry, Rt-Pcr And Fluorescence Microscopy", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Microscopy", "Immune_System-Function_enhanced/numbers_increased": "bulk CD8+ T cells IFN-γ,CXCR3,CXCL11 CD31+ Tbet", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CXCL11 / I-TAC; CD8; CD31 / PECAM-1; T cells; CD8+ T cells; CXCR3", "Immune_System-Function_inhibited/numbers_decreased": "Treg (CD4+Foxp3+) phenotypes in the TME", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MO5 (B16.OVA) tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1715", "Drug": "Anti-CTLA-4 + PLX4720", "Drug_category": "others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "22934253", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "a chow diet containing 417 mg/kg PLX4720 + Mice were injected intraperitoneal with the anti-CTLA-4 mAbs dissolved in HBSS. Dosing per injection was 200 μg for the hamster-derived anti-CTLA-4 mAb clone 9H10 (BioXcell, BE0131) and 100 μg for the mouse-derived anti-CTLA-4 mAb clone 9D9 (BioXcell, BE0164)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD45+ leukocytes, CD8+ and CD4+ T cells in the melanomas ,frequency of NK-cells, myeloid derived suppressor cells (MDSCs), macrophages", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD8; CD45; Myeloid-derived suppressor cells / MDSCs; Macrophages; T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "Tyr::CreERT2PTENF−/−BRAFF-V600E/+", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1730", "Drug": "AR-42 and/or DNA vaccine (DNA encoding CRT/E7)", "Drug_category": "others/combination", "Drugbank_ID": "DB12707", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C)[C@H](C(=O)NC1=CC=C(C=C1)C(=O)NO)C1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "23715898", "Cancer_Type": "Cervical Cancer", "Cancer_Type_Description": "Cervical Cancer", "System": null, "Dose": "AR-42 was given daily at a dose of 30 mg/kg body weight via oral gavage. The DNA vaccine (2 μg/mouse) was given at 3-day intervals via gene gun", "Technique": "Kaplan-Meier Survival Analysis, Flow Cytometry", "Controlled_Technique": "Flow cytometry; Survival analysis (Kaplan–Meier)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells IFN-γ(IFN-γ-producing CD8+ T cells ) Improved survival", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; T cells; CD8+ T cells; IFN-γ-producing cells; Survival outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "6918848", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "TC-1 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1734", "Drug": "Lenalidomide and cyclophosphamide", "Drug_category": "others/combination", "Drugbank_ID": "DB00480, DB00531", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O, ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Combination", "PMID": "23765229", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - A20 Murine Lymphoma", "System": null, "Dose": null, "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "splenic Treg", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687, D07760", "Drug_Pubchem": "216326, 2907", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1735", "Drug": "Lenalidomide and lymphoma Id DNA fusion vaccine", "Drug_category": "others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "23765229", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - A20 Murine Lymphoma", "System": null, "Dose": "5mg/kg/day", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "anti-Id antibodies", "Controlled_Terms_Function_enhanced_Number_increased": "anti-Id antibodies", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": "216326", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1736", "Drug": "Lymphoma Id DNA fusion vaccine", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "23765229", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - A20 Murine Lymphoma", "System": null, "Dose": "5mg/kg/day", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "anti-Id antibodies", "Controlled_Terms_Function_enhanced_Number_increased": "anti-Id antibodies", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1739", "Drug": "Ad5-OVA plus low-dose 5-fluorouracil (5-FU)", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "23840786", "Cancer_Type": "Thymoma", "Cancer_Type_Description": "Thymoma", "System": null, "Dose": "10^8 pfu (2.7×10^9 virus particles) of Ad5-OVA ± i.p. administration of 40 mg/kg 5-FU", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8(+) T lymphocytes", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "MDSCs", "Controlled_Terms_Negative_Regulation": "Myeloid-derived suppressor cells / MDSCs", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "E.G7", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1741", "Drug": "Α-lactalbumin vaccine and Sunitinib", "Drug_category": "others/combination", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Combination", "PMID": "24105638", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Mammary Carcinoma", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD11b+Gr1+ myeloid derived suppressor cells (MDSCs), T regulatory cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1 mouse mammary carcinoma", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1748", "Drug": "Sorafenib and YC-1, a soluble guanylyl cyclase (sGC) activator", "Drug_category": "others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "24418169", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "sorafenib (30 mg/kg/day) and YC-1 (10 mg/kg/day)", "Technique": "Immunohistochemistry Assay", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "Apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis / caspase activation", "Immune_System-Function_inhibited/numbers_decreased": "p-STAT3, cyclin D1, and survivin,p-STAT3, cyclin D1, and survivin", "Controlled_Terms_Function_inhibited_Number_decreased": "STAT3 signaling", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "nude", "Cell_line_used_to_induce_tumor_in_mice": "HCCLM3", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1749", "Drug": "Sorafenib and YC-1, a soluble guanylyl cyclase (sGC) activator", "Drug_category": "others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "24418169", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "sorafenib (30 mg/kg/day) and YC-1 (10 mg/kg/day)", "Technique": "Immunohistochemistry Assay", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "Apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis / caspase activation", "Immune_System-Function_inhibited/numbers_decreased": "p-STAT3, cyclin D1, and survivin,p-STAT3, cyclin D1, and survivin", "Controlled_Terms_Function_inhibited_Number_decreased": "STAT3 signaling", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "nude", "Cell_line_used_to_induce_tumor_in_mice": "HepG2 cell", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1752", "Drug": "Dasatinib + OVA peptide-based dendritic cell vaccination therapy", "Drug_category": "others/combination", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Combination", "PMID": "24734217", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "0.01–1 mg/day", "Technique": "Immunofluorescence Staining And Fluorescence Microscopy,Flow Cytometry", "Controlled_Technique": "Flow cytometry; Immunofluorescence assay; Microscopy; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "Type1 CD8+ effector T cell and DC infiltration", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Dendritic cells; T cells; Th1 / type 1 T-cell response; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "CD11b+Gr1+ myeloid-derived suppressor cells (MDSC) and CD4+Foxp3+ regulatory T (Treg)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD11b / ITGAM; FOXP3; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": "3062316", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "M05 melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1758", "Drug": "PLX4720+Anti IFN-y", "Drug_category": "others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "24736544", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "417mg/kg PLX4720+IFNγ(250μg/mouse)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD11b+/Gr-1+", "Controlled_Terms_Function_enhanced_Number_increased": "CD11b / ITGAM", "Immune_System-Function_inhibited/numbers_decreased": "CD4+ and CD8+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD8; T cells; CD8+ T cells", "Immune_System_function_unaffected": "TAMs or TIDCs", "Controlled_Terms_Unaffected": "Tumor-associated macrophages / TAMs; Dendritic cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "BrafV600E/Pten", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1759", "Drug": "PLX4720+GK1.5 mAbs", "Drug_category": "others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "24736544", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "417mg/kg PLX4720+GK1.5 mAbs", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD8+ or CD4+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD8; T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "BrafV600E/Pten", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1760", "Drug": "PLX4720+TIB210", "Drug_category": "others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "24736544", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "417mg/kg PLX4720 + TIB210", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD8+ or CD4+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD8; T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "BrafV600E/Pten", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1761", "Drug": "Cyclophosphamide + adoptive transfer (AT) of tumor-specific CD4+ T cells", "Drug_category": "others/combination", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Combination", "PMID": "24780756", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "B-Cell Lymphoma", "System": null, "Dose": null, "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "inflammatory myeloid cells consisting of monocytic and granulocytic subsets", "Controlled_Terms_Unaffected": "inflammatory myeloid cells consisting of monocytic and granulocytic subsets", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": "2907", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "B-cell lymphoma cell line A20 (A20HA)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1762", "Drug": "PLX4720 + anti-mouse PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "24903021", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "BRAFi (200 ppm) was initiated at day 0. 100μg of anti-PD-1 (29F.1A12) antibody was administered i.p. at days 1, 3, and 5", "Technique": "Flow Cytometry, Immunohistochemical Staining", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD3+ T cells, CD8+ T cells in the tumor , The CD8/Treg ratio, polyfunctional CD8+ T cells producing both IFNγ and TNFα in the mice treated with anti-PD-1 and BRAFi", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; TNF-α / TNF; CD8; CD3; PD-1 / PDCD1; Regulatory T cells / Tregs; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "BP cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1763", "Drug": "PLX4720 + anti-mouse PD-L1", "Drug_category": "others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "24903021", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "BRAFi (200 ppm) was initiated at day 0. ), 200μg anti-PD-L1 (10F.9G2), or isotype antibody was administered i.p. at days 1, 3, and 5", "Technique": "Flow Cytometry, Immunohistochemical Staining", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD3+ T cells, The CD8/Treg ratio", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD3; Regulatory T cells / Tregs; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "BP cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1768", "Drug": "PLX4720 +dasatinib", "Drug_category": "others/combination", "Drugbank_ID": "DB06999, DB01254", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf,\n Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F,\n CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Combination", "PMID": "24994118", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer", "System": null, "Dose": "PLX4720-impregnated chow (417 mg/kg) and 50 mg/kg dasatinib", "Technique": "Immunohistochemical Analysis", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cell infiltration was observed in tumors, infiltrating B220+ B cells, marker of monocytes and macrophages, F4/80 Caspase 3 cleavage- marker of apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Macrophages; Monocytes; B cells; T cells; CD8+ T cells; Apoptosis / caspase activation; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": "24180719, 3062316", "Animal_Strain_used": "B6129SF1/J", "Cell_line_used_to_induce_tumor_in_mice": "TBP-3743", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1769", "Drug": "PLX4720+Dasatinib", "Drug_category": "others/combination", "Drugbank_ID": "DB06999, DB01254", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf,\n Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F,\n CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Combination", "PMID": "24994118", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer - (Anaplastic)", "System": null, "Dose": "PLX4720-impregnated\n chow (417 mg/kg), orally gavaged with 50 mg/kg dasatinib five days per week", "Technique": "Immunohistochemial Analysis", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": "24180719, 3062316", "Animal_Strain_used": "B6129SF1/J syngeneic", "Cell_line_used_to_induce_tumor_in_mice": "105 TBP-3743 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1770", "Drug": "Pmel-ACT+ LBH589 (Panobinostat)", "Drug_category": "others/combination", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Combination", "PMID": "25054063", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "LBH589 (Panobinostat): 5 mg/kg+ \"5 × 106 gp100-specific Pmel\n T cells\"+ \"gp10025-33 peptide pulsed dendritic\n cell vaccination\"", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Pmel T cells (CD8+ Thy1.1+) IFN-γ ,TNF, and IL-10, IL-6 CD25, OX-40", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-6; IL-10; TNF-α / TNF; CD8; CD25 / IL2RA; T cells", "Immune_System-Function_inhibited/numbers_decreased": "T regulatory cells (CD3+ CD4+ FoxP3+)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD3; FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": "CD40L, 4-1BB, or CD27", "Controlled_Terms_Unaffected": "CD40L / CD154", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10019", "Drug_Pubchem": "6918837", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "B16-F10", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1773", "Drug": "PLX4720", "Drug_category": "others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": null, "PMID": "25183499", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "PLX4720 (417 mg/kg) for 10 days", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "increased CD8+ T cells by proportion of CD45+ cells but not the absolute number, increased CD4 +T cells by proportion of CD45+ cells but not the absolute number,", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD45; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "Foxp3+ Tregs,CD11b+Gr1+", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": "T-bet, GATA3, and RORγt", "Controlled_Terms_Unaffected": "T-bet, GATA3, and RORγt", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "C57BL/6 (Braf/Pten model)", "Cell_line_used_to_induce_tumor_in_mice": "Braf/Pten tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1777", "Drug": "PD184352 and BMS-345541", "Drug_category": "others/combination", "Drugbank_ID": "DB12429", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "FC1=C(F)C(NC2=CC=C(I)C=C2Cl)=C(C=C1)C(=O)NOCC1CC1", "Single/Combination": "Combination", "PMID": "25256614", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "25 mg/kg/day PD184352 and 40 mg/kg/day BMS-345541", "Technique": "Immunofluorescence Staining", "Controlled_Technique": "Immunofluorescence assay; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "pan macrophage marker CD68, and also the M1 and M2 macrophage markers CD86 and CD163, in the tumors from mice treated with the MEKi/IKKi combination when compared to the MEKi and IKKi only treatment", "Controlled_Terms_Function_inhibited_Number_decreased": "CD86; CD68; CD163; Macrophages; M2 macrophage phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "6918454", "Animal_Strain_used": "C57J/B6", "Cell_line_used_to_induce_tumor_in_mice": "BRafV600E-4434", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1778", "Drug": "5-fluorouracil (5-FU)+IFN-a", "Drug_category": "others/combination", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "25368252", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": null, "Dose": "5-FU (35 mg/g/d; IP from day 5 to day 9)+murine IFN-a on days 5, 7, 9 (500 IU/g, SC).", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8 T cells, infiltrating NK cells, dendritic cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Dendritic cells; NK cells; T cells; CD8+ T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00584", "Drug_Pubchem": "3385", "Animal_Strain_used": "C57BL/6 (B6)", "Cell_line_used_to_induce_tumor_in_mice": "Panc02 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1862", "Drug": "Trametinib + anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "27622011", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "0.6mg/kg of trametinib + 4 doses of 200 ug of PD-1", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD3+CD8+ cells in the tumors,CD3+CD4+ cells in the tumors,", "Controlled_Terms_Unaffected": "CD4; CD8; CD3", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1781", "Drug": "Golvatinib + lenvatinib", "Drug_category": "others/combination", "Drugbank_ID": "DB11977, DB09078", "Target/s_or_mechanism_of_action": "An orally bioavailable dual kinase inhibitor of c-Met (hepatocyte growth factor receptor) and VEGFR-2 (vascular endothelial growth factor receptor-2) tyrosine kinases with potential antineoplastic activity. Golvatinib binds to and inhibits the activities of both c-Met and VEGFR-2, which may inhibit tumor cell growth and survival of tumor cells that overexpress these receptor tyrosine kinases. c-Met and VEGFR-2 are upregulated in a variety of various tumor cell types and play important roles in tumor cell growth, migration and angiogenesis.\n Lenvatinib is a receptor tyrosine kinase (RTK) inhibitor that inhibits the kinase activities of vascular endothelial growth factor (VEGF) receptors VEGFR1 (FLT1), VEGFR2 (KDR), and VEGFR3 (FLT4). Lenvatinib also inhibits other RTKs that have been implicated in pathogenic angiogenesis, tumor growth, and cancer progression in addition to their normal cellular functions, including fibroblast growth factor (FGF) receptors FGFR1, 2, 3, and 4; the platelet derived growth factor receptor alpha (PDGFRα), KIT, and RET", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC1)C1CCN(CC1)C(=O)NC1=CC(OC2=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C(F)=C2)=CC=N1,\n COC1=C(C=C2C(OC3=CC=C(NC(=O)NC4CC4)C(Cl)=C3)=CC=NC2=C1)C(N)=O", "Single/Combination": "Combination", "PMID": "25458359", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid -Human Thyroid Cancer", "System": null, "Dose": "golvatinib 100 mg/kg + lenvatinib 10 mg/kg", "Technique": "Immunohistochemical Analysis, Flow Cytometry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "myeloid cells (CD11b+), macrophages (F4/80+ in Flow cytometry, CD11b+F4/80+ in immunohistochemistry)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Macrophages", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09919", "Drug_Pubchem": "16118392, 9823820", "Animal_Strain_used": "Nude (CAnN.Cg-Foxn1nu/CrlCrlj; female, 5–6 weeks old)", "Cell_line_used_to_induce_tumor_in_mice": "K1/angiopoietin-2 (Ang2)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1784", "Drug": "Golvatinib + lenvatinib", "Drug_category": "others/combination", "Drugbank_ID": "DB11977, DB09078", "Target/s_or_mechanism_of_action": "An orally bioavailable dual kinase inhibitor of c-Met (hepatocyte growth factor receptor) and VEGFR-2 (vascular endothelial growth factor receptor-2) tyrosine kinases with potential antineoplastic activity. Golvatinib binds to and inhibits the activities of both c-Met and VEGFR-2, which may inhibit tumor cell growth and survival of tumor cells that overexpress these receptor tyrosine kinases. c-Met and VEGFR-2 are upregulated in a variety of various tumor cell types and play important roles in tumor cell growth, migration and angiogenesis.\n Lenvatinib is a receptor tyrosine kinase (RTK) inhibitor that inhibits the kinase activities of vascular endothelial growth factor (VEGF) receptors VEGFR1 (FLT1), VEGFR2 (KDR), and VEGFR3 (FLT4). Lenvatinib also inhibits other RTKs that have been implicated in pathogenic angiogenesis, tumor growth, and cancer progression in addition to their normal cellular functions, including fibroblast growth factor (FGF) receptors FGFR1, 2, 3, and 4; the platelet derived growth factor receptor alpha (PDGFRα), KIT, and RET", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC1)C1CCN(CC1)C(=O)NC1=CC(OC2=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C(F)=C2)=CC=N1,\n COC1=C(C=C2C(OC3=CC=C(NC(=O)NC4CC4)C(Cl)=C3)=CC=NC2=C1)C(N)=O", "Single/Combination": "Combination", "PMID": "25458359", "Cancer_Type": "Uterus", "Cancer_Type_Description": "Endometrial - Human Endometrial Cancer", "System": null, "Dose": "golvatinib 100 mg/kg + lenvatinib 10 mg/kg", "Technique": "Immunohistochemical Analysis, Flow Cytometry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "macrophage population", "Controlled_Terms_Function_inhibited_Number_decreased": "Macrophages", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09919", "Drug_Pubchem": "16118392, 9823820", "Animal_Strain_used": "Nude (CAnN.Cg-Foxn1nu/CrlCrlj; female, 5–6 weeks old)", "Cell_line_used_to_induce_tumor_in_mice": "AN3CA tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1788", "Drug": "Sorafenib + AMD3100", "Drug_category": "others/combination", "Drugbank_ID": "DB00398, DB06809", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.\n Plerixafor inhibits the CXCR4 chemokine receptors on CD34+ cells and reversibly blocks binding of the ligand, stromal cell-derived factor-1-alpha (SDF-1α). By blocking the interaction between SDF-1α and CXCR4 with plerixafor, mobilization of progenitor cells is triggered. Filgrastim, a granulocyte-colony stimulating factor, is added to enhance CD34+ cell mobilization, thus increasing the yield of stem cells- an important determinant of graft adequacy.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1,\n C(N1CCCNCCNCCCNCC1)C1=CC=C(CN2CCCNCCNCCCNCC2)C=C1", "Single/Combination": "Combination", "PMID": "25529917", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "sorafenib at a dose of 50mg/kg (in PBS/1%Tween80, MGH Pharmacy), and with the CXCR4 inhibitor AMD3100 (10mg/kg bodyweight, s.c. by osmotic minipumps, Sigma)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "F4/80+ TAMs, and CD11b+Gr-1+ and CD45+CXCR4+ myeloid cells, CD4+CD25+FoxP3+ Tregs in HCA-1 tumors, M2-type markers in TAMs without affecting that of M1-type markers", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD25 / IL2RA; CD11b / ITGAM; CD45; FOXP3; Regulatory T cells / Tregs; Tumor-associated macrophages / TAMs; CXCR4", "Immune_System_function_unaffected": "CD4+ and CD8+ T-lymphocytes", "Controlled_Terms_Unaffected": "CD4; CD8", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524,\n D08971", "Drug_Pubchem": "216239, \n 65015", "Animal_Strain_used": "C3H", "Cell_line_used_to_induce_tumor_in_mice": "HCA-1 tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1789", "Drug": "Sorafenib + AMD3100 + anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB00398, DB06809", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.\n Plerixafor inhibits the CXCR4 chemokine receptors on CD34+ cells and reversibly blocks binding of the ligand, stromal cell-derived factor-1-alpha (SDF-1α). By blocking the interaction between SDF-1α and CXCR4 with plerixafor, mobilization of progenitor cells is triggered. Filgrastim, a granulocyte-colony stimulating factor, is added to enhance CD34+ cell mobilization, thus increasing the yield of stem cells- an important determinant of graft adequacy.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1,\n C(N1CCCNCCNCCCNCC1)C1=CC=C(CN2CCCNCCNCCCNCC2)C=C1", "Single/Combination": "Combination", "PMID": "25529917", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "sorafenib at a dose of 50mg/kg (in PBS/1%Tween80, MGH Pharmacy), and with the CXCR4 inhibitor AMD3100 (10mg/kg bodyweight, s.c. by osmotic minipumps, Sigma), PD-1 (100μg i.p. every 3 days, for a total of 5 times).", "Technique": "Immunoflorescence staining, immunohistochemistry, ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "intratumoral penetration and activation of CD8+ T-lymphocytes in HCC IFN-γ, IL-2 and TNF-α apoptosis- cleaved caspase 3", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-2; TNF-α / TNF; CD8; Apoptosis / caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524,\n D08971", "Drug_Pubchem": "216239, \n 65015", "Animal_Strain_used": "Mst1–/– Mst2F/–", "Cell_line_used_to_induce_tumor_in_mice": "induced liver fibrosis with carbon tetrachloride (CCl4) treatment (20%v/v in olive oil, 150µL gavage, 3 times per week) for 12 weeks", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1790", "Drug": "Sorafenib + AMD3100 + anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB00398, DB06809", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.\n Plerixafor inhibits the CXCR4 chemokine receptors on CD34+ cells and reversibly blocks binding of the ligand, stromal cell-derived factor-1-alpha (SDF-1α). By blocking the interaction between SDF-1α and CXCR4 with plerixafor, mobilization of progenitor cells is triggered. Filgrastim, a granulocyte-colony stimulating factor, is added to enhance CD34+ cell mobilization, thus increasing the yield of stem cells- an important determinant of graft adequacy.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1,\n C(N1CCCNCCNCCCNCC1)C1=CC=C(CN2CCCNCCNCCCNCC2)C=C1", "Single/Combination": "Combination", "PMID": "25529917", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "sorafenib at a dose of 50mg/kg (in PBS/1%Tween80, MGH Pharmacy), and with the CXCR4 inhibitor AMD3100 (10mg/kg bodyweight, s.c. by osmotic minipumps, Sigma), PD-1 (100μg i.p. every 3 days, for a total of 5 times).", "Technique": "Immunoflorescence staining, immunohistochemistry, ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "intratumoral penetration and activation of CD8+ T-lymphocytes in HCC IFN-γ, IL-2 and TNF-α apoptosis- cleaved caspase 3", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-2; TNF-α / TNF; CD8; Apoptosis / caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524,\n D08971", "Drug_Pubchem": "216239, \n 65015", "Animal_Strain_used": "C3H", "Cell_line_used_to_induce_tumor_in_mice": "HCA-1 tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1791", "Drug": "Bortezomib( a proteasome inhibitor) and SAHA( Vorinostat)", "Drug_category": "others/combination", "Drugbank_ID": "DB00188, DB02546", "Target/s_or_mechanism_of_action": "Bortezomib is a reversible inhibitor of the 26S proteasome, which is made up of a 20S core complexed with a 19S regulatory complex. Individual β-subunits allow specific catalytic action of the 20S core.\n Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C)C[C@H](NC(=O)[C@H](CC1=CC=CC=C1)NC(=O)C1=CN=CC=N1)B(O)O,\n ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "25591912", "Cancer_Type": "Cervical Cancer", "Cancer_Type_Description": "Cervical Cancer", "System": null, "Dose": "bortezomib (1 mg/kg, once every 3 days), SAHA (30 mg/kg, once per day)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "E7-specific CD8+ T cells, CD8+ T cells in the tumor IFN-γ by CD8+ T cells significantly lower tumor volume", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; T cells; CD8+ T cells; Tumor growth / burden outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03150,D06320", "Drug_Pubchem": "387447, 5311", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "TC-1 tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1794", "Drug": "Dabrafenib+ACT", "Drug_category": "others/combination", "Drugbank_ID": "DB08912", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Murine Melanoma", "System": null, "Dose": "three million gp10025-33 peptide activated pmel-1 splenocytes+ 30 mg/kg of dabrafenib", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+Thy1.1+ (adoptively transferred pmel-1 effector) and CD3+CD8+ (both endogenous and adoptively transferred effector) cells MHC expression, PD-L1", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD3; PD-L1 / CD274; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": "decreased percentage of MO-MDSC in spleen", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "tumour-associated macrophages (TAMs, F4/80+CD11b+), increased MO-MDSCs (Ly6ChighLy6GlowCD11b+) and decreased PMN-MDSCs (Ly6ClowLy6GhighCD11b+) in tumors", "Controlled_Terms_Negative_Regulation": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; PMN-MDSCs / granulocytic MDSCs; Tumor-associated macrophages / TAMs; Macrophages", "KEGG_Drug_ID": "D10064", "Drug_Pubchem": "44462760", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1795", "Drug": "Dabrafenib+trametinib+ACT", "Drug_category": "others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Murine Melanoma", "System": null, "Dose": "three million gp10025-33 peptide activated pmel-1 splenocytes+ 0.6mg/kg of trametinib+30 mg/kg of dabrafenib", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+Thy1.1+ (adoptively transferred pmel-1 effector) and CD3+CD8+ (both endogenous and adoptively transferred effector) cells MHC expression, PD-L1", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD3; PD-L1 / CD274; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD11b+ cells in spleen", "Controlled_Terms_Unaffected": "CD11b / ITGAM", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "tumour-associated macrophages (TAMs, F4/80+CD11b+), T regulatory cells (Tregs, CD4+CD25+FOXp3+) showed significantly increased percentage in the tumours, increased MO-MDSCs (Ly6ChighLy6GlowCD11b+) and decreased PMN-MDSCs (Ly6ClowLy6GhighCD11b+) in tumors", "Controlled_Terms_Negative_Regulation": "CD4; CD25 / IL2RA; CD11b / ITGAM; FOXP3; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; PMN-MDSCs / granulocytic MDSCs; Tumor-associated macrophages / TAMs; Macrophages", "KEGG_Drug_ID": "D10064, D10175", "Drug_Pubchem": "44462760, 11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1796", "Drug": "Dobrafenib+ Trametinib", "Drug_category": "others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "dabrafenib (30 mg/kg) and trametinib(0.15mg/kg)", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064, D10175", "Drug_Pubchem": "44462760, 11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "murine melanoma SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1797", "Drug": "Pmel-1 ACT+Dabrafenib", "Drug_category": "others/combination", "Drugbank_ID": "DB08912", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "ACT (3 million)+Dobrafenib (30 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+Thy1.1+, CD3+CD8+\n (both endogenous and adoptively transferred\n effector) cells, Ly6CHiLy6GLoCD11b+, F4/80+CD11b+, T regulatory cells (Tregs; CD4+CD25+FOXp3+)", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD3; CD25 / IL2RA; CD11b / ITGAM; FOXP3; Regulatory T cells / Tregs", "Immune_System-Function_inhibited/numbers_decreased": "Ly6CLoLy6GHiCD11b+", "Controlled_Terms_Function_inhibited_Number_decreased": "Ly6CLoLy6GHiCD11b+", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064", "Drug_Pubchem": "44462760", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "murine melanoma SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1798", "Drug": "Pmel-1 ACT+Dabrafenib", "Drug_category": "others/combination", "Drugbank_ID": "DB08912", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "ACT (3 million)+Dobrafenib (30 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+Thy1.1+ IFN-y", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD3", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064", "Drug_Pubchem": "44462760", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "murine melanoma SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1799", "Drug": "Pmel-1 ACT+Dabrafenib +anti PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB08912", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "ACT (3 million)+Dobrafenib (30 mg/kg)+anti PD-1 (200 ug)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064", "Drug_Pubchem": "44462760", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "murine melanoma SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1800", "Drug": "Pmel-1 ACT+dabrafenib+trametinib", "Drug_category": "others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "ACT (3 million)+dabrafenib(30 mg/kg) and trametinib", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+Thy1.1+ IFN-y", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD3", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064, D10175", "Drug_Pubchem": "44462760, 11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "murine melanoma SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1801", "Drug": "Pmel-1 ACT+dabrafenib+trametinib+ anti PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "ACT (3 million)+dabrafenib(30 mg/kg) +trametinib+ anti PD-1(200 ug)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064, D10175", "Drug_Pubchem": "44462760, 11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "murine melanoma SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1802", "Drug": "Pmel-1 ACT+Dobrafenib+ Trametinib", "Drug_category": "others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "ACT of gp10025-33 peptide–activated\n splenocytes obtained from pmel-1mice (3 million)+dabrafenib(30 mg/kg) and trametinib", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+Thy1.1+, CD3+CD8+\n (both endogenous and adoptively transferred\n effector) cells, Ly6CHiLy6GLoCD11b+, F4/80+CD11b+ IFN-y", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; CD3; CD11b / ITGAM", "Immune_System-Function_inhibited/numbers_decreased": "Ly6CLoLy6GHiCD11b+", "Controlled_Terms_Function_inhibited_Number_decreased": "Ly6CLoLy6GHiCD11b+", "Immune_System_function_unaffected": "T regulatory cells (Tregs; CD4+CD25+FOXp3+)", "Controlled_Terms_Unaffected": "CD4; CD25 / IL2RA; FOXP3; Regulatory T cells / Tregs", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064, D10175", "Drug_Pubchem": "44462760, 11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "murine melanoma SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1803", "Drug": "Pmel-1 ACT+Trametinib", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "ACT (3 million)+Trametinib(0.6 mg/kg)", "Technique": "Flow Cytometery", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+Thy1.1+, CD3+CD8+\n (both endogenous and adoptively transferred\n effector) cells, Ly6CHiLy6GLoCD11b+, F4/80+CD11b+", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD3; CD11b / ITGAM", "Immune_System-Function_inhibited/numbers_decreased": "Ly6CLoLy6GHiCD11b+", "Controlled_Terms_Function_inhibited_Number_decreased": "Ly6CLoLy6GHiCD11b+", "Immune_System_function_unaffected": "T regulatory cells (Tregs; CD4+CD25+FOXp3+)", "Controlled_Terms_Unaffected": "CD4; CD25 / IL2RA; FOXP3; Regulatory T cells / Tregs", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "murine melanoma SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1804", "Drug": "Pmel-1 ACT+Trametinib", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "ACT (3 million)+Trametinib(0.6 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+Thy1.1+ IFN-y", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD3", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "murine melanoma SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1805", "Drug": "Pmel-1 ACT+Trametinib+ anti PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "ACT (3 million)+Trametinib(0.6 mg/kg)+ anti PD-1 (200 ug)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "PD-L1", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "murine melanoma SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1806", "Drug": "Trametinib+ACT", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "25787767", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Murine Melanoma", "System": null, "Dose": "three million gp10025-33 peptide activated pmel-1 splenocytes+ 0.6mg/kg of trametinib", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+Thy1.1+ (adoptively transferred pmel-1 effector) and CD3+CD8+ (both endogenous and adoptively transferred effector) cells MHC expression, PD-L1", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD3; PD-L1 / CD274; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD11b+ cells in spleen", "Controlled_Terms_Unaffected": "CD11b / ITGAM", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "increased MO-MDSCs (Ly6ChighLy6GlowCD11b+) and decreased PMN-MDSCs (Ly6ClowLy6GhighCD11b+) in tumors", "Controlled_Terms_Negative_Regulation": "Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; PMN-MDSCs / granulocytic MDSCs", "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1807", "Drug": "Sorafenib + anti-CTLA-4", "Drug_category": "others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "25845968", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma (RCC)", "System": null, "Dose": "Sorafenib (10 mg/kg) and anti-CTLA-4 Ab (100 g/mouse)", "Technique": "Immunohostochemistry", "Controlled_Technique": "Immunohostochemistry", "Immune_System-Function_enhanced/numbers_increased": "CD4- cells and CD8-cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "RENCA cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1809", "Drug": "Sunitinib + SFVeE6,7 immunization", "Drug_category": "others/combination", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Combination", "PMID": "25949902", "Cancer_Type": "Cervical Cancer", "Cancer_Type_Description": "Cervical Cancer", "System": null, "Dose": "20 or 40 mg/kg body weight i.p", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs,Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "TC-1 tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1812", "Drug": "Metronomic Cyclophosphamide + DepoVax vaccine containing HPV16E749–57 peptide antigen", "Drug_category": "others/combination", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Combination", "PMID": "25960932", "Cancer_Type": "Hpv16-Expressing Tumors", "Cancer_Type_Description": "Hpv16-Expressing Tumors", "System": null, "Dose": "(20 mg/kg/day) CPA in combination with a 10 μg R9F-PADRE antigen (DPX-R9F) DepoVax vaccine containing HPV16E749-57 (R9F) peptide antigen (DPX-R9F).", "Technique": "IFNγ ELISPOT assay +Flow cytometry+RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); ELISpot/FluoroSpot assay", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells,increased T-cell infiltration IFNγ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; T cells; CD8+ T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": "2907", "Animal_Strain_used": "C57BL6", "Cell_line_used_to_induce_tumor_in_mice": "C3 tumor line", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1814", "Drug": "Cyclophosphamide + lysate/CpG oligodeoxynucleotide (ODN)", "Drug_category": "others/combination", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Combination", "PMID": "26082836", "Cancer_Type": "Brain Cancer", "Cancer_Type_Description": "Neuroblastoma", "System": null, "Dose": "100 mg/kg", "Technique": "ELISPOT assay, Flow cytometry", "Controlled_Technique": "Flow cytometry; ELISpot/FluoroSpot assay", "Immune_System-Function_enhanced/numbers_increased": "CD4 and CD8 T cells, DC activation IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; Dendritic cells; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": "2907", "Animal_Strain_used": "Male A/J", "Cell_line_used_to_induce_tumor_in_mice": "AgN2a", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1818", "Drug": "A-GITR", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "26239999", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal - Metastatic Renal Cell Cancer", "System": null, "Dose": "a-GITR (100 µg, i.p.)", "Technique": "Flow cytometry, real-time quantitative\n PCR (q-PCR)", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD69 and NKG2D CD8 T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD69; T cells; CD8+ T cells; NKG2D ligand / receptor pathway", "Immune_System-Function_inhibited/numbers_decreased": "CD41FoxP3 Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "B6", "Cell_line_used_to_induce_tumor_in_mice": "RENCA cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1849", "Drug": "CD40 monoclonal antibody (mAb) therapy + sunitinib", "Drug_category": "others/combination", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Combination", "PMID": "27385210", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Fibrosarcoma", "System": null, "Dose": "30 μg agonistic rat-anti-mouse CD40 antibody +sunitinib- dose of 50 mg/kg", "Technique": "Flow cytometry,Immunofluorescence Staining", "Controlled_Technique": "Flow cytometry; Immunofluorescence assay; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "CD86 on cDCs (B220−CD11b+/−CD11c+), intratumoral CD8+ T-cells ICAM-1 and VCAM-1", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD86; CD11b / ITGAM; CD11c / ITGAX; T cells; VCAM-1; ICAM-1 / CD54", "Immune_System-Function_inhibited/numbers_decreased": "CD11b+Gr1+ MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "T241 fibrosarcoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1999", "Drug": "Peptide R", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31661001", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": null, "Dose": "Pep R (2 mg/kg, 5 days per week for 2 weeks)", "Technique": "Immunostaining, Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC); Immunostaining/image analysis", "Immune_System-Function_enhanced/numbers_increased": "Granzyme B (GRZB) positive immune cells", "Controlled_Terms_Function_enhanced_Number_increased": "Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": "FoxP3 positive Treg cells CXCR4,CXCL12 decreased in tumors PD-L1 reduction", "Controlled_Terms_Function_inhibited_Number_decreased": "CXCL12 / SDF-1; PD-L1 / CD274; FOXP3; Regulatory T cells / Tregs; Immune checkpoint pathway; CXCR4", "Immune_System_function_unaffected": "CXCR7, PD-1 expression", "Controlled_Terms_Unaffected": "PD-1 / PDCD1; CXCR7", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57Bl/6", "Cell_line_used_to_induce_tumor_in_mice": "MC38 (1 × 106)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1819", "Drug": "Sunitinib plus a-GITR induced", "Drug_category": "others/combination", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Combination", "PMID": "26239999", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal - Metastatic Renal Cell Cancer", "System": null, "Dose": ", a-GITR (100 µg, i.p.), or Sunitinib (20 mg/kg weight, oral gavage)", "Technique": "Flow cytometry, real-time quantitative\n PCR (q-PCR)", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "lymphocytic infiltration, localization of leukocytes in or around tumor foci , infiltration of CD8 T\n cells, NK cells, DCs and macrophages within the livers IFN-g expression in CD8 T cells, IL-12 and TNF alpha. CXCR3 and its ligands CXCL9/MIG, CXCL10/IP-10 and CXCL11/I-TAC CD69 and NKG2D on CD8 T cells, Ki67 protein\n in both NK cells and CD 8 T cells , CD40, CD80,\n CD86 and MHC-II on macrophages and DCs", "Controlled_Terms_Function_enhanced_Number_increased": "IL-12; TNF-α / TNF; CXCL9 / MIG; CXCL10 / IP-10; CXCL11 / I-TAC; CD8; CD69; CD80; CD86; CD40; MHC class II; Macrophages; Dendritic cells; NK cells; T cells; CD8+ T cells; NKG2D ligand / receptor pathway; CXCR3; Cell proliferation / Ki-67; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "liver-infiltrating CD4 T cells, CD41FoxP3 Tregs, CD11b1Gr-11\n MDSC infiltration CCL2/MCP1, CXCL12/SDF-1a, S100A8/9, CCL17 and CCL22, TGF-b, IL-10 PD1, CTLA-4,, GATA-3 and FoxP3 as well as the MDSC-associated gene products arginase-1 and IDO-1", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-10; CCL2 / MCP-1; CXCL12 / SDF-1; CD4; PD-1 / PDCD1; CTLA-4; FOXP3; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; T cells; CD4+ T cells; IDO1; Arginase-1 / ARG1; Immune-cell infiltration", "Immune_System_function_unaffected": "IL-17 ROR-gt", "Controlled_Terms_Unaffected": "IL-17 / IL-17A", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "B6", "Cell_line_used_to_induce_tumor_in_mice": "RENCA cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1820", "Drug": "Sorafenib + TLR3 agonist: lysine-stabilized polyinosinic-polycytidylic-acid (poly-ICLC)", "Drug_category": "others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "26287667", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "20 μl of poly-ICLC (40 μg/dose) + 8.5–11.5 μg Sorafenib per gram of body weight per day", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "NK cells and T cells Apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; T cells; Apoptosis / caspase activation", "Immune_System-Function_inhibited/numbers_decreased": "PD-1 expressing CD 8 cells", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-1 / PDCD1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Hepa 1-6 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1822", "Drug": "LBH589 (panobinostat) +PD-1 blocking antibody", "Drug_category": "others/combination", "Drugbank_ID": "DB06603", "Target/s_or_mechanism_of_action": "Panobinostat is a potent inhibitor of histone deacetylase, which is responsible for the regulation of gene transcription, cellular differentiation, cell-cycle progression, and apoptosis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=C(CCNCC2=CC=C(\\C=C\\C(=O)NO)C=C2)C2=CC=CC=C2N1", "Single/Combination": "Combination", "PMID": "26297712", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "LBH589 (15mg/kg) (Monday, Wednesday and Friday), PD-1 blocking antibody (3mg/kg) (Tuesday and Thursday)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "improved survival", "Controlled_Terms_Function_enhanced_Number_increased": "Survival outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10019", "Drug_Pubchem": "6918837", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "B16F10", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1829", "Drug": "Murine anti–PD-1 antibody and mTOR inhibitor (rapamycin; )/Sirolimus", "Drug_category": "others/combination", "Drugbank_ID": "DB00877", "Target/s_or_mechanism_of_action": "Sirolimus works by inhibiting T-lymphocyte activation and proliferation stimulated by antigens and cytokines such as interleukin (IL)-2, IL-4, and IL-15.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "26637667", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Tumors", "System": null, "Dose": null, "Technique": "Immunohistochemical Staining", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD3+T cells A marker of apoptosis, cleaved caspase-3,", "Controlled_Terms_Function_enhanced_Number_increased": "CD3; T cells; Apoptosis / caspase activation", "Immune_System-Function_inhibited/numbers_decreased": "FoxP3 Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00753", "Drug_Pubchem": "5284616", "Animal_Strain_used": "C57BL/6 KRAS LA2", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1831", "Drug": "BRAF inhibitor (BRAF-I) Vemurafenib and IFN-a +HLA-A2-\n NY-ESO-1 peptide157-165-complex- specific T-cells", "Drug_category": "others/combination", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Combination", "PMID": "26851802", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "1x106 cells/\n mouse", "Technique": "Flow Cytometry, Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09996", "Drug_Pubchem": "42611257", "Animal_Strain_used": "SCID", "Cell_line_used_to_induce_tumor_in_mice": "BRAFV600E M21 melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1832", "Drug": "BRAF inhibitor (BRAF-I) Vemurafenib and IFN-a +HLA-A2-\n NY-ESO-1 peptide157-165-complex- specific T-cells", "Drug_category": "others/combination", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Combination", "PMID": "26851802", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "1x106 cells/\n mouse", "Technique": "Flow Cytometry, Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09996", "Drug_Pubchem": "42611257", "Animal_Strain_used": "NSG", "Cell_line_used_to_induce_tumor_in_mice": "BRAFV600E SK-MEL-37 melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1835", "Drug": "BRAFi PLX4720+Anti PD-L1", "Drug_category": "others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "26943572", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer", "System": null, "Dose": "PLX4720-impregnated chow (417 mg/kg) and anti PD-L1 200ug/mouse/I.P dose every other day (4 total doses)", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "B6129SF1/J", "Cell_line_used_to_induce_tumor_in_mice": "105 genetically engineered murine ATC; TBP 3743\n BRAFV600E/WT P53-/- cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1836", "Drug": "Anti-PD-1 and romidepsin", "Drug_category": "others/combination", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Combination", "PMID": "26964571", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": null, "Dose": "Romidepsin - i.p. (2 mg/kg) on days 14, 16 and 18 after tumor inoculation. Anti-PD-1 - i i.p. (300 μg/mouse per injection) on days 15, 17 and 19 after tumor inoculation", "Technique": "RT-PCR, Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD4 and CD8 T IFNγ Cxcl10 and Cxcl9", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CXCL9 / MIG; CXCL10 / IP-10; CD4; CD8", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06637", "Drug_Pubchem": "57515973", "Animal_Strain_used": "129S4/SvJaeJ", "Cell_line_used_to_induce_tumor_in_mice": "LKR cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1838", "Drug": "Trametinib + ALT-803", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "26980764", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Tumors", "System": null, "Dose": "trametinib (1.0 mg/kg) from day 9–13. On day 10, Cell Trace labelled OT-I T cells (CD45.2+) were injected i.p. and mice were treated i.p. with ALT-803 (0.2 mg/kg) or PBS", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "overcome trametinib-induced CD8+ T cell suppression in the tumor microenvironment.", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "Ly5.1 (CD45.1+)", "Cell_line_used_to_induce_tumor_in_mice": "ID8-OVA cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1840", "Drug": "Cediranib and MEDI3617", "Drug_category": "others/combination", "Drugbank_ID": "DB04849", "Target/s_or_mechanism_of_action": "Cediranib inhibits vacular endothelial growth factor (VEGF) receptor tyrosine kinase (RTK).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OCCCN1CCCC1)N=CN=C2OC1=C(F)C2=C(NC(C)=C2)C=C1", "Single/Combination": "Combination", "PMID": "27044097", "Cancer_Type": "Brain cancer", "Cancer_Type_Description": "Glioblastoma", "System": null, "Dose": "cediranib (6 mg/kg) + MEDI3617 (10 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "M1/M2 ratio", "Controlled_Terms_Function_enhanced_Number_increased": "M1 macrophage phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08881", "Drug_Pubchem": "9933475", "Animal_Strain_used": "nude or C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Gl261 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1841", "Drug": "MEDI3617", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "27044097", "Cancer_Type": "Brain cancer", "Cancer_Type_Description": "Glioblastoma", "System": null, "Dose": "MEDI3617 (10 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "increased TAMs compared with cediranib-treated tumors", "Controlled_Terms_Function_enhanced_Number_increased": "Tumor-associated macrophages / TAMs", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "nude or C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Gl261 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1850", "Drug": "CD40 monoclonal antibody (mAb) therapy + sunitinib", "Drug_category": "others/combination", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Combination", "PMID": "27385210", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "30 μg agonistic rat-anti-mouse CD40 antibody +sunitinib- dose of 50 mg/kg", "Technique": "Flow cytometry,Immunofluorescence Staining", "Controlled_Technique": "Flow cytometry; Immunofluorescence assay; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "CD86 on cDCs (B220−CD11b+/−CD11c+), intratumoral CD8+ T-cells ICAM-1 and VCAM-1", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD86; CD11b / ITGAM; CD11c / ITGAX; T cells; VCAM-1; ICAM-1 / CD54", "Immune_System-Function_inhibited/numbers_decreased": "CD11b+Gr1+ MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Murine B16.F10 melanoma", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1852", "Drug": "Cetuximab + IL-21", "Drug_category": "others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "27435400", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Adenocarcinoma", "System": null, "Dose": "5 μg IL-21, 0.5 mg/kg cetuximab", "Technique": "NK cells depletion studies", "Controlled_Technique": "Immune suppression/blocking/depletion assay", "Immune_System-Function_enhanced/numbers_increased": "NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03455", "Drug_Pubchem": "46507042", "Animal_Strain_used": "01B74 nude athymic nude", "Cell_line_used_to_induce_tumor_in_mice": "Panc02EGFR tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1853", "Drug": "Imatinib + PD-1/PD-L1 blockade", "Drug_category": "others/combination", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Combination", "PMID": "27470968", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastrointestinal Stromal Tumor (GIST)", "System": null, "Dose": null, "Technique": "Flow cytometry, Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "intratumoral cytokine-producing CD8+ T cells.", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "PD-1 and PD-L1 expression on tumor cells phosphorylated KIT, phosphorylated STAT1, IDO and TGFβ and its upstream mediator phosphorylated SMAD2", "Controlled_Terms_Function_inhibited_Number_decreased": "TGF-β; PD-L1 / CD274; PD-1 / PDCD1; Immune checkpoint pathway; STAT1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": "5291", "Animal_Strain_used": "KitV558Δ/+", "Cell_line_used_to_induce_tumor_in_mice": "spontaneous", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1857", "Drug": "Dabrafenib plus trametinib", "Drug_category": "others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "27622011", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - SM1 Murine Melanoma", "System": null, "Dose": "30 mg/kg of dabrafenib or/and 0.6mg/kg of trametinib", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+CD8+cells, CD3+CD4+cells, Ly6ClowLy6GhighCD11b+ (PMN-MDSC), Ly6ChighLy6GlowCD11b+ (MO-MDSC), F4/80+CD11b+ (TAMS), CD4+\n CD25+ FOXp3+ (Tregs) PD-L1", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD3; CD25 / IL2RA; CD11b / ITGAM; PD-L1 / CD274; FOXP3; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; PMN-MDSCs / granulocytic MDSCs; Tumor-associated macrophages / TAMs; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064, D10175", "Drug_Pubchem": "44462760, 11707110", "Animal_Strain_used": "BRAFV600E mutant transgenic", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1858", "Drug": "Dabrafenib+ trametinib +anti-\n PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "27622011", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - SM1 Murine Melanoma", "System": null, "Dose": "30 mg/kg of dabrafenib or/and 0.6mg/kg of trametinib", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+CD8+cells, CD3+CD4+cells, Ly6ClowLy6GhighCD11b+ (PMN-MDSC), Ly6ChighLy6GlowCD11b+ (MO-MDSC), F4/80+CD11b+ (TAMS), CD4+\n CD25+ FOXp3+ (Tregs) PD-L1", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD3; CD25 / IL2RA; CD11b / ITGAM; PD-L1 / CD274; FOXP3; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; PMN-MDSCs / granulocytic MDSCs; Tumor-associated macrophages / TAMs; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064, D10175", "Drug_Pubchem": "44462760, 11707110", "Animal_Strain_used": "BRAFV600E mutant transgenic", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1859", "Drug": "Dabrafenib+anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB08912", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1", "Single/Combination": "Combination", "PMID": "27622011", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "30 mg/kg of dabrafenib + 4 doses of 200 ug of PD-1", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD3+CD8+ cells in the tumors,CD3+CD4+ cells in the tumors,", "Controlled_Terms_Unaffected": "CD4; CD8; CD3", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064", "Drug_Pubchem": "44462760", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1860", "Drug": "Dabrafenib+trametinib", "Drug_category": "others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "27622011", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "30 mg/kg of dabrafenib+0.6mg/kg of trametinib", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+CD8+ cells in the tumors,CD3+CD4+ cells in the tumors, MDSCs (CD11b+) in the tumors and spleens, mature TAMs\n (F4/80+CD11b+) in tumors, CD4+CD25+FOXp3+ Tregs in tumors PD-L1", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD3; CD25 / IL2RA; CD11b / ITGAM; PD-L1 / CD274; FOXP3; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; Tumor-associated macrophages / TAMs; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064, D10175", "Drug_Pubchem": "44462760, 11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1861", "Drug": "Dabrafenib+Trametinib+anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "27622011", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "30 mg/kg of dabrafenib+0.6mg/kg of trametinib+4 doses of 200 ug of PD-1", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+CD8+ cells in the tumors,CD3+CD4+ cells in the tumors, MDSCs (CD11b+) in the tumors and spleens, mature TAMs\n (F4/80CCD11bC) in tumors, CD4+CD25+FOXp3+ Tregs in tumors PD-L1", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD3; CD25 / IL2RA; CD11b / ITGAM; PD-L1 / CD274; FOXP3; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; Tumor-associated macrophages / TAMs; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064, D10175", "Drug_Pubchem": "44462760, 11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "SM1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1865", "Drug": "Sunitinib +LCP-Trp2 vaccine- targeted polymeric micelle nano-delivery system (SUNb-PM)", "Drug_category": "others/combination", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Combination", "PMID": "27863995", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "VAC was injected on day 14 at a dose of 0.3 mg/kg; SUNOS and SUNb-PM were p.o. or i.v. administered on days 14, 16, and 18 at a dose of 30 mg/kg or 10 mg/kg, respectively.", "Technique": "Flow cytometry, Western blot analysis,RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "cytotoxic T-cell infiltration Th1 cytokine expression", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; Th1 / type 1 T-cell response; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs and Tregs Stat3 and AKT", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; STAT3 signaling; AKT signaling", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "B16F10 melanoma cell lines", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1866", "Drug": "Celecoxib and sunitinib", "Drug_category": "others/combination", "Drugbank_ID": "DB00482, DB01268", "Target/s_or_mechanism_of_action": "celecoxib is a selective noncompetitive inhibitor of cyclooxygenase-2 (COX-2) enzyme. \n sunitinib Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=CC=C(C=C1)C1=CC(=NN1C1=CC=C(C=C1)S(N)(=O)=O)C(F)(F)F,\n CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Combination", "PMID": "27926489", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma", "System": null, "Dose": "sunitinib 40 mg/kg/d", "Technique": "Flow Cytometry, Western Blot", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "CD4+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; T cells; CD4+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs, Tregs STAT-3", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00567,D06402", "Drug_Pubchem": "2662, 5329102", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "Renca cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1869", "Drug": "Trametinib + PLX4720", "Drug_category": "others/combination", "Drugbank_ID": "DB08911, DB06999", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity. \n PLX4720 Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1,\n CCCS(=O(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "28123875", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "BRAFi [B] PLX4720 was provided in chow; MEKi [M] trametinib was dosed by daily oral gavage at 15 µg (on average 0.75 mg/kg)", "Technique": "Flow Cytometry, Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD3+ T cell infiltration, CD4+ and CD8+ T cell subsets ,Tregs and cancer-associated B cells,intratumoral IFNγ positive CD8+ T cells intratumoral IFNγ positive CD8+ T cells The infiltrating CD8+ T cells expressed high levels of PD-1 in about 50% of the cells , a marker shown to be associated with tumor-antigen-specific T cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; CD3; PD-1 / PDCD1; Regulatory T cells / Tregs; B cells; T cells; CD8+ T cells; Antigen-specific recognition; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "macrophages with a M2-like phenotype PD-L1", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; Macrophages; Immune checkpoint pathway; M2 macrophage phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110, 24180719", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "D4M.3A mouse melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1870", "Drug": "Trametinib + PLX4720 + anti-PD-1 combination", "Drug_category": "others/combination", "Drugbank_ID": "DB08911, DB06999", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity. \n PLX4720 Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1,\n CCCS(=O(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "28123875", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "BRAFi [B] PLX4720 was provided in chow; MEKi [M] trametinib was dosed by daily oral gavage at 15 µg (on average 0.75 mg/kg); PI3Ki [P] BKM120 daily oral gavage at 400 µg (on average 20 mg/kg) + anti-PD-1 or isotype mAb (twice weekly 100 µg intraperitoneal", "Technique": "Flow Cytometry, Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "infiltrating CD3+ T cells, IFNγ+ CD8+ T cell proportion, the granzyme B+ CD8+ T cell", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; CD3; T cells; CD8+ T cells; Granzyme B / GZMB; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110, 24180719", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "D4M.3A mouse melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1871", "Drug": "Trametinib + PLX4720 + BKM120", "Drug_category": "others/combination", "Drugbank_ID": "DB08911, DB06999, DB11666", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity. \n PLX4720 Target: Serine/threonine-protein kinase B-raf,\n Buparlisib has been used in trials studying the treatment and basic science of Lymphoma, Metastases, Lung Cancer, Solid Tumors, and Breast Cancer, among others.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1,\n CCCS(=O(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F, \n NC1=CC(=C(C=N1)C1=NC(=NC(=C1)N1CCOCC1)N1CCOCC1)C(F)(F)F", "Single/Combination": "Combination", "PMID": "28123875", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "BRAFi [B] PLX4720 was provided in chow; MEKi [M] trametinib was dosed by daily oral gavage at 15 µg (on average 0.75 mg/kg); PI3Ki [P] BKM120 daily oral gavage at 400 µg (on average 20 mg/kg)", "Technique": "Flow Cytometry, Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "increased CD3+ T cell, Tregs and cancer-associated B cells, intratumoral IFNγ positive CD8+ T cells intratumoral IFNγ positive CD8+ T cells The infiltrating CD8+ T cells expressed high levels of PD-1 in about 50% of the cells , a marker shown to be associated with tumor-antigen-specific T cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; CD3; PD-1 / PDCD1; Regulatory T cells / Tregs; B cells; T cells; CD8+ T cells; Antigen-specific recognition; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "macrophages with a M2-like phenotype PD-L1", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; Macrophages; Immune checkpoint pathway; M2 macrophage phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175, \n D10584", "Drug_Pubchem": "11707110, 24180719, 16654980", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "D4M.3A mouse melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1872", "Drug": "Trametinib + PLX4720 + BKM120 + anti-PD-1 combination", "Drug_category": "others/combination", "Drugbank_ID": "DB08911, DB06999, DB11666", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity. \n PLX4720 Target: Serine/threonine-protein kinase B-raf,\n Buparlisib has been used in trials studying the treatment and basic science of Lymphoma, Metastases, Lung Cancer, Solid Tumors, and Breast Cancer, among others.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1,\n CCCS(=O(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F, \n NC1=CC(=C(C=N1)C1=NC(=NC(=C1)N1CCOCC1)N1CCOCC1)C(F)(F)F", "Single/Combination": "Combination", "PMID": "28123875", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "BRAFi [B] PLX4720 was provided in chow; MEKi [M] trametinib was dosed by daily oral gavage at 15 µg (on average 0.75 mg/kg); PI3Ki [P] BKM120 daily oral gavage at 400 µg (on average 20 mg/kg) + anti-PD-1 or isotype mAb (twice weekly 100 µg intraperitoneal", "Technique": "Flow Cytometry, Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "infiltrating CD3+ T cells, IFNγ+ CD8+ T cell proportion, the granzyme B+ CD8+ T cell", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; CD3; T cells; CD8+ T cells; Granzyme B / GZMB; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175, \n D10584", "Drug_Pubchem": "11707110, 24180719, 16654980", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "D4M.3A mouse melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1873", "Drug": "Vorinostat +IKK inhibitor -Bay 117085", "Drug_category": "others/combination", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "28167529", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": null, "Dose": "IKK inhibitor -Bay 117085 (5 mg/kg) and vorinostat (50 mg/kg)", "Technique": "ELISA, Western Blotting,Densitometry", "Controlled_Technique": "Western blot/immunoblot analysis; Enzyme-linked immunosorbent assay (ELISA); Immunostaining/image analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "proangiogenic chemokine IL-8 (CXCL-8)", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-8 / CXCL8", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06320", "Drug_Pubchem": "5311", "Animal_Strain_used": "athymic nude", "Cell_line_used_to_induce_tumor_in_mice": "SKOV3 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1877", "Drug": "Sorafenib +HER-2-targeted cellular vaccine (3T3neuGM)", "Drug_category": "others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "28282575", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Breast Tumor", "System": null, "Dose": "(30 mg/kg)", "Technique": "ELISPOT assay", "Controlled_Technique": "ELISpot/FluoroSpot assay", "Immune_System-Function_enhanced/numbers_increased": "CD4+ and CD8+ T cells,41BB receptor expression on Thy1.2+ HER-2-specific CD8+ T cell IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "regulatory T cells and MDSC", "Controlled_Terms_Unaffected": "Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "FVB/N", "Cell_line_used_to_induce_tumor_in_mice": "NT2.5 tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1881", "Drug": "JQ1, an inhibitor of the BET family of bromodomain proteins", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "JQ1 is a thienotriazolodiazepine and a potent inhibitor of the BET family of bromodomain proteins which include BRD2, BRD3, BRD4, and the testis-specific protein BRDT in mammals. BET inhibitors structurally similar to JQ1 are being tested in clinical trials for a variety of cancers including NUT midline carcinoma.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "O=C(C[C@H]1C2=NN=C(N2C3=C(C(C4=CC=C(C=C4)Cl)=N1)C(C)=C(S3)C)C)OC(C)(C)C", "Single/Combination": "Single Drug", "PMID": "28408401", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": null, "Dose": "25 mg/kg daily", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD4+Foxp3+ Tregs Foxp3, CTLA-4, and PD-1-on CD4+Foxp3+ Tregs phospho-STAT5,", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; PD-1 / PDCD1; CTLA-4; FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "46907787", "Animal_Strain_used": "Genetically engineered harboring Kras+/LSL-G12DTrp53L/L (KP)", "Cell_line_used_to_induce_tumor_in_mice": "For lung tumor induction, mice received 1 × 106 CFU Cre-encoding adenovirus intranasally at 5–6 weeks of age", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1883", "Drug": "Entinostat and azacytidine", "Drug_category": "others/combination", "Drugbank_ID": "DB11841, DB00928", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers.\n As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1, \n NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Combination", "PMID": "28498806", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": null, "Dose": "azacytidine 2mg/kg, entinostat 5mg/kg", "Technique": "Quantitative PCR", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CIITA,CD74 expression, HLA-DPA1", "Controlled_Terms_Function_enhanced_Number_increased": "CIITA", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338,\n D03021", "Drug_Pubchem": "4261, 9444", "Animal_Strain_used": "SCID", "Cell_line_used_to_induce_tumor_in_mice": "ovarian PDX tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1884", "Drug": "Entinostat and azacytidine", "Drug_category": "others/combination", "Drugbank_ID": "DB11841, DB00928", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers.\n As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1, \n NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Combination", "PMID": "28498806", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": null, "Dose": "azacytidine 2 mg/kg, entinostat 5 mg/kg", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC II and CD74 proteins in ovarian tumors", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class II", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338,\n D03021", "Drug_Pubchem": "4261, 9444", "Animal_Strain_used": "MISIIR-Tag", "Cell_line_used_to_induce_tumor_in_mice": "spontaneously develop ovarian tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1886", "Drug": "Vorinostat (V) + mithramycin A (MA)", "Drug_category": "others/combination", "Drugbank_ID": "vorinostat (V): DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM). Mithramycin (also known as Plicamycin) is an antineoplastic antibiotic produced by Streptomyces plicatus. Mithramycin A is a DNA/RNA polymerase inhibitor, DNA-binding transcriptional inhibitor, antibiotic, and observed to facilitate tumor necrosis factor (TNF)-α and Fas ligand-induced apoptosis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1,\n C[C@@H]1[C@H]([C@@H](C[C@@H](O1)O[C@@H]2C[C@@H](O[C@@H]", "Single/Combination": "Combination", "PMID": "28536458", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin Cancer - Merkel Cell Carcinoma-Skin Cancer", "System": null, "Dose": "60mg/kg vorinostat in combination with 0.2 mg/kg", "Technique": "Immunohistochemistry,RT-qPCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "HLA class-I surface expression APM components LMP2, LMP7 and TAP2", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I; TAP2; Antigen processing and presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "vorinostat (V): D06320", "Drug_Pubchem": "vorinostat (V): 5311", "Animal_Strain_used": "NOD.CB17/Prkdc scid", "Cell_line_used_to_induce_tumor_in_mice": "WaGa tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1888", "Drug": "UNC2025 plus XRT", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "28605477", "Cancer_Type": "Brain cancer", "Cancer_Type_Description": "Glioblastoma", "System": null, "Dose": "external beam radiotherapy (XRT) (5 Gy q.o.d. fractions on days 7, 9, and 11) + UNC2025 (65 mg/kg via oral gavage daily starting day 7", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "GAMs with M2 phenotype", "Controlled_Terms_Function_inhibited_Number_decreased": "M2 phenotype-associated glioma-associated macrophages (GAMs)", "Immune_System_function_unaffected": "F4-80+ cells", "Controlled_Terms_Unaffected": "F4-80+ cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57Bl/6", "Cell_line_used_to_induce_tumor_in_mice": "TRP-MSCV-luc cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1889", "Drug": "XRT", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "28605477", "Cancer_Type": "Brain cancer", "Cancer_Type_Description": "Glioblastoma", "System": null, "Dose": "external beam radiotherapy (XRT) (5 Gy q.o.d. fractions on days 7, 9, and 11)", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "F4-80+ cells", "Controlled_Terms_Unaffected": "F4-80+ cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57Bl/6", "Cell_line_used_to_induce_tumor_in_mice": "TRP-MSCV-luc cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1891", "Drug": "Entinostat + anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "28698201", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma", "System": null, "Dose": "entinostat (5mg/kg), anti-PD-1 (10mg/kg)", "Technique": "Flow Cytometry, Proteome Profiler Analysis (Ary028)", "Controlled_Technique": "Flow cytometry; Protein array/profiler assay", "Immune_System-Function_enhanced/numbers_increased": "tumor infiltrating CD8+ T cells IL-1ra and innate anti-tumor response (IL-4 & IL-12p40), T cell attractants & anti-endothelial markers (CXCL9, CXCL10 ), tumor proliferation inhibitory cytokines (IL-4 & IL-13 ), T cell chemoattractant (E-selectin ), and anti-tumor marker (IL-12p40 )", "Controlled_Terms_Function_enhanced_Number_increased": "IL-4; IL-12; IL-13; CXCL9 / MIG; CXCL10 / IP-10; CD8; T cells; CD8+ T cells; Cell proliferation / Ki-67; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "CD4+FoxP3+ cells, TAMs MDSC activation cytokines-G-CSF, GM-CS, IL-1β & IL-10 (despite increase in number of MDSC,s)", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-1 family; IL-10; G-CSF; CD4; FOXP3; Myeloid-derived suppressor cells / MDSCs; Tumor-associated macrophages / TAMs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "BALB/c or C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "luciferin tagged RENCA cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1894", "Drug": "Regorafenib and NU", "Drug_category": "others/combination", "Drugbank_ID": "DB08896", "Target/s_or_mechanism_of_action": "Regorafenib is a small molecule inhibitor of multiple membrane-bound and intracellular kinases involved in normal cellular functions and in pathologic processes such as oncogenesis, tumor angiogenesis, and maintenance of the tumor microenvironment. \n NU7441 (KU-57788) is a highly potent and selective DNA-PK inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=CC(OC2=CC(F)=C(NC(=O)NC3=CC=C(Cl)C(=C3)C(F)(F)F)C=C2)=CC=N1, \n C1COCCN1C2=CC(=O)C3=C(O2)C(=CC=C3)C4=CC=CC5=C4SC6=CC=CC=C56", "Single/Combination": "Combination", "PMID": "28775208", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "NU7026 (6 mg/kg) + Reg (8 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "intratumoral CD45+ leukocytes and CD8+ T cells MHC-I", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD45; MHC class I; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "CD155, semaphorin 4D, CEACAM1, and galectin-9", "Controlled_Terms_Function_inhibited_Number_decreased": "CD155 / PVR", "Immune_System_function_unaffected": "intratumoral dendritic cells, macrophages, myeloid-derived suppressor cells, or natural killer cells", "Controlled_Terms_Unaffected": "Myeloid-derived suppressor cells / MDSCs; Macrophages; Dendritic cells; NK cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10138", "Drug_Pubchem": "11167602, 11327430", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "B16-F1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1897", "Drug": "Anti-CTLA-4 + MEK inhibitor selumetinib", "Drug_category": "others/combination", "Drugbank_ID": "DB11689", "Target/s_or_mechanism_of_action": "The mechanism of action of selumetinib is as a Mitogen-Activated Protein Kinase Kinase 1 Inhibitor, and Mitogen-Activated Protein Kinase Kinase 2 Inhibitor.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C=NC2=C(F)C(NC3=C(Cl)C=C(Br)C=C3)=C(C=C12)C(=O)NOCCO", "Single/Combination": "Combination", "PMID": "28807001", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "25 mg/kg, twice daily", "Technique": "Flow Cytometry Analysis", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "tumor-infiltrating CD8+ T-cell, intratumoral MHC-II+ Ly6C+ intermediary differentiating monocytes", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; MHC class II; Monocytes; T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "tumor-infiltrating Tregs, tumor-infiltrating gMDSC/neutrophil , MHCIIlo/− TAMs and pDCs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs; PMN-MDSCs / granulocytic MDSCs; Tumor-associated macrophages / TAMs; Neutrophils / granulocytes; Immune-cell infiltration", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09666", "Drug_Pubchem": "10127622", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1899", "Drug": "Pemetrexed + sildenafil", "Drug_category": "others/combination", "Drugbank_ID": "DB00642, DB00203", "Target/s_or_mechanism_of_action": "Pemetrexed is an antifolate containing the pyrrolopyrimidine-based nucleus that exerts its antineoplastic activity by disrupting folate-dependent metabolic processes essential for cell replication. \n sildenafil is a potent and selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5) in the corpus cavernosum, where PDE5 is responsible for degradation of cGMP", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)C2=C(NC=C2CCC2=CC=C(C=C2)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N1,\n CCCC1=NN(C)C2=C1N=C(NC2=O)C1=CC(=CC=C1OCC)S(=O)(=O)N1CCN(C)CC1", "Single/Combination": "Combination", "PMID": "28812434", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": null, "Dose": "pemetrexed (Day 1, 25\n mg/kg) C sildenafil (Days 1–3, 5.0 mg/kg)], sodium valproate\n (50 mg/kg)", "Technique": "Immuno-Histochemical Analyses", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "M1 macrophages, NK cells, total T cell levels and activated T cell levels, MHCA", "Controlled_Terms_Function_enhanced_Number_increased": "Macrophages; NK cells; T cells; M1 macrophage phenotype", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07472, \n D08514", "Drug_Pubchem": "446556, \n 5212", "Animal_Strain_used": "C57/BL6", "Cell_line_used_to_induce_tumor_in_mice": "0.5x106 Lewis Lung Carcinoma cancer cell", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1900", "Drug": "Pemetrexed + sildenafil + anti CTLA 4", "Drug_category": "others/combination", "Drugbank_ID": "DB00642, DB00203", "Target/s_or_mechanism_of_action": "Pemetrexed is an antifolate containing the pyrrolopyrimidine-based nucleus that exerts its antineoplastic activity by disrupting folate-dependent metabolic processes essential for cell replication. \n sildenafil is a potent and selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5) in the corpus cavernosum, where PDE5 is responsible for degradation of cGMP", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)C2=C(NC=C2CCC2=CC=C(C=C2)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N1,\n CCCC1=NN(C)C2=C1N=C(NC2=O)C1=CC(=CC=C1OCC)S(=O)(=O)N1CCN(C)CC1", "Single/Combination": "Combination", "PMID": "28812434", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": null, "Dose": "\"pemetrexed (Day 1, 25\n mg/kg) C sildenafil (Days 1–3, 5.0 mg/kg)], sodium valproate\n (50 mg/kg)\" + anti-CTLA4 IgG (100 mg)", "Technique": "Immuno-Histochemical Analyses", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "MHCA", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07472, \n D08514", "Drug_Pubchem": "446556, \n 5212", "Animal_Strain_used": "C57/BL6", "Cell_line_used_to_induce_tumor_in_mice": "0.5x106 Lewis Lung Carcinoma cancer cell", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1901", "Drug": "Pemetrexed + sildenafil + Anti PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB00642, DB00203", "Target/s_or_mechanism_of_action": "Pemetrexed is an antifolate containing the pyrrolopyrimidine-based nucleus that exerts its antineoplastic activity by disrupting folate-dependent metabolic processes essential for cell replication. \n sildenafil is a potent and selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5) in the corpus cavernosum, where PDE5 is responsible for degradation of cGMP", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)C2=C(NC=C2CCC2=CC=C(C=C2)C(=O)N[C@@H](CCC(O)=O)C(O)=O)N1,\n CCCC1=NN(C)C2=C1N=C(NC2=O)C1=CC(=CC=C1OCC)S(=O)(=O)N1CCN(C)CC1", "Single/Combination": "Combination", "PMID": "28812434", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": null, "Dose": "\"pemetrexed (Day 1, 25\n mg/kg) C sildenafil (Days 1–3, 5.0 mg/kg)], sodium valproate\n (50 mg/kg)\" + anti-PD-1\n IgG (100 mg)", "Technique": "Immuno-Histochemical Analyses", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "M1 macrophages, NK cells, total T cell levels and activated T cell levels, MHCA", "Controlled_Terms_Function_enhanced_Number_increased": "Macrophages; NK cells; T cells; M1 macrophage phenotype", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07472, \n D08514", "Drug_Pubchem": "446556, \n 5212", "Animal_Strain_used": "C57/BL6", "Cell_line_used_to_induce_tumor_in_mice": "0.5x106 Lewis Lung Carcinoma cancer cell", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1903", "Drug": "NK cells + entinostat", "Drug_category": "others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "28919994", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Osteosarcoma", "System": null, "Dose": "Mice received 5 mg/kg of entinostat or 200 μL of DMSO (control) by oral gavage three times a week for 5 weeks. A total of 50 × 106 NK cells were injected via the tail vein twice a week for 5 weeks", "Technique": "Quantitative RT-PCR,bioluminescent imaging (BLI),immunohistochemical staining", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunohistochemistry (IHC); Bioluminescence/luciferase assay", "Immune_System-Function_enhanced/numbers_increased": "MICA and MICB", "Controlled_Terms_Function_enhanced_Number_increased": "NKG2D ligand / receptor pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "overall survival of mice treated with NK cells + entinostat was not improved", "Controlled_Terms_Unaffected": "NK cells; Survival outcome", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "nu/nu", "Cell_line_used_to_induce_tumor_in_mice": "LM7 cells/ genetically modified LM7 OS cell line that expresses firefly luciferase to identify onset of micrometastasis in the lung more precisely", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1906", "Drug": "Trametinib and α-OX-40 antibody", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "28928458", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "trametinib (1 mg/kg/daily)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8 T-cell frequency, proliferation was also enhanced in CD8+ T cells, IFNγ production from CD4+ FOXP3− T cells and enhanced proliferation of these T cells, macrophages (CD11b+ F4/80+) IFNγ production by CD8+ T cells T-cell markers such as Tbet+ and CCR7+, associated with a TH1-like memory response", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; CD11b / ITGAM; FOXP3; Macrophages; T cells; Th1 / type 1 T-cell response; CD8+ T cells; Cell proliferation / Ki-67", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs (CD11b+ Ly6C+)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "AT3ova", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1907", "Drug": "Trametinib with α-4-1BB", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "28928458", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "trametinib (1 mg/kg/daily)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8 T-cell frequency, proliferation was also enhanced in CD8+ T cells, IFNγ production from CD4+ FOXP3− T cells and enhanced proliferation of these T cells, macrophages (CD11b+ F4/80+) IFNγ production by CD8+ T cells T-cell markers such as Tbet+ and CCR7+, associated with a TH1-like memory response", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; CD11b / ITGAM; FOXP3; Macrophages; T cells; Th1 / type 1 T-cell response; CD8+ T cells; Cell proliferation / Ki-67", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs (CD11b+ Ly6C+)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "AT3ova", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1908", "Drug": "7A7", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29056908", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung", "System": null, "Dose": "7A7 (56 μg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "a strong induction of H-2Kb and H-2Db expression, MHC-I expression", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "D122", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2000", "Drug": "Anti -PD-1 +peptide R", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "31661001", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - B16 Melanoma", "System": null, "Dose": "murine anti-PD-1 [RMP1–14] (5 mg/kg, twice week for 2 weeks), Pep R (2 mg/kg, 5 days per week for 2 weeks)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Granzyme B (GRZB) positive immune cells, ratio CD8+ T cells/Tregs", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Regulatory T cells / Tregs; T cells; CD8+ T cells; Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": "FoxP3 positive Treg cells,pDC (CD 45+ cells) CXCR4 decreased in tumors", "Controlled_Terms_Function_inhibited_Number_decreased": "FOXP3; Regulatory T cells / Tregs; CXCR4", "Immune_System_function_unaffected": "PD-1 expression", "Controlled_Terms_Unaffected": "PD-1 / PDCD1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57Bl/6", "Cell_line_used_to_induce_tumor_in_mice": "B16-hCXCR4 (5 × 105)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1910", "Drug": "Pazopanib + anti-PD-1 IgG", "Drug_category": "others/combination", "Drugbank_ID": "DB06589", "Target/s_or_mechanism_of_action": "Pazopanib is a second-generation multitargeted tyrosine kinase inhibitor against vascular endothelial growth factor receptor-1, -2, and -3, platelet-derived growth factor receptor-alpha, platelet-derived growth factor receptor-beta, and c-kit.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN(C1=CC2=NN(C)C(C)=C2C=C1)C1=CC=NC(NC2=CC=C(C)C(=C2)S(N)(=O)=O)=N1", "Single/Combination": "Combination", "PMID": "29137331", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "pazopanib 25 mg/kg (Days 1, 2, 3)+ anti-PD-1 IgG (100 μg)", "Technique": "Immuno-Histostaining", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "F4/80+\n macrophages (M1 macrophages), NK cells, neutrophils and activated\n T cells", "Controlled_Terms_Function_enhanced_Number_increased": "Macrophages; Neutrophils / granulocytes; NK cells; T cells; M1 macrophage phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D05380", "Drug_Pubchem": "10113978", "Animal_Strain_used": "C57B6", "Cell_line_used_to_induce_tumor_in_mice": "mouse B16 melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1911", "Drug": "Pazopanib + AR42", "Drug_category": "others/combination", "Drugbank_ID": "DB06589,DB12707", "Target/s_or_mechanism_of_action": "Pazopanib is a second-generation multitargeted tyrosine kinase inhibitor against vascular endothelial growth factor receptor-1, -2, and -3, platelet-derived growth factor receptor-alpha, platelet-derived growth factor receptor-beta, and c-kit.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN(C1=CC2=NN(C)C(C)=C2C=C1)C1=CC=NC(NC2=CC=C(C)C(=C2)S(N)(=O)=O)=N1,\n CC(C)[C@H](C(=O)NC1=CC=C(C=C1)C(=O)NO)C1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "29137331", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "pazopanib 25 mg/kg (Days 1, 2, 3)+AR42 15 mg/kg (Days 1 and 3)", "Technique": "Immuno-Histostaining", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "F4/80+\n macrophages (M1 macrophages), NK cells, neutrophils and activated\n T cells", "Controlled_Terms_Function_enhanced_Number_increased": "Macrophages; Neutrophils / granulocytes; NK cells; T cells; M1 macrophage phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D05380", "Drug_Pubchem": "10113978, 6918848", "Animal_Strain_used": "C57B6", "Cell_line_used_to_induce_tumor_in_mice": "mouse B16 melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1912", "Drug": "Pazopanib + AR42 + anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB06589,DB12707", "Target/s_or_mechanism_of_action": "Pazopanib is a second-generation multitargeted tyrosine kinase inhibitor against vascular endothelial growth factor receptor-1, -2, and -3, platelet-derived growth factor receptor-alpha, platelet-derived growth factor receptor-beta, and c-kit.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN(C1=CC2=NN(C)C(C)=C2C=C1)C1=CC=NC(NC2=CC=C(C)C(=C2)S(N)(=O)=O)=N1,\n CC(C)[C@H](C(=O)NC1=CC=C(C=C1)C(=O)NO)C1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "29137331", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "pazopanib 25 mg/kg (Days 1, 2, 3)+ AR42 15 mg/kg (Days 1 and 3)+ anti-PD-1 IgG (100 μg)", "Technique": "Immuno-Histostaining", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "F4/80+\n macrophages (M1 macrophages), NK cells, neutrophils and activated\n T cells IL-6, IL-12, CCL2, CCL3,\n CCL5, CXCL9 and CXCL2, TGF\n beta", "Controlled_Terms_Function_enhanced_Number_increased": "IL-6; IL-12; CCL2 / MCP-1; CCL3 / MIP-1α; CCL5 / RANTES; CXCL9 / MIG; Macrophages; Neutrophils / granulocytes; NK cells; T cells; M1 macrophage phenotype", "Immune_System-Function_inhibited/numbers_decreased": "IL1a\n levels", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-1 family", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D05380", "Drug_Pubchem": "10113978, 6918848", "Animal_Strain_used": "C57B6", "Cell_line_used_to_induce_tumor_in_mice": "mouse B16 melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1913", "Drug": "Pazopanib + sodium valproate + anti-PD-1 IgG", "Drug_category": "others/combination", "Drugbank_ID": "DB06589, DB00313", "Target/s_or_mechanism_of_action": "Pazopanib is a second-generation multitargeted tyrosine kinase inhibitor against vascular endothelial growth factor receptor-1, -2, and -3, platelet-derived growth factor receptor-alpha, platelet-derived growth factor receptor-beta, and c-kit.\n Valproic acid exhibits its pharmacologic effects in a couple of ways, such as by acting on GABA (γ aminobutyric acid) levels in the CNS, blocking voltage-gated ion channels, and inhibiting histone deacetylase", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN(C1=CC2=NN(C)C(C)=C2C=C1)C1=CC=NC(NC2=CC=C(C)C(=C2)S(N)(=O)=O)=N1,\n CCCC(CCC)C(O)=O", "Single/Combination": "Combination", "PMID": "29137331", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "pazopanib 25 mg/kg (Days 1, 2, 3)+ sodium valproate 50 mg/kg (Days 1, 2, 3) + anti-PD-1 IgG (100 μg)", "Technique": "Immuno-Histostaining", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "F4/80+\n macrophages (M1 macrophages), NK cells, neutrophils and activated\n T cells IL-6, IL-12, CCL2, CCL3,\n CCL5, CXCL9 and CXCL2", "Controlled_Terms_Function_enhanced_Number_increased": "IL-6; IL-12; CCL2 / MCP-1; CCL3 / MIP-1α; CCL5 / RANTES; CXCL9 / MIG; Macrophages; Neutrophils / granulocytes; NK cells; T cells; M1 macrophage phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D05380, D00399", "Drug_Pubchem": "10113978, 3121", "Animal_Strain_used": "C57B6", "Cell_line_used_to_induce_tumor_in_mice": "mouse B16 melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1914", "Drug": "Pazopanib+ sodium valproate", "Drug_category": "others/combination", "Drugbank_ID": "DB06589, DB00313", "Target/s_or_mechanism_of_action": "Pazopanib is a second-generation multitargeted tyrosine kinase inhibitor against vascular endothelial growth factor receptor-1, -2, and -3, platelet-derived growth factor receptor-alpha, platelet-derived growth factor receptor-beta, and c-kit.\n Valproic acid exhibits its pharmacologic effects in a couple of ways, such as by acting on GABA (γ aminobutyric acid) levels in the CNS, blocking voltage-gated ion channels, and inhibiting histone deacetylase", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN(C1=CC2=NN(C)C(C)=C2C=C1)C1=CC=NC(NC2=CC=C(C)C(=C2)S(N)(=O)=O)=N1,\n CCCC(CCC)C(O)=O", "Single/Combination": "Combination", "PMID": "29137331", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "pazopanib 25 mg/kg (Days 1, 2, 3)+ sodium valproate 50 mg/kg (Days 1, 2, 3)", "Technique": "Immuno-Histostaining", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "F4/80+\n macrophages (M1 macrophages), NK cells, neutrophils and activated\n T cells", "Controlled_Terms_Function_enhanced_Number_increased": "Macrophages; Neutrophils / granulocytes; NK cells; T cells; M1 macrophage phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D05380, D00399", "Drug_Pubchem": "10113978, 3121", "Animal_Strain_used": "C57B6", "Cell_line_used_to_induce_tumor_in_mice": "mouse B16 melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1915", "Drug": "Decitabine (DAC) in combination with allogeneic NK cells generated from CD34+ hematopoietic stem and progenitor cells (HSPC-NK cells)", "Drug_category": "others/combination", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Combination", "PMID": "29138222", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": null, "Dose": "DAC (1.25 mg/m2)", "Technique": "Flow cytometry, RT PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "NK cell–mediated killing. perforin, and TRAIL NKp44 expression,upregulation of NKG2D- and DNAM-1-activating ligands on AML cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; Perforin / PRF1; NKG2D ligand / receptor pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03665", "Drug_Pubchem": "451668", "Animal_Strain_used": "NOD/SCID/IL2Rgnull (NSG)", "Cell_line_used_to_induce_tumor_in_mice": "THP-1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1918", "Drug": "Vorinostat + anti-PD-1+ anti-CTLA-4", "Drug_category": "others/combination", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "29371976", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "vorinostat (50 mg/Kg i.p.), anti-PD-1 (10 mg/Kg i.p.) combined with anti-CTLA-4 (10mg/Kg i.p.)", "Technique": "RNA in situ hybridization analysis on formalin fixed paraffin embedded (FFPE) tissues, TUNEL assay", "Controlled_Technique": "Apoptosis/cell viability assay; RNA in situ hybridization (RISH)", "Immune_System-Function_enhanced/numbers_increased": "CD4+ T cells, CD8+ T cells PD-L1 expression in tumor cells reduced the tumor burden, survival increase, apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; PD-L1 / CD274; T cells; CD8+ T cells; CD4+ T cells; Apoptosis / caspase activation; Immune checkpoint pathway; Survival outcome; Tumor growth / burden outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06320", "Drug_Pubchem": "5311", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1919", "Drug": "PD-1 Ab +sorafenib and DC-TEX", "Drug_category": "others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "29413757", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "sorafenib (50 mg/kg/day) and PD-1 Ab (200 μg)", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "AFP", "Controlled_Terms_Function_inhibited_Number_decreased": "AFP", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "hepa1-6 cell", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1921", "Drug": "Sorafenib + dendritic cells with exosomes derived from tumor cells (DC-TEX)", "Drug_category": "others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "29413757", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "50 mg/kg +DCs were pulsed with exosomes (4×106, injected intravenously)", "Technique": "Flow Cytometry, Immunohistochemistry And ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA); Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+T cells IFN-γ and IL-2", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-2; CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "CD4+CD25+FoxP3+ Tregs IL-10 and TGF-β", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-10; TGF-β; CD4; CD25 / IL2RA; FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "hepa1-6 cell", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1922", "Drug": "Imatinib + anti CD 40", "Drug_category": "others/combination", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Combination", "PMID": "29467128", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastrointestinal Stromal Tumor (GIST)", "System": null, "Dose": "one dose of an agonistic CD40 antibody (clone FGK4.5, 100 μg intraperitoneal [i.p.]) or rat IgG2a (clone 2A3, 100 μg i.p.) on day 0, which indicates first day of treatment. Imatinib (600 mg/L in drinking water; Novartis) was started on day 3 and continued until the end of the experiment,", "Technique": "Flow cytometry, Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "Macrophages and CD8+ T Cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Macrophages; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD4+ T cells and B cells", "Controlled_Terms_Unaffected": "CD4; B cells; T cells; CD4+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": "5291", "Animal_Strain_used": "KitV558Δ/+", "Cell_line_used_to_induce_tumor_in_mice": "spontaneous", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1930", "Drug": "Antibody-Drug Conjugate, Trastuzumab Deruxtecan (DS-8201a) + anti PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "29703841", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "DS-8201a (10 mg/kg once a week, twice, i.v.)+ anti-PD1 (5 mg/kg, twice a week, 2 cycles, i.v.)", "Technique": "Survival Was Analyzed By The Kaplan–Meier Method", "Controlled_Technique": "Survival analysis (Kaplan–Meier)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03257", "Drug_Pubchem": "46507516", "Animal_Strain_used": "(BALB/c)", "Cell_line_used_to_induce_tumor_in_mice": "5 million CT26.WT-hHER2 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1932", "Drug": "JQ1+ACY-1215", "Drug_category": "others/combination", "Drugbank_ID": "DB12376", "Target/s_or_mechanism_of_action": "Ricolinostat (ACY-1215) is an orally available selective HDAC6 inhibitor.\n JQ1 is a thienotriazolodiazepine and a potent inhibitor of the BET family of bromodomain proteins which include BRD2, BRD3, BRD4, and the testis-specific protein BRDT in mammals. BET inhibitors structurally similar to JQ1 are being tested in clinical trials for a variety of cancers including NUT midline carcinoma.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1, O=C(C[C@H]1C2=NN=C(N2C3=C(C(C4=CC=C(C=C4)Cl)=N1)C(C)=C(S3)C)C)OC(C)(C)C", "Single/Combination": "Combination", "PMID": "29760044", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung - Small Cell Lung Cancer", "System": null, "Dose": "JQ1(25 mg/kg daily)+ACY-1215( (50 mg/kg daily)", "Technique": "Flow Cytometery", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cells, HLA-DR expression on tumor cells MHC II on tumor cells", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class II; NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10661", "Drug_Pubchem": "53340666, 46907787", "Animal_Strain_used": "SCLC xenograft models", "Cell_line_used_to_induce_tumor_in_mice": "NCl-H60", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1933", "Drug": "JQ1+ACY-1215", "Drug_category": "others/combination", "Drugbank_ID": "DB12376", "Target/s_or_mechanism_of_action": "Ricolinostat (ACY-1215) is an orally available selective HDAC6 inhibitor.\n JQ1 is a thienotriazolodiazepine and a potent inhibitor of the BET family of bromodomain proteins which include BRD2, BRD3, BRD4, and the testis-specific protein BRDT in mammals. BET inhibitors structurally similar to JQ1 are being tested in clinical trials for a variety of cancers including NUT midline carcinoma.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1, O=C(C[C@H]1C2=NN=C(N2C3=C(C(C4=CC=C(C=C4)Cl)=N1)C(C)=C(S3)C)C)OC(C)(C)C", "Single/Combination": "Combination", "PMID": "29760044", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung - Small Cell Lung Cancer", "System": null, "Dose": "JQ1(25 mg/kg daily)+ACY-1215( (50 mg/kg daily)", "Technique": "Flow Cytometery", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cells, HLA-DR expression on tumor cells MHC II on tumor cells", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class II; NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10661", "Drug_Pubchem": "53340666, 46907787", "Animal_Strain_used": "SCLC xenograft models", "Cell_line_used_to_induce_tumor_in_mice": "GLC-16", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1935", "Drug": "Decitabine (DAC, a DNA demethylation drug) and γδ T cells", "Drug_category": "others/combination", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Combination", "PMID": "29910819", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Osteosarcoma", "System": null, "Dose": "DAC -1 µg/g of body weight, γδ T cells (5 × 107 in 100 µL PBS)", "Technique": "Western Blotting", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "MICB and ULBP1 proteins in OS tumor tissues", "Controlled_Terms_Function_enhanced_Number_increased": "NKG2D ligand / receptor pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03665", "Drug_Pubchem": "451668", "Animal_Strain_used": "BALB/c-nu", "Cell_line_used_to_induce_tumor_in_mice": "HOS cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1940", "Drug": "Romidepsin + IBET151", "Drug_category": "others/combination", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Combination", "PMID": "30249811", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "Romidepsin (1 mg/kg single dose at the time of vaccination) + IBET151 (30 mg/kg single dose at the time of vaccination)", "Technique": "Flow Cytometry, Luminex", "Controlled_Technique": "Flow cytometry; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "Gag- (epitope AL11) specific CD8+\n T cells, CD8+ T cells that produced IFN-g IL-6", "Controlled_Terms_Function_enhanced_Number_increased": "IL-6; CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "total number of circulating CD8+ T cells or the percentage of regulatory Foxp3+ CD4 T cells", "Controlled_Terms_Unaffected": "CD4; CD8; FOXP3; T cells; CD8+ T cells; CD4+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06637", "Drug_Pubchem": "57515973", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Ad5.Gag vaccination", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1941", "Drug": "Romidepsin + IBET151", "Drug_category": "others/combination", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C=C1/NC(=O)[C@H]2CSSCC\\C=C\\[C@H](CC(=O)N[C@H](C(C)C)C(=O)N2)OC(=O)[C@@H](NC1=O)C(C)C", "Single/Combination": "Combination", "PMID": "30249811", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "Ad5.SIINFEKL + Romidepsin (1 mg/kg single dose at the time of vaccination) + IBET151 (30 mg/kg single dose at the time of vaccination)", "Technique": "Flow Cytometry, Luminex", "Controlled_Technique": "Flow cytometry; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "OVA-specific SIINFEKL+CD8+\n T cells IL-6", "Controlled_Terms_Function_enhanced_Number_increased": "IL-6; CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06637", "Drug_Pubchem": "57515973", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "mice were primed with Ad26.OVA (107 vp) followed by the\n s.c. injection of 500,000 B16-OVA cells 28 d later.", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1943", "Drug": "Entinostat in combination with anti–PD-1 or anti–CTLA-4", "Drug_category": "others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "30341213", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "anti–PD-1, 100 μg/mouse via intraperitoneal injection (i.p.)or anti–CTLA-4, 100 μg/mouse,ENT dosing solution (5 mg/kg)", "Technique": "Flow Cytometry,Immunosuppression Assays,Colorimetric Arginase Activity Assay", "Controlled_Technique": "Flow cytometry; Colorimetric/biochemical activity assay; Immune suppression/blocking/depletion assay", "Immune_System-Function_enhanced/numbers_increased": "shifts the TME from an M-MDSC to a G-MDSC dominated milieu,infiltration of CD8+ T effector cells(active) improved survival", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; PMN-MDSCs / granulocytic MDSCs; Immune-cell infiltration; Survival outcome", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 expression on G-MDSC Arg-1 by MDSCs-a marker of immunosupressive activity of MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; Myeloid-derived suppressor cells / MDSCs; PMN-MDSCs / granulocytic MDSCs; Immune checkpoint pathway", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "female neu-N", "Cell_line_used_to_induce_tumor_in_mice": "NT2.5 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1996", "Drug": "Anti-CD3 + Anti-PD-1+ Trametinib 10 nm", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "31648326", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": null, "Dose": "Anti-CD3 5 ug/mL + Anti-PD-1 10 ug/mL+ Trametinib 10 nm", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 and PD-L2 expression", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; PD-L2 / PDCD1LG2; Immune checkpoint pathway", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "AML mouse model", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1944", "Drug": "Entinostat in combination with anti–PD-1 or anti–CTLA-4", "Drug_category": "others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "30341213", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Adenocarcinoma", "System": null, "Dose": "anti–PD-1, 100 μg/mouse via intraperitoneal injection (i.p.)or anti–CTLA-4, 100 μg/mouse,ENT dosing solution (5 mg/kg)", "Technique": "Flow Cytometry,Immunosuppression Assays", "Controlled_Technique": "Flow cytometry; Immune suppression/blocking/depletion assay", "Immune_System-Function_enhanced/numbers_increased": "shifts the TME from an M-MDSC to a G-MDSC dominated milieu,infiltration of CD8+ T effector cells(active) improved survival", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; PMN-MDSCs / granulocytic MDSCs; Immune-cell infiltration; Survival outcome", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 expression on G-MDSC Arg-1 by MDSCs-a marker of immunosupressive activity of MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; Myeloid-derived suppressor cells / MDSCs; PMN-MDSCs / granulocytic MDSCs; Immune checkpoint pathway", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "(Panc02)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1953", "Drug": "MEK inhibitor trametinib + anti-PD-L1", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "30546955", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": null, "Dose": "trametinib (1 mg/kg) by oral gavage once daily and/or an anti-PD-L1 mAb (10 mg/kg) by intraperitoneal (i.p.) injection twice weekly.", "Technique": "Flow cytometry,qRT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD3+CD8+ tumor infiltrating lymphocytes (TILs) CXCL9 and CXCL10 T cell activation marker CD25", "Controlled_Terms_Function_enhanced_Number_increased": "CXCL9 / MIG; CXCL10 / IP-10; CD8; CD3; CD25 / IL2RA; T cells; Tumor-infiltrating lymphocytes / TILs; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "neutrophils (CD11b+Ly6G+) Erk1/2 activation in tumor tissues", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Neutrophils / granulocytes", "Immune_System_function_unaffected": "TAMs (CD11b+F4/80+)", "Controlled_Terms_Unaffected": "CD11b / ITGAM; Tumor-associated macrophages / TAMs", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "C3H", "Cell_line_used_to_induce_tumor_in_mice": "SCCVII cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1960", "Drug": "Sunitinib and MD5-1 combination", "Drug_category": "others/combination", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Combination", "PMID": "30713805", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Mammary Carcinoma", "System": null, "Dose": "35 mg/kg", "Technique": "Flow cytometry, Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells and dendritic cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Dendritic cells; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1 mammary carcinoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1961", "Drug": "Sunitinib and MD5-1 combination", "Drug_category": "others/combination", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Combination", "PMID": "30713805", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Carcinoma", "System": null, "Dose": "35 mg/kg", "Technique": "Flow cytometry, Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells and dendritic cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Dendritic cells; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "(CT26) carcinoma", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1965", "Drug": "Trametinib+anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Combination", "PMID": "30771521", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": null, "Dose": "trametinib for three days prior to initiation of combination or single treatment follwed by MEKi (0.25, 0.5, and 1 mg/kg)+ anti-PD-1 (200ug) for three weeks", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "percentage of CD4+ and CD8+ cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8", "Immune_System-Function_inhibited/numbers_decreased": "PMN-MDSCs, CD45+/CD11b+/Ly6Ghigh/Ly6Clow", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; CD45; Myeloid-derived suppressor cells / MDSCs; PMN-MDSCs / granulocytic MDSCs", "Immune_System_function_unaffected": "monocytic-MDSCs CD45+/CD11b+/Ly6G-/Ly6Chigh", "Controlled_Terms_Unaffected": "CD11b / ITGAM; CD45; Myeloid-derived suppressor cells / MDSCs", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09996", "Drug_Pubchem": "42611257", "Animal_Strain_used": "PKL (Lung tumors were induced by Ad-Cre in the transgenic mouse model)", "Cell_line_used_to_induce_tumor_in_mice": "3 × 105 PKL5–2 cells into the right flank of mice", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1966", "Drug": "Trametinib+anti-PD-L1", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Combination", "PMID": "30771521", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": null, "Dose": "trametinib for three days prior to initiation of combination or single treatment follwed by MEKi (0.25, 0.5, and 1 mg/kg) + anti-PD-L1(200ug twice a week) for three weeks", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "percentage of CD4+ and CD8+ cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8", "Immune_System-Function_inhibited/numbers_decreased": "PMN-MDSCs, CD45+/CD11b+/Ly6Ghigh/Ly6Clow", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; CD45; Myeloid-derived suppressor cells / MDSCs; PMN-MDSCs / granulocytic MDSCs", "Immune_System_function_unaffected": "monocytic-MDSCs CD45+/CD11b+/Ly6G-/Ly6Chigh", "Controlled_Terms_Unaffected": "CD11b / ITGAM; CD45; Myeloid-derived suppressor cells / MDSCs", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09996", "Drug_Pubchem": "42611257", "Animal_Strain_used": "PKL (Lung tumors were induced by Ad-Cre in the transgenic mouse model)", "Cell_line_used_to_induce_tumor_in_mice": "3 × 105 PKL5–2 cells into the right flank of mice", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1968", "Drug": "CXCR4 inhibitor AMD 3100 /\n Plerixafor\"+ αPD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB06809", "Target/s_or_mechanism_of_action": "Plerixafor inhibits the CXCR4 chemokine receptors on CD34+ cells and reversibly blocks binding of the ligand, stromal cell-derived factor-1-alpha (SDF-1α). By blocking the interaction between SDF-1α and CXCR4 with plerixafor, mobilization of progenitor cells is triggered.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C(N1CCCNCCNCCCNCC1)C1=CC=C(CN2CCCNCCNCCCNCC2)C=C1", "Single/Combination": "Combination", "PMID": "30802149", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": null, "Dose": "AMD3100 (3 mg/kg of mouse body weight) 10 times every other day from d 20 post–tumor implantation + αPD-1 (200 μg per mouse) every other day starting from d 23 for 9 doses.", "Technique": "ELISA, Flow cytometery", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ and CD4+ T cells intratumoral filteration, FN-γ expressing on CD8+ and CD4+ T cells, CD8+ IL-2+ cells , CD44+CD27+CD4+ and CD44+CD27+CD8+ memory T cells , forkhead box P3 (FoxP3)+CD25−CD4+ T cells in the tumor, IL-2+CD40L+FoxP3+CD25− cells, M1 macrophagess F4/80+CD11b+ cells (CD163-MHCII+) IL-2", "Controlled_Terms_Function_enhanced_Number_increased": "IL-2; CD4; CD8; CD25 / IL2RA; CD40L / CD154; CD11b / ITGAM; CD163; MHC class II; FOXP3; T cells; CD4+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "CD4+FoxP3+CD25+ Treg cells in tumor, CD11b+ GR-1+ , M2 macrophages F4/80+CD11b+ cells (CD163+MHC II−) , PD-L1+CD38+ cells CXCL12", "Controlled_Terms_Function_inhibited_Number_decreased": "CXCL12 / SDF-1; CD4; CD25 / IL2RA; CD11b / ITGAM; CD163; PD-L1 / CD274; MHC class II; FOXP3; Regulatory T cells / Tregs; Macrophages; Immune checkpoint pathway; M2 macrophage phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08971", "Drug_Pubchem": "65015", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "luciferase-expressing syngeneic ID8-luc cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1969", "Drug": "ΑPD-1", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "30802149", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": null, "Dose": "αPD-1 (200 μg per mouse) every other day starting from d 23 for 9 doses.", "Technique": "ELISA, Flow cytometery", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ and CD4+ T cells intratumoral filteration, FN-γ expressing on CD8+ and CD4+ T cells, CD4+ and CD8+ memory T cells , M1 macrophagess F4/80+CD11b+ cells (CD163-MHCII+) IL-2", "Controlled_Terms_Function_enhanced_Number_increased": "IL-2; CD4; CD8; CD11b / ITGAM; CD163; MHC class II; T cells; CD4+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "M2 macrophages F4/80+CD11b+ cells (CD163+MHC II−) CXCL12", "Controlled_Terms_Function_inhibited_Number_decreased": "CXCL12 / SDF-1; CD11b / ITGAM; CD163; MHC class II; Macrophages; M2 macrophage phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "luciferase-expressing syngeneic ID8-luc cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1998", "Drug": "Anti -PD-1 +peptide R", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "31661001", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": null, "Dose": "murine anti-PD-1 [RMP1–14] (5 mg/kg, twice week for 2 weeks), Pep R (2 mg/kg, 5 days per week for 2 weeks)", "Technique": "Immunostaining, Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC); Immunostaining/image analysis", "Immune_System-Function_enhanced/numbers_increased": "Granzyme B (GRZB) positive immune cells", "Controlled_Terms_Function_enhanced_Number_increased": "Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": "FoxP3 positive Treg cells CXCR4,CXCL12 decreased in tumors PD-L1 reduction", "Controlled_Terms_Function_inhibited_Number_decreased": "CXCL12 / SDF-1; PD-L1 / CD274; FOXP3; Regulatory T cells / Tregs; Immune checkpoint pathway; CXCR4", "Immune_System_function_unaffected": "CXCR7, PD-1 expression", "Controlled_Terms_Unaffected": "PD-1 / PDCD1; CXCR7", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57Bl/6", "Cell_line_used_to_induce_tumor_in_mice": "MC38 (1 × 106)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1971", "Drug": "Nexturastat A + anti-PD-1 immune checkpoint blockade", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCCN(CC1=CC=C(C=C1)C(=O)NO)C(=O)NC2=CC=CC=C2", "Single/Combination": "Combination", "PMID": "30992475", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Murine Melanoma", "System": null, "Dose": "3 mg/kg anti-PD-1, 15 mg/kg NextA", "Technique": "Kaplan-Meier survival plot, Flow cytometry,qRT-PCR, immunoblot", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Survival analysis (Kaplan–Meier)", "Immune_System-Function_enhanced/numbers_increased": "ratio M1/M2 of TAMs, CD8+ lymphocytes in tumor,effector memory T cell, infiltration of NK and NKT cells IFNγ and IL-2 MHC class I expression, MHC class II reduction in tumor, robust increase in overall survival", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-2; CD8; MHC class II; MHC class I; Tumor-associated macrophages / TAMs; NKT cells; T cells; Immune-cell infiltration; Survival outcome", "Immune_System-Function_inhibited/numbers_decreased": "M2 macrophages, pDC , MDSC population IL-10 and TGFβ PD-L1 in tumor cells", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-10; TGF-β; PD-L1 / CD274; Myeloid-derived suppressor cells / MDSCs; Macrophages; Immune checkpoint pathway; M2 macrophage phenotype", "Immune_System_function_unaffected": "B7-H3 and B7-H4, galectin-9, ICOS-L, CD80, CD86, CD70, and HVEM", "Controlled_Terms_Unaffected": "CD80; CD86", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "71462653", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "SM1 murine melanoma tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1973", "Drug": "JQ1 (BET inhibitor) in combination with ricolinostat", "Drug_category": "others/combination", "Drugbank_ID": "DB12376", "Target/s_or_mechanism_of_action": "JQ1 is a thienotriazolodiazepine and a potent inhibitor of the BET family of bromodomain proteins which include BRD2, BRD3, BRD4, and the testis-specific protein BRDT in mammals. BET inhibitors structurally similar to JQ1 are being tested in clinical trials for a variety of cancers including NUT midline carcinoma. Ricolinostat (ACY-1215) is an orally available selective HDAC6 inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "O=C(C[C@H]1C2=NN=C(N2C3=C(C(C4=CC=C(C=C4)Cl)=N1)C(C)=C(S3)C)C)OC(C)(C)C,\n ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "31015208", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": null, "Dose": "50 mg/kg JQ1, 50 mg/kg ricolinostat intraperitoneally once per day for 5 days per week for 3 weeks", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "significant reduction in disease burden,apoptosis (active caspase-3)", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis / caspase activation", "Immune_System-Function_inhibited/numbers_decreased": "MM cell proliferation (PCNA),expression of c-MYC and BCL-2", "Controlled_Terms_Function_inhibited_Number_decreased": "Cell proliferation / Ki-67", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10661", "Drug_Pubchem": "46907787, 53340666", "Animal_Strain_used": "SCID", "Cell_line_used_to_induce_tumor_in_mice": "RPMI-8226 tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1974", "Drug": "CTGF/E7 DNA vaccine and everolimus", "Drug_category": "others/combination", "Drugbank_ID": "DB01590", "Target/s_or_mechanism_of_action": "Everolimus is a mammalian target of rapamycin (mTOR) kinase inhibitor used to treat various types of malignancies", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "[H][C@@]1(C[C@@H](C)[C@]2([H])CC(=O)[C@H](C)\\C=C(C)\\[C@@H](O)[C@@H](OC)C(=O)[C@H](C)C[C@H](C)\\C=C\\C=C\\C=C(C)\\[C@H](C[C@]3([H])CC[C@@H](C)[C@@](O)(O3)C(=O)C(=O)N3CCCC[C@@]3([H])C(=O)O2)OC)CC[C@@H](OCCO)[C@@H](C1)OC", "Single/Combination": "Combination", "PMID": "31052575", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": null, "Dose": "everolimus: 1 mg/kg , On day 11, the tumor-bearing mice were treated with 2 µg CTGF/E7 DNA vaccine twice per week for two weeks", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD86+MHC IIhi DCs in tumor-infiltrating lymphocytes (TILs), E7-specific CD8+ T cells, E7-specific IFN-γ-secreting CD8+ T cells IFN-γ CD86+MHC IIhi DCs better disease control and longer survivals", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; CD86; Dendritic cells; T cells; CD8+ T cells; Tumor-infiltrating lymphocytes / TILs; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02714", "Drug_Pubchem": "46505248", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "TC-1 tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1975", "Drug": "MCAR T cells", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31078430", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "GPC3 mCAR T cells administered on days 9 and 13 after subcutaneous injection of Hepa1-6-chGPC3 tumor cells", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Increased mCAR T cell infiltration and a higher percentage of CAR+ IFN-γ+ T cells in tumor tissues", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Hepa1-6-chGPC3 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1977", "Drug": "Sorafenib + huCAR T cells", "Drug_category": "others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "31078430", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "one dose of 2 × 106 huCAR T cells+ 7.5 mg/kg sorafenib for 2 consecutive weeks", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "huCAR T cell accumulation in tumor tissues", "Controlled_Terms_Function_enhanced_Number_increased": "T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "NOD/Scid IL2RγCnull (NSG)", "Cell_line_used_to_induce_tumor_in_mice": "GPC3+ PLC/PRF/5 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1978", "Drug": "Sorafenib + mCAR T cells", "Drug_category": "others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "31078430", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "GPC3 mCAR T cells administered on days 9 and 13 after subcutaneous injection of Hepa1-6-chGPC3 tumor cells + 7.5 mg/kg per day sorafenib from days 8 to 18", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Increased mCAR T cell infiltration and a higher percentage of CAR+ IFN-γ+ T cells in tumor tissues", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Hepa1-6-chGPC3 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1979", "Drug": "Sorafenib + mCAR T cells", "Drug_category": "others/combination", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Combination", "PMID": "31078430", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "GPC3 mCAR T cells administered on days 9 and 13 after subcutaneous injection of Hepa1-6-chGPC3 tumor cells + 30 mg/kg per day sorafenib from days 8 to 18", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Increased mCAR T cell infiltration and a higher percentage of CAR+ IFN-γ+ T cells in tumor tissues", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Hepa1-6-chGPC3 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1980", "Drug": "Fluorouracil +Docosahexaenoic acid (DHA)", "Drug_category": "others/combination", "Drugbank_ID": "DB00544,DB03756", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA, DHA inhibits endotoxin-stimulated production of IL-6 and IL-8 in human endothelial cells. Derivatives of DHA are anti-inflammatory lipid mediators.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O, \n CC\\C=C/C\\C=C/C\\C=C/C\\C=C/C\\C=C/C\\C=C/CCC(O)=O", "Single/Combination": "Combination", "PMID": "31217433", "Cancer_Type": "Thymoma", "Cancer_Type_Description": "Thymoma", "System": null, "Dose": "(50 mg/kg)", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "IL-1β release by MDSC", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-1 family; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00584,\n C06429", "Drug_Pubchem": "3385,\n 445580", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "EL4 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1981", "Drug": "Fluorouracil +Docosahexaenoic acid (DHA)", "Drug_category": "others/combination", "Drugbank_ID": "DB00544,DB03756", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA, DHA inhibits endotoxin-stimulated production of IL-6 and IL-8 in human endothelial cells. Derivatives of DHA are anti-inflammatory lipid mediators.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O, \n CC\\C=C/C\\C=C/C\\C=C/C\\C=C/C\\C=C/C\\C=C/CCC(O)=O", "Single/Combination": "Combination", "PMID": "31217433", "Cancer_Type": "Thymoma", "Cancer_Type_Description": "Thymoma", "System": null, "Dose": "(50 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "JNK in MDSC", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs; MAPK signaling", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00584,\n C06429", "Drug_Pubchem": "3385,\n 445580", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "EL4 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1982", "Drug": "OKI-179 plus anti-PD1", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "novel oral Class I histone deacetylase (HDAC) inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "31235619", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphomas", "System": null, "Dose": "anti-PD1 (10mg/kg/dose) , OKI-179 (60mg/kg/dose)", "Technique": "Kaplan-Meier Curve Of Recipient Mice", "Controlled_Technique": "Survival analysis (Kaplan–Meier)", "Immune_System-Function_enhanced/numbers_increased": "inhibited tumor growth, suurvival", "Controlled_Terms_Function_enhanced_Number_increased": "Tumor growth / burden outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "A20 lymphomas", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2003", "Drug": "Peptide R", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31661001", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - B16 Melanoma", "System": null, "Dose": "Pep R (2 mg/kg, 5 days per week for 2 weeks)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Granzyme B (GRZB) positive immune cells, ratio CD8+ T cells/Tregs", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Regulatory T cells / Tregs; T cells; CD8+ T cells; Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": "FoxP3 positive Treg cells,neutrophils infiltration, pDC (CD 45+ cells) CXCR4 decreased in tumors", "Controlled_Terms_Function_inhibited_Number_decreased": "FOXP3; Regulatory T cells / Tregs; Neutrophils / granulocytes; CXCR4; Immune-cell infiltration", "Immune_System_function_unaffected": "PD-1 expression", "Controlled_Terms_Unaffected": "PD-1 / PDCD1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57Bl/6", "Cell_line_used_to_induce_tumor_in_mice": "B16-hCXCR4 (5 × 105)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2004", "Drug": "Peptide R54", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31661001", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "Peptide R54 (GL BiochemShangay LTD) (2 mg/kg ip, 5 days week/3 weeks)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Granzyme B (GRZB) positive immune cells", "Controlled_Terms_Function_enhanced_Number_increased": "Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": "CXCR4 PD-L1 CXCR4 expression, p-ERK and KI67, pERK1/2, pP38 MAPK, pAKT and p4EBP", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; Immune checkpoint pathway; MAPK signaling; CXCR4; Cell proliferation / Ki-67", "Immune_System_function_unaffected": "DTC-PES43 cells CXCL12 and cognate receptor CXCR7 expression", "Controlled_Terms_Unaffected": "CXCL12 / SDF-1; CXCR7", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "Athymic Nude-Foxn1nu", "Cell_line_used_to_induce_tumor_in_mice": "PES43 (2.5 × 106) melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2005", "Drug": "Peptide R54+nivolumab", "Drug_category": "others/combination", "Drugbank_ID": "DB09035", "Target/s_or_mechanism_of_action": "The ligands PD-L1 and PD-L2 bind to the PD-1 receptor on T-cells, inhibiting the action of these cells. Tumor cells express PD-L1 and PD-L2. Nivolumab binds to PD-1, preventing PD-L1 and PD-L2 from inhibiting the action of T-cells, restoring a patient's tumor-specific T-cell response", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "31661001", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "anti-human PD-1/(CD279) IgG4 (S228P) (nivolumab) monoclonal antibody (5 mg/kg ip, twice week/3 weeks)+ Peptide R54 (GL BiochemShangay LTD) (2 mg/kg ip, 5 days week/3 weeks)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "DTC-PES43 cells CXCR4 PD-L1 CXCR4 expression, p-ERK and KI67", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; Immune checkpoint pathway; MAPK signaling; CXCR4; Cell proliferation / Ki-67", "Immune_System_function_unaffected": "CXCL12 and cognate receptor CXCR7 expression", "Controlled_Terms_Unaffected": "CXCL12 / SDF-1; CXCR7", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10316", "Drug_Pubchem": "348000000", "Animal_Strain_used": "Athymic Nude-Foxn1nu", "Cell_line_used_to_induce_tumor_in_mice": "PES43 (2.5 × 106) melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2008", "Drug": "PLX4720+TLR7A", "Drug_category": "others/combination", "Drugbank_ID": "DB06999", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F", "Single/Combination": "Combination", "PMID": "31702822", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "3 × 105 D4M cells injected subcutaneously (s.c.)+ BRAFi containg Chow(417 mg PLX4720/kg) +2 mg/kg of\n the TLR7A at Day 19 (middle of sensitive phase)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD69+\n NK and T cells, PD-1+ T cells, IFN-γ production by NK and T cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD69; PD-1 / PDCD1; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "TNF-α NKG2D", "Controlled_Terms_Unaffected": "TNF-α / TNF; NKG2D ligand / receptor pathway", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "BRAFV600E/PTEN D4M-3A (RRID:CVCL_0P27)25 murine\n melanoma cell line", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2011", "Drug": "Domatinostat (4SC-202) + agonistic 4-1BB antibody", "Drug_category": "others/combination", "Drugbank_ID": "DB13101", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C=C(C=N1)C1=CC=C(C=C1)S(=O)(=O)N1C=CC(\\C=C\\C(=O)NC2=CC=CC=C2N)=C1", "Single/Combination": "Combination", "PMID": "31703604", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "20 mg/kg domatinostat twice daily ; agonistic anti-4-1BB antibody was administered at 10 mg/kg", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "reduce tumor volumes", "Controlled_Terms_Function_enhanced_Number_increased": "reduce tumor volumes", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "15985904", "Animal_Strain_used": "C57BL/6 J", "Cell_line_used_to_induce_tumor_in_mice": "C38 tumor fragments", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2012", "Drug": "Domatinostat (4SC-202) + PD-L1 blockade", "Drug_category": "others/combination", "Drugbank_ID": "DB13101", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C=C(C=N1)C1=CC=C(C=C1)S(=O)(=O)N1C=CC(\\C=C\\C(=O)NC2=CC=CC=C2N)=C1", "Single/Combination": "Combination", "PMID": "31703604", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "20 mg/kg domatinostat twice daily, 10 mg/kg anti-PD-L1 antibody twice a week", "Technique": "Kaplan-Meier Event-Free Survival Plots", "Controlled_Technique": "Survival analysis (Kaplan–Meier)", "Immune_System-Function_enhanced/numbers_increased": "prolonged event-free survival of the animals", "Controlled_Terms_Function_enhanced_Number_increased": "Survival outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "15985904", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26 cell", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2013", "Drug": "Domatinostat (4SC-202) + PD-L1 blockade", "Drug_category": "others/combination", "Drugbank_ID": "DB13101", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C=C(C=N1)C1=CC=C(C=C1)S(=O)(=O)N1C=CC(\\C=C\\C(=O)NC2=CC=CC=C2N)=C1", "Single/Combination": "Combination", "PMID": "31703604", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "60 mg/kg domatinostat once daily or 20 mg/kg domatinostat twice daily ); anti-PD-1", "Technique": "Kaplan-Meier Event-Free Survival Plots", "Controlled_Technique": "Survival analysis (Kaplan–Meier)", "Immune_System-Function_enhanced/numbers_increased": "prolonged the median event-free survival", "Controlled_Terms_Function_enhanced_Number_increased": "Survival outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "15985904", "Animal_Strain_used": "C57BL/6 J", "Cell_line_used_to_induce_tumor_in_mice": "C38 tumor fragments", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2014", "Drug": "Domatinostat (4SC-202) + PD-L1 blockade +LAG3 blockade", "Drug_category": "others/combination", "Drugbank_ID": "DB13101", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C=C(C=N1)C1=CC=C(C=C1)S(=O)(=O)N1C=CC(\\C=C\\C(=O)NC2=CC=CC=C2N)=C1", "Single/Combination": "Combination", "PMID": "31703604", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "60 mg/kg domatinostat once daily or 20 mg/kg domatinostat twice daily ); anti-PD-1 and anti-LAG3 antibodies were administered at 10 mg/kg", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "reduce tumor volumes", "Controlled_Terms_Function_enhanced_Number_increased": "reduce tumor volumes", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "15985904", "Animal_Strain_used": "C57BL/6 J", "Cell_line_used_to_induce_tumor_in_mice": "C38 tumor fragments", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2017", "Drug": "Entinostat (MS275) +PD1 blockade", "Drug_category": "others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "31720815", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "20 mg/kg ENT,200 μg\n anti-PD1", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T-cell function, intratumoral T-cell clonal expansion", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "TS/A tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2019", "Drug": "Vorinostat (SAHA) plus tumor lysates", "Drug_category": "others/combination", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "31737100", "Cancer_Type": "Brain cancer", "Cancer_Type_Description": "Glioma", "System": null, "Dose": "SAHA (100 mg/kg)", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "longer period of survival", "Controlled_Terms_Function_enhanced_Number_increased": "Survival outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06320", "Drug_Pubchem": "5311", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "GL261 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2021", "Drug": "BRAFi PLX4720 + MEKi PD0325901", "Drug_category": "others/combination", "Drugbank_ID": "DB06999, DB07101", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf.\n PD0325901 is a selective, cell permeable inhibitor of the MEK/ERK pathway that inhibits the activation and downstream signaling of MEK.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F,\n [H][C@@](O)(CO)CONC(=O)C1=C(NC2=CC=C(I)C=C2F)C(F)=C(F)C=C1", "Single/Combination": "Combination", "PMID": "31796433", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "combination BRAFi + MEKi chow (200 ppm PLX4720 plus 7 ppm PD0325901)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ and CD4+ cells in tumors, activated (CD44+) and proliferating (Ki67+) T cells in tumors MHC-II on tumor-infiltrating DCs", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; MHC class II; Dendritic cells; T cells; Cell proliferation / Ki-67; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "tumor-associated macrophages (TAM) and myeloid-derived suppressor cells (MDSCs) were decreased intra-tumorally, IDO-1, FasL, LGasS9, and OX40L on CD45.2-negative and CD45.2-positive cells within tumors TNFα from intra-tumoral and splenic CD4+ and CD8+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "TNF-α / TNF; CD4; CD8; CD45; Myeloid-derived suppressor cells / MDSCs; Tumor-associated macrophages / TAMs; Macrophages; T cells; CD8+ T cells; IDO1", "Immune_System_function_unaffected": "IFNγ, IL-2 from intra-tumoral and splenic CD4+ and CD8+ T cells", "Controlled_Terms_Unaffected": "IFN-γ; IL-2; CD4; CD8; T cells; CD8+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719, 9826528", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "D4M3.A cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2056", "Drug": "Domatinostat + agonistic anti-4-1BB", "Drug_category": "others/combination", "Drugbank_ID": "DB17521", "Target/s_or_mechanism_of_action": "Domatinostat modulates tumor immune microenvironment; agonistic 4-1BB stimulation enhances T-cell costimulation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C=C(C=N1)C2=CC=C(C=C2)S(=O)(=O)N3C=CC(=C3)/C=C/C(=O)NC4=CC=CC=C4N", "Single/Combination": "Combination", "PMID": "31703604", "Cancer_Type": "Adenocarcinoma", "Cancer_Type_Description": null, "System": null, "Dose": "Domatinostat 20 mg/kg twice daily + anti-4-1BB 10 mg/kg every 3 days", "Technique": "Tumor-volume measurement; response analysis", "Controlled_Technique": "Tumor growth/survival analysis", "Immune_System-Function_enhanced/numbers_increased": "Antitumor T-cell response increased; 14/20 animals responded", "Controlled_Terms_Function_enhanced_Number_increased": "T cells", "Immune_System-Function_inhibited/numbers_decreased": "NR", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "NR", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Inhibitory/exhaustion-associated immune regulation was counteracted through 4-1BB costimulation", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "15985904", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "C38 murine colon carcinoma", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2022", "Drug": "BRAFi PLX4720 + MEKi PD0325901", "Drug_category": "others/combination", "Drugbank_ID": "DB06999, DB07101", "Target/s_or_mechanism_of_action": "Target: Serine/threonine-protein kinase B-raf.\n PD0325901 is a selective, cell permeable inhibitor of the MEK/ERK pathway that inhibits the activation and downstream signaling of MEK.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCS(=O)(=O)NC1=CC=C(F)C(C(=O)C2=CNC3=C2C=C(Cl)C=N3)=C1F,\n [H][C@@](O)(CO)CONC(=O)C1=C(NC2=CC=C(I)C=C2F)C(F)=C(F)C=C1", "Single/Combination": "Combination", "PMID": "31796433", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "combination BRAFi + MEKi chow (200 ppm PLX4720 plus 7 ppm PD0325901)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ and CD4+ cells in tumors, activated (CD44+) and proliferating (Ki67+) T cells in tumors MHC-II on tumor-infiltrating DCs", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; MHC class II; Dendritic cells; T cells; Cell proliferation / Ki-67; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "tumor-associated macrophages (TAM) and myeloid-derived suppressor cells (MDSCs) were decreased intra-tumorally, IDO-1, FasL, LGasS9, and OX40L on CD45.2-negative and CD45.2-positive cells within tumors TNFα from intra-tumoral and splenic CD4+ and CD8+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "TNF-α / TNF; CD4; CD8; CD45; Myeloid-derived suppressor cells / MDSCs; Tumor-associated macrophages / TAMs; Macrophages; T cells; CD8+ T cells; IDO1", "Immune_System_function_unaffected": "IFNγ, IL-2 from intra-tumoral and splenic CD4+ and CD8+ T cells", "Controlled_Terms_Unaffected": "IFN-γ; IL-2; CD4; CD8; T cells; CD8+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "24180719, 9826528", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "YUMM1.7 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2023", "Drug": "Chidamide (CS055/HBI-8000/Tucidinostat) and Rituximab", "Drug_category": "others/combination", "Drugbank_ID": "DB06334, DB00073", "Target/s_or_mechanism_of_action": "Histone deacetylase inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=CC(F)=CC=C1NC(=O)C1=CC=C(CNC(=O)\\C=C\\C2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "31907371", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Diffuse Large B Cell Lymphoma (DLBCL)", "System": null, "Dose": "The dose of Rituximab for in vivo use is 200 µg/mice, equivalent to 10 µg/ml. The dose of Chidamide for mice is 3.9 mg/kg, equivalent to 10 µM", "Technique": "Immunohistochemistry,Kaplan Meier overall survival (OS) curves", "Controlled_Technique": "Immunohistochemistry (IHC); Survival analysis (Kaplan–Meier)", "Immune_System-Function_enhanced/numbers_increased": "CD20 prlonged survival and improved response", "Controlled_Terms_Function_enhanced_Number_increased": "CD20 / MS4A1; Survival outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10993, \n D02994", "Drug_Pubchem": "12136798, 46505820", "Animal_Strain_used": "BALB/c nude", "Cell_line_used_to_induce_tumor_in_mice": "DLBCL OCI-Ly7", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2036", "Drug": "VPA (valpromide) + anti- PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB00313", "Target/s_or_mechanism_of_action": "Valproic acid exhibits its pharmacologic effects in a couple of ways, such as by acting on GABA (γ aminobutyric acid) levels in the CNS, blocking voltage-gated ion channels, and inhibiting histone deacetylase", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCC(CCC)C(O)=O", "Single/Combination": "Combination", "PMID": "32158627", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "VPA and anti-PD-1 (200 μg/\n mouse on day 4, 7 and 8)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00399", "Drug_Pubchem": "3121", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "EL4", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2037", "Drug": "VPA (valpromide) + anti- PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB00313", "Target/s_or_mechanism_of_action": "Valproic acid exhibits its pharmacologic effects in a couple of ways, such as by acting on GABA (γ aminobutyric acid) levels in the CNS, blocking voltage-gated ion channels, and inhibiting histone deacetylase", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCCC(CCC)C(O)=O", "Single/Combination": "Combination", "PMID": "32158627", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "VPA (500 mg/kg) and anti-PD-1 (200 μg/\n mouse on days 7, 10 and 13)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00399", "Drug_Pubchem": "3121", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "B16-F10", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2040", "Drug": "MEKi GDC-0623/CD40 Ab", "Drug_category": "others/combination", "Drugbank_ID": "DB11982", "Target/s_or_mechanism_of_action": "Not Available", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "OCCONC(=O)C1=C(NC2=C(F)C=C(I)C=C2)N2C=NC=C2C=C1", "Single/Combination": "Combination", "PMID": "32358491", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Murine Colon Carcinoma", "System": null, "Dose": "Mice were treated daily with 30 mg kg−1 GDC-0623 or vehicle for ~2 weeks (gray rectangle). Anti-CD40 or control Ab were administered on treatment days 3, 5, 7 as well as 1 day prior to biomarker analyses", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD206+ M2-like macrophages,Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD206 / MRC1; Regulatory T cells / Tregs; Macrophages; M2 macrophage phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "42642654", "Animal_Strain_used": "C57BL/6-Ly5.1", "Cell_line_used_to_induce_tumor_in_mice": "MC-38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2043", "Drug": "MEKi GDC-0623/CD40 Ab", "Drug_category": "others/combination", "Drugbank_ID": "DB11982", "Target/s_or_mechanism_of_action": "Not Available", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "OCCONC(=O)C1=C(NC2=C(F)C=C(I)C=C2)N2C=NC=C2C=C1", "Single/Combination": "Combination", "PMID": "32358491", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Tumor", "System": null, "Dose": "Mice were treated daily with 30 mg kg−1 GDC-0623 or vehicle for ~2 weeks (gray rectangle). Anti-CD40 or control Ab were administered on treatment days 3, 5, 7 as well as 1 day prior to biomarker analyses", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD206+ M2-like macrophages,Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD206 / MRC1; Regulatory T cells / Tregs; Macrophages; M2 macrophage phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "42642654", "Animal_Strain_used": "C57BL/6-Ly5.1", "Cell_line_used_to_induce_tumor_in_mice": "PDA30364", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2044", "Drug": "MRX-2843", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "MRX-2843 is a potent and orally active inhibitor of MERTK and FLT3", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "32642716", "Cancer_Type": "Brain cancer", "Cancer_Type_Description": "Glioblastoma", "System": null, "Dose": "MRX-2843 administration started on day 7 (oral gavage daily, 50 mg/kg) after intracranial injection of GL261 cells", "Technique": "Multiplex Fluorescence IHC, Flow cytometry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC); Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "CD80high/CD86high positive pro-inflammatory macrophages", "Controlled_Terms_Function_enhanced_Number_increased": "Macrophages", "Immune_System-Function_inhibited/numbers_decreased": "macrophages and microglia (CD206+ CD11c+) in the tumor microenvironment in vivo, CD163high/CD206high positive anti-inflammatory macrophages CD206 expression was decreased within the tumor site compared to control", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11c / ITGAX; CD206 / MRC1; Macrophages", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "Syngeneic orthotopic glioblastoma mouse model (BALB/c)", "Cell_line_used_to_induce_tumor_in_mice": "GL261 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2046", "Drug": "Anti PD-1 + abemaciclib", "Drug_category": "others/combination", "Drugbank_ID": "DB12001", "Target/s_or_mechanism_of_action": "Abemaciclib selectively inhibits CDK4 and CDK6 with low nanomolar potency, inhibits Rb phosphorylation resulting in a G1 arrest and inhibition of proliferation, and its activity is specific for Rb-proficient cells", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN1CCN(CC2=CC=C(NC3=NC=C(F)C(=N3)C3=CC(F)=C4N=C(C)N(C(C)C)C4=C3)N=C2)CC1", "Single/Combination": "Combination", "PMID": "32929370", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": null, "Dose": "abemaciclib (50 mg/kg) daily +anti-PD-1 mAb (200 μg) every 3 days for a total period of 21 days after three weeks after cell implantation", "Technique": "Flow Cytometery", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "increased infiltration of CD8+ T\n cells expressing CD69, CD107a or IFN-γ, CD4+ T cells\n expressing CD69, CD107a or IFN-γ, and CD19+ B cells,", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; CD69; CD19; B cells; T cells; CD4+ T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10688", "Drug_Pubchem": "46220502", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "ID8 (ID8-luc) cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2048", "Drug": "B7-H3 × CD3 BiAb with MEK inhibitor trametinib", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "32984002", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small-Cell Lung Cancer (NSCLC) And Bladder Cancer (BC)", "System": null, "Dose": "2 million cells + trametinib (0.6 mg/kg)", "Technique": "FFow cytometry and CCK-8 assay, H$E staining", "Controlled_Technique": "Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "CD3+ T cells CD31 and caspase-3", "Controlled_Terms_Function_enhanced_Number_increased": "CD3; CD31 / PECAM-1; T cells; Apoptosis / caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "NOD-SCID", "Cell_line_used_to_induce_tumor_in_mice": "T24", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2049", "Drug": "B7-H3 × CD3 BiAb with MEK inhibitor trametinib", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "32984002", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small-Cell Lung Cancer (NSCLC) And Bladder Cancer (BC)", "System": null, "Dose": "2 million cells+ trametinib (0.6 mg/kg), 8 × 106 T cells+100U IL-2, 2 mg/kg BiAb", "Technique": "Flow cytometry and CCK-8 assay", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "CD3+ T cells CD31 and caspase-3", "Controlled_Terms_Function_enhanced_Number_increased": "CD3; CD31 / PECAM-1; T cells; Apoptosis / caspase activation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "NOD-SCID", "Cell_line_used_to_induce_tumor_in_mice": "H460", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2052", "Drug": "ACY1215 and anti-PD-L1", "Drug_category": "others/combination", "Drugbank_ID": "DB12376", "Target/s_or_mechanism_of_action": "Ricolinostat (ACY-1215) is an orally available selective HDAC6 inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "ONC(=O)CCCCCCNC(=O)C1=CN=C(N=C1)N(C1=CC=CC=C1)C1=CC=CC=C1", "Single/Combination": "Combination", "PMID": null, "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": null, "Dose": "ACY1215 (50 mg/kg, daily)) +anti-PD-L1 (10mg/kg, twice a week)", "Technique": "Flow Cytometery", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "IFNγ+ CD8 cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD4 T cells", "Controlled_Terms_Unaffected": "CD4; T cells; CD4+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10661", "Drug_Pubchem": "53340666", "Animal_Strain_used": "ARID1Aflox/flox/PIK3CAH1047R OCCC mouse model", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2057", "Drug": "Domatinostat + anti-PD-1 + anti-LAG3", "Drug_category": "others/combination", "Drugbank_ID": "DB17521", "Target/s_or_mechanism_of_action": "Domatinostat increases antigen presentation/CTL activity; anti-PD-1 and anti-LAG3 inhibit checkpoint-mediated T-cell suppression", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C=C(C=N1)C2=CC=C(C=C2)S(=O)(=O)N3C=CC(=C3)/C=C/C(=O)NC4=CC=CC=C4N", "Single/Combination": "Combination", "PMID": "31703604", "Cancer_Type": "Adenocarcinoma", "Cancer_Type_Description": null, "System": null, "Dose": "Domatinostat 20 mg/kg twice daily or 60 mg/kg once daily + anti-PD-1 10 mg/kg + anti-LAG3 10 mg/kg", "Technique": "Tumor-volume measurement; response analysis; event-free survival", "Controlled_Technique": "Tumor growth/survival analysis", "Immune_System-Function_enhanced/numbers_increased": "Antitumor T-cell response increased; response rate increased; reported response in 80% of animals in the triple-combination experiment", "Controlled_Terms_Function_enhanced_Number_increased": "T cells", "Immune_System-Function_inhibited/numbers_decreased": "PD-1 and LAG3-mediated inhibitory signaling blocked", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-1 / PDCD1; LAG-3", "Immune_System_function_unaffected": "NR", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Negative immune-checkpoint regulation through PD-1/LAG3 reduced", "Controlled_Terms_Negative_Regulation": "PD-1 / PDCD1; LAG-3", "KEGG_Drug_ID": null, "Drug_Pubchem": "15985904", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "C38 murine colon carcinoma", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2058", "Drug": "Domatinostat + anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB17521", "Target/s_or_mechanism_of_action": "Domatinostat increases antigen presentation and CTL activity; anti-PD-1 blocks PD-1-mediated T-cell inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C=C(C=N1)C2=CC=C(C=C2)S(=O)(=O)N3C=CC(=C3)/C=C/C(=O)NC4=CC=CC=C4N", "Single/Combination": "Combination", "PMID": "31703604", "Cancer_Type": "Adenocarcinoma", "Cancer_Type_Description": null, "System": null, "Dose": "Domatinostat 20 mg/kg twice daily + anti-PD-1 10 mg/kg twice weekly", "Technique": "Tumor-volume measurement; event-free survival; flow cytometry", "Controlled_Technique": "Tumor growth/survival analysis; Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CTL activity/function increased; antitumor response increased; tumor control increased", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; Tumor growth / burden outcome", "Immune_System-Function_inhibited/numbers_decreased": "PD-1-mediated inhibitory signaling blocked", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-1 / PDCD1", "Immune_System_function_unaffected": "NR", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Negative immune-checkpoint regulation through PD-1 reduced", "Controlled_Terms_Negative_Regulation": "PD-1 / PDCD1", "KEGG_Drug_ID": null, "Drug_Pubchem": "15985904", "Animal_Strain_used": "BALB/c and C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "CT26 and C38 murine colon carcinoma", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2063", "Drug": "Trastuzumab deruxtecan (T-DXd)", "Drug_category": "others/combination", "Drugbank_ID": "DB14962", "Target/s_or_mechanism_of_action": "Fcγ-receptor activation; antibody-dependent cellular phagocytosis (ADCP); ICD", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "40175391", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "HER2-positive", "System": null, "Dose": "Phagocytosis flow cytometry; ELISA; flow cytometry", "Technique": "Macrophage HLA-A2, HLA-DR, CD80, CD40 and CCR7; antigen-presentation and chemokine genes; inflammatory cytokines", "Controlled_Technique": "Cytokine/chemokine analysis", "Immune_System-Function_enhanced/numbers_increased": "NR", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Macrophages were not susceptible to T-DXd or payload cytotoxicity in vitro", "Controlled_Terms_Function_inhibited_Number_decreased": "Macrophages", "Immune_System_function_unaffected": "CD47 upregulation may limit phagocytosis", "Controlled_Terms_Unaffected": "CD4", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D11529", "Drug_Pubchem": "384585505", "Animal_Strain_used": "Au565 cells", "Cell_line_used_to_induce_tumor_in_mice": "1 µg/mL for 4-hour ADCP assays; separate co-culture conditions", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2076", "Drug": "IL-12 + trabectedin + anti-PD-L1", "Drug_category": "others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "DNA minor-groove binding; DNA damage", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39777457", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Murine TNBC", "System": null, "Dose": "IL-12 and trabectedin as above; anti-PD-L1 dose to verify in full protocol", "Technique": "Mouse tumor model; tumor growth and immune profiling", "Controlled_Technique": "Tumor growth/survival analysis; Immune-cell profiling/phenotyping", "Immune_System-Function_enhanced/numbers_increased": "Enhanced tumor control; increased IFN-γ and effector CD8+ T-cell proportion; decreased Tregs and total MDSCs", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; T cells; Tumor growth / burden outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06199", "Drug_Pubchem": "108150", "Animal_Strain_used": "BALB/c mice", "Cell_line_used_to_induce_tumor_in_mice": "4T1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2077", "Drug": "IL-12 + trabectedin", "Drug_category": "others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "DNA minor-groove binding; DNA damage", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39777457", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Murine TNBC", "System": null, "Dose": "IL-12 0.5 μg IP, 3×/week + trabectedin 0.15 mg/kg IV, 1×/week", "Technique": "Tumor growth, plasma cytokines, mass cytometry, spatial profiling", "Controlled_Technique": "Tumor growth/survival analysis; Cytokine/chemokine analysis; Immune-cell profiling/phenotyping", "Immune_System-Function_enhanced/numbers_increased": "Reduced tumor burden, MDSCs and M2-like macrophages; increased IFN-γ and intratumoral CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; Myeloid-derived suppressor cells / MDSCs; Macrophages; T cells; Tumor growth / burden outcome", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06199", "Drug_Pubchem": "108150", "Animal_Strain_used": "BALB/c mice", "Cell_line_used_to_induce_tumor_in_mice": "4T1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2078", "Drug": "IL-12 + trabectedin", "Drug_category": "others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "DNA minor-groove binding; DNA damage", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39777457", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Murine TNBC", "System": null, "Dose": "IL-12 0.5 μg IP, 3×/week + trabectedin 0.15 mg/kg IV, 1×/week", "Technique": "Mouse tumor model; tumor growth", "Controlled_Technique": "Tumor growth/survival analysis", "Immune_System-Function_enhanced/numbers_increased": "Significantly reduced tumor volume compared with controls and single-agent treatments", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06199", "Drug_Pubchem": "108150", "Animal_Strain_used": "BALB/c mice", "Cell_line_used_to_induce_tumor_in_mice": "EMT6", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2079", "Drug": "Olaparib + AZD1775 + anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB09074 + DB11740 + N/A", "Target/s_or_mechanism_of_action": "DNA-damage/STING activation + blockade of PD-1 inhibitory signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC1)C2=NC3=C(N2C4=CC=CC=C4C5=CC=CC=C5)C=CC(=C3)C(=O)N and CN1CCN(CC1)C2=CC=C(C=C2)NC3=NC4=C(C(=O)N(C4=CC=C3)CC=C)N(C5=CC=CC(=C5)C(C)(C)O)", "Single/Combination": "Combination", "PMID": "37582853", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "BRCA1/2-wild-type TNBC with moderate pre-existing TILs", "System": null, "Dose": "Olaparib 40 mg/kg + AZD1775 30 mg/kg orally 5 days/week + anti-PD-1 200 µg/mouse i.p. on days 1, 5, 8, 12", "Technique": "flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8⁺ and CD4⁺ effector T cells; CD4⁺/FOXP3⁻ T cells ; CD4⁺ cells expressing IFNγ ; tumor MHC-I", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; FOXP3; T cells; MHC class I; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "PD-1-mediated T-cell inhibition blocked", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-1 / PDCD1; T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-1/PD-L1 negative regulation inhibited", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-1 / PDCD1", "KEGG_Drug_ID": "D09713 + D11361 + N/A", "Drug_Pubchem": "23725625 + 24856436 + N/A", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "AT3OVA", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2080", "Drug": "Olaparib + AZD1775", "Drug_category": "others/combination", "Drugbank_ID": "DB09074 + DB11740", "Target/s_or_mechanism_of_action": "PARP/WEE1 inhibition → DNA damage + cGAS-STING signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC1)C2=NC3=C(N2C4=CC=CC=C4C5=CC=CC=C5)C=CC(=C3)C(=O)N and CN1CCN(CC1)C2=CC=C(C=C2)NC3=NC4=C(C(=O)N(C4=CC=C3)CC=C)N(C5=CC=CC(=C5)C(C)(C)O)", "Single/Combination": "Combination", "PMID": "37582853", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "BRCA1/2-wild-type TNBC", "System": null, "Dose": "40 mg/kg olaparib + 30 mg/kg AZD1775, oral, 5 days/week", "Technique": "flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC-I (H2Kb/H2Db) , MHC-II , CD80, CD86,  CD4⁺ T cells ; CD8:Treg ratio ; mature MHC-II⁺ DCs ; CD8⁺ and CD4⁺ IFNγ/granzyme B production ; CD4⁺ Ki67⁺PD1+ cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; CD80; CD86; PD-1 / PDCD1; Regulatory T cells / Tregs; T cells; Granzyme B / GZMB; MHC class I; MHC class II; Cell proliferation / Ki-67; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09713 + D11361", "Drug_Pubchem": "23725625 + 24856436", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "AT3OVA", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2081", "Drug": "Olaparib + AZD1775 + ADU-S100", "Drug_category": "others/combination", "Drugbank_ID": "DB09074 + DB11740 + N/A", "Target/s_or_mechanism_of_action": "DNA damage/replication stress + direct STING activation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC1)C2=NC3=C(N2C4=CC=CC=C4C5=CC=CC=C5)C=CC(=C3)C(=O)N and CN1CCN(CC1)C2=CC=C(C=C2)NC3=NC4=C(C(=O)N(C4=CC=C3)CC=C)N(C5=CC=CC(=C5)C(C)(C)O)", "Single/Combination": "Combination", "PMID": "37582853", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "BRCA1/2-wild-type TNBC", "System": null, "Dose": "Reduced-dose of olaparib and AZD1775 (40 mg) + ADU-S100 40 µg/tumor i.t. days 1, 3, 5", "Technique": "flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "MHC-I, MHC-II , tumor-infiltrating CD8⁺ T cells, CD8⁺ IFNγ , CD11c⁺CD11b⁻ DCs , CD103⁺ DCs , CD80/CD86⁺ DCs,", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; CD11b / ITGAM; CD11c / ITGAX; CD80; CD86; T cells; MHC class I; MHC class II; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "Tumor-cell CD80, CD86 and PD-L1 were not significantly changed", "Controlled_Terms_Unaffected": "CD8; CD80; CD86; PD-L1 / CD274", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "No significant PD-L1 induction,  therefore negative PD-L1 regulation was not increased", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": "D09713 + D11361 + N/A", "Drug_Pubchem": "23725625 + 24856436 + N/A", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "AT3", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2114", "Drug": "Vinblastine (VBL)", "Drug_category": "others/combination", "Drugbank_ID": "DB00570", "Target/s_or_mechanism_of_action": "Binds tubulin/microtubules and inhibits microtubule polymerization.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC[C@]1(O)C[C@@H]2CN(CCc3c([nH]c4ccccc34)[C@@](C(=O)OC)(c3cc4c(cc3OC)N(C)[C@H]3[C@@](O)(C(=O)OC)[C@H](OC(C)=O)[C]5(CC)C=CCN6CC[C@]43[C@@H]65)C2)C1", "Single/Combination": "Combination", "PMID": "37652576", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": null, "Dose": "VBL 1.25 mg/kg + anti-PD-1 100 µg/mouse", "Technique": "CD8⁺ T-cell antitumor response, macrophage reprogramming", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "M2-like phenotype", "Controlled_Terms_Function_enhanced_Number_increased": "Macrophages", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08675", "Drug_Pubchem": "241903", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2082", "Drug": "Olaparib + AZD1775", "Drug_category": "others/combination", "Drugbank_ID": "DB09074 + DB11740", "Target/s_or_mechanism_of_action": "Combined PARP/WEE1 inhibition → replication catastrophe, DNA damage and cGAS-STING activation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC1)C2=NC3=C(N2C4=CC=CC=C4C5=CC=CC=C5)C=CC(=C3)C(=O)N and CN1CCN(CC1)C2=CC=C(C=C2)NC3=NC4=C(C(=O)N(C4=CC=C3)CC=C)N(C5=CC=CC(=C5)C(C)(C)O)", "Single/Combination": "Combination", "PMID": "37582853", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "BRCA1/2-wild-type TNBC", "System": null, "Dose": "50 mg/kg olaparib + 50 mg/kg AZD1775, oral, 5 days/week", "Technique": "flow cytometry, immune profiling", "Controlled_Technique": "Flow cytometry; Immune-cell profiling/phenotyping", "Immune_System-Function_enhanced/numbers_increased": "Tumor MHC-I ; CD11c⁺CD11b⁻ DCs ; MHC-II⁺ DCs ; CD80/CD83⁺ DC maturation ; CD8⁺/CD4⁺ T cells showed increased numbers (not always significant); CD8:Treg ratio", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD11b / ITGAM; CD11c / ITGAX; CD80; CD83; Regulatory T cells / Tregs; Dendritic cells; T cells; MHC class I; MHC class II; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "CD80/CD86 on tumor cells ↓", "Controlled_Terms_Function_inhibited_Number_decreased": "CD8; CD80; CD86", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 significantly increased indicates activation of PD-1/PD-L1 immune suppression", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-1 / PDCD1", "KEGG_Drug_ID": "D09713 + D11361", "Drug_Pubchem": "23725625 + 24856436", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "AT3", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2083", "Drug": "Olaparib + AZD1775", "Drug_category": "others/combination", "Drugbank_ID": "DB09074 + DB11740", "Target/s_or_mechanism_of_action": "Combined PARP/WEE1 inhibition → replication catastrophe, DNA damage and cGAS-STING activation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC1)C2=NC3=C(N2C4=CC=CC=C4C5=CC=CC=C5)C=CC(=C3)C(=O)N and CN1CCN(CC1)C2=CC=C(C=C2)NC3=NC4=C(C(=O)N(C4=CC=C3)CC=C)N(C5=CC=CC(=C5)C(C)(C)O)", "Single/Combination": "Combination", "PMID": "37582853", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "BRCA1/2-wild-type TNBC", "System": null, "Dose": "50 mg/kg olaparib + 50 mg/kg AZD1775, oral, 5 days/week", "Technique": "flow cytometry, immune profiling", "Controlled_Technique": "Flow cytometry; Immune-cell profiling/phenotyping", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09713 + D11361", "Drug_Pubchem": "23725625 + 24856436", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1ch9", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2084", "Drug": "Entinostat + anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "HDAC inhibitors", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3", "Single/Combination": "Combination", "PMID": "31720815", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast cancer", "System": null, "Dose": "20 mg/kg/day", "Technique": "flow cytometry, gene-expression analysis", "Controlled_Technique": "Flow cytometry; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T-cell , CD4+ Tcell", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "BALB/c mice", "Cell_line_used_to_induce_tumor_in_mice": "TS/A", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2085", "Drug": "B102 + anti-PD-L1", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "B102 activates cGAS-STING/type-I IFN pathway; anti-PD-L1 blocks PD-L1 checkpoint signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "38182579", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Triple-negative breast cancer", "System": null, "Dose": "15 mg/kg B102 + anti-PD-L1; syngeneic orthotopic model", "Technique": "Anti-tumor immune response ↑; tumor growth inhibition ↑", "Controlled_Technique": "Tumor growth/survival analysis", "Immune_System-Function_enhanced/numbers_increased": "IFNβ, CCL5, CXCL10, activation of the cGAS–STING signaling pathway", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-β; CCL5 / RANTES; CXCL10 / IP-10; cGAS–STING signaling", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 inhibitory signaling ↓", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "Female BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2086", "Drug": "B302 + anti-PD-L1", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "B302 activates cGAS-STING/type-I IFN pathway; anti-PD-L1 blocks PD-L1 checkpoint signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "38182579", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Triple-negative breast cancer", "System": null, "Dose": "50 mg/kg B302 + anti-PD-L1; syngeneic orthotopic model", "Technique": "Anti-tumor immune response ↑; tumor growth inhibition ↑", "Controlled_Technique": "Tumor growth/survival analysis", "Immune_System-Function_enhanced/numbers_increased": "IFNβ, CCL5, CXCL10, activation of the cGAS–STING signaling pathway", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-β; CCL5 / RANTES; CXCL10 / IP-10; cGAS–STING signaling", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 inhibitory signaling ↓", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "Female BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2087", "Drug": "Trametinib+anti‐CD73 antibody", "Drug_category": "others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "Selective MEK1/MEK2 inhibition → inhibition of RAS–RAF–MEK–ERK signaling; paradoxically causes sustained p38 activation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Combination", "PMID": "34165921", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "4T1 mouse mammary carcinoma", "System": null, "Dose": "daily MEKi (1 mg·kg−1), anti‐CD73 antibody (TY/23, days 5, 9, 13, and 17)", "Technique": "flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "enrichment of CD45+CD3− in tumors", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD3; CD45", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": "11707110", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2088", "Drug": "Entinostat+Ad-Twist vaccine+N-803 (1 μg, s.c.)", "Drug_category": "others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "HDAC inhibition, particularly HDAC1/HDAC3; immunomodulatory effects include reduction of Tregs and MDSCs and reduction of VISTA expression on multiple immune-cell populations.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3", "Single/Combination": "Combination", "PMID": "31645354", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": null, "System": null, "Dose": "12 mg/kg/day in CEA-Tg/NSG mice, 3 mg/kg/day for Balb/c mice", "Technique": "Flow cytometry, ELISPOT, cytokine analysis, tumor-growth/survival analysis, immune-cell depletion, NanoString gene-expression analysis, chemokine analysis, immunological rechallenge, in-vitro PBMC experiments", "Controlled_Technique": "Flow cytometry; ELISpot/FluoroSpot assay; Cytokine/chemokine analysis; Survival analysis (Kaplan–Meier); In-vivo/in-vitro immunological assay; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "Elevated the proinflammatory cytokines IFNγ (3-fold) and TNFα (2-fold),increase in splenic CD4+ T cells, CD8⁺ T-cell tumor infiltration increased; activated CD8⁺ T cells increased, increased expression of CD25 and Ki67 on CD8⁺ T cells, increase in granzyme B", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; TNF-α / TNF; CD4; CD8; CD25 / IL2RA; T cells; Granzyme B / GZMB; Cell proliferation / Ki-67; Immune-cell infiltration; Cytokines", "Immune_System-Function_inhibited/numbers_decreased": "Elevated the proinflammatory cytokines IFNγ (3-fold) and TNFα (2-fold),increase in splenic CD4+ T cells, CD8⁺ T-cell tumor infiltration increased; activated CD8⁺ T cells increased, increased expression of CD25 and Ki67 on CD8⁺ T cells, increase in granzyme B", "Controlled_Terms_Function_inhibited_Number_decreased": "IFN-γ; TNF-α / TNF; CD4; CD8; CD25 / IL2RA; T cells; Granzyme B / GZMB; Cell proliferation / Ki-67; Immune-cell infiltration; Cytokines", "Immune_System_function_unaffected": "Frequency of activated (CD44hi) or total CD4+ T cells remained unchanged", "Controlled_Terms_Unaffected": "CD4; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "elevated programmed death-ligand 1 (PD-L1)", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "BALB/c mice, CEA-transgenic mice", "Cell_line_used_to_induce_tumor_in_mice": "4T1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2089", "Drug": "Macrocarpal I", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Binds TUBB2B and PARP1; disrupts microtubule polymerization and DNA repair; promotes immunogenic tumor-cell death", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C)C[C@@H]([C@@H]1CC[C@@]([C@H]2[C@]1(CC[C@H](C2)C(C)(C)O)C)(C)O)C3=C(C(=C(C(=C3O)C=O)O)C=O)O", "Single/Combination": "Single", "PMID": "39987121", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Mouse colon adenocarcinoma syngeneic tumor model", "System": null, "Dose": "60 mg/kg intraperitoneally once daily for 7 days; n=8 mice/group", "Technique": "Mouse tumor model; tumor growth measurement; tumor-infiltrating immune-cell isolation; flow cytometry", "Controlled_Technique": "Tumor growth/survival analysis; Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "remarkable enhancement of ICD activation, increased the infiltration of total T cells, CD4+ and CD8+ T cells, Granzyme B+ CD8+ T cells, dendritic cells, CD8+/Treg ratio", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; Regulatory T cells / Tregs; Dendritic cells; T cells; Granzyme B / GZMB; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "Decreased tumor-infiltrating FOXP3+ CD4+ regulatory T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; FOXP3; Regulatory T cells / Tregs; T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "10028546", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "MC38K", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2092", "Drug": "Macrocarpal I + anti-PD-1 antibody", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Macrocarpal I targets TUBB2B and PARP1 and promotes immunogenic cell death; anti-PD-1 blocks PD-1-mediated immune inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C)C[C@@H]([C@@H]1CC[C@@]([C@H]2[C@]1(CC[C@H](C2)C(C)(C)O)C)(C)O)C3=C(C(=C(C(=C3O)C=O)O)C=O)O", "Single/Combination": "Combination", "PMID": "39987121", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Mouse colon adenocarcinoma syngeneic tumor model MC38K", "System": null, "Dose": "Macrocarpal I: 60 mg/kg intraperitoneally daily for 7 days; anti-PD-1: 200 µg/injection intraperitoneally every 2 days", "Technique": "Combination treatment; tumor growth monitoring; tumor-infiltrating immune-cell flow cytometry", "Controlled_Technique": "Tumor growth/survival analysis; Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "marked enhancement of the ICD effect , ncrease in the infiltration of total T cells, CD4+ T cells CD8+ T cells and Granzyme B+ CD8+ T cells, substantial increase in intratumoral DCs cell population , CD8+/Treg ratio", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; Regulatory T cells / Tregs; T cells; Granzyme B / GZMB; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "decrease in Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "10028546", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "MC38K", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2093", "Drug": "HBI-8000 + anti-PD-1 mAb", "Drug_category": "others/combination", "Drugbank_ID": "DB06334", "Target/s_or_mechanism_of_action": "Epigenetic immune modulation + PD-1 checkpoint blockade", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC(=CN=C1)/C=C/C(=O)NCC2=CC=C(C=C2)C(=O)NC3=C(C=C(C=C3)F)N", "Single/Combination": "Combination", "PMID": "34461854", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Murine colon carcinoma", "System": null, "Dose": "HBI-8000 50 mg/kg daily + anti-PD-1 10 mg/kg twice weekly", "Technique": "Syngeneic tumor model + NanoString profiling", "Controlled_Technique": "Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "dendritic cells, macrophages, NK/cytotoxic cells, CD45 cells, antigen presentation, MHC expression, immune-effector signatures,  increased expression of the immune checkpoints PD-1, PD-L1, CTLA-4, and CD86 (CD28L), CD276/B7-H3 and CD244, lymphocyte activation gene-3 (LAG-3), T cell immunoreceptor with Ig and ITIM domains (TIGIT), ecto-5′-nucleotidase (NT5E/CD73), signal regulatory protein α (SIRPα), nuclear factor of activated T cells 4 (NFATC4), and poliovirus receptor (CD155), increased T-effector and interferon-γ gene scores, which, along with increases in granzyme B (GZMB) and perforin-1 (PRF1)", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; CD45; CD86; CD155 / PVR; PD-L1 / CD274; PD-1 / PDCD1; CTLA-4; LAG-3; TIGIT; Macrophages; Dendritic cells; NK cells; T cells; Granzyme B / GZMB; Perforin / PRF1; CD276 / B7-H3; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "PD-1 signaling inhibited", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-1 / PDCD1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-1-mediated negative regulation inhibited", "Controlled_Terms_Negative_Regulation": "PD-1 / PDCD1", "KEGG_Drug_ID": "D10993", "Drug_Pubchem": "12136798", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2094", "Drug": "Entinostat+Ad-CEA+N-803 (1 μg, s.c.)", "Drug_category": "others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "HDAC inhibition, particularly HDAC1/HDAC3; immunomodulatory effects include reduction of Tregs and MDSCs and reduction of VISTA expression on multiple immune-cell populations.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3", "Single/Combination": "Combination", "PMID": "31645354", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": null, "System": null, "Dose": "12 mg/kg/day in CEA-Tg/NSG mice, 3 mg/kg/day for Balb/c mice", "Technique": "Flow cytometry, ELISPOT, cytokine analysis, tumor-growth/survival analysis, immune-cell depletion, NanoString gene-expression analysis, chemokine analysis, immunological rechallenge, in-vitro PBMC experiments", "Controlled_Technique": "Flow cytometry; ELISpot/FluoroSpot assay; Cytokine/chemokine analysis; Survival analysis (Kaplan–Meier); In-vivo/in-vitro immunological assay; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "Elevated the proinflammatory cytokines IFNγ (3-fold) and TNFα (2-fold),increase in splenic CD4+ T cells, CD8⁺ T-cell tumor infiltration increased; activated CD8⁺ T cells increased, increased expression of CD25 and Ki67 on CD8⁺ T cells, increase in granzyme B", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; TNF-α / TNF; CD4; CD8; CD25 / IL2RA; T cells; Granzyme B / GZMB; Cell proliferation / Ki-67; Immune-cell infiltration; Cytokines", "Immune_System-Function_inhibited/numbers_decreased": "Elevated the proinflammatory cytokines IFNγ (3-fold) and TNFα (2-fold),increase in splenic CD4+ T cells, CD8⁺ T-cell tumor infiltration increased; activated CD8⁺ T cells increased, increased expression of CD25 and Ki67 on CD8⁺ T cells, increase in granzyme B", "Controlled_Terms_Function_inhibited_Number_decreased": "IFN-γ; TNF-α / TNF; CD4; CD8; CD25 / IL2RA; T cells; Granzyme B / GZMB; Cell proliferation / Ki-67; Immune-cell infiltration; Cytokines", "Immune_System_function_unaffected": "No change in level of IL-10, Tumor infiltration of G-MDSCs and M-MDSCs", "Controlled_Terms_Unaffected": "IL-10; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; PMN-MDSCs / G-MDSCs; Immune-cell infiltration", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "elevated programmed death-ligand 1 (PD-L1)", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "BALB/c mice, CEA-transgenic mice", "Cell_line_used_to_induce_tumor_in_mice": "MC38-CEA", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2095", "Drug": "CKI27 + anti-GITR (DTA-1) + anti-CTLA-4 (9D9)", "Drug_category": "others/combination", "Drugbank_ID": "DB14779", "Target/s_or_mechanism_of_action": "KI27 inhibits MEK1/2–ERK signaling; DTA-1 agonizes GITR/TNFRSF18 and provides T-cell costimulation; 9D9 blocks CTLA-4-mediated inhibitory signaling and promotes T-cell activation/Treg depletion", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C)N1C2=NC=NC(=C2C(=N1)C3=CC4=C(C=C3)OC(=N4)N)N", "Single/Combination": "Combination", "PMID": "38885362", "Cancer_Type": "Colon Cancer; Lung Cancer", "Cancer_Type_Description": "Lung cancer / colon cancer", "System": null, "Dose": "LLC: 5 mg/kg orally, 4 days on/3 days off (4-on/3-off); Anti-GITR -1 mg/mouse, i.p., single dose on day 1, Anti-CTLA-4-100 µg/mouse, i.p., twice weekly beginning day 1", "Technique": "low cytometry TIL profiling", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "CD8⁺ T-cell, CD4⁺ effector T-cell, CD8⁺/CD4⁺ effector-memory and memory phenotypes,  cytotoxic T-cell function, CD8:Treg ratio, cytotoxic/effector genes including Gzma, Gzmm, Tbx21 and Eomes", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; Regulatory T cells / Tregs; T cells", "Immune_System-Function_inhibited/numbers_decreased": "Intratumoral Tregs, MDSCs, CTLA-4/CD25 expression on Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD25 / IL2RA; CTLA-4; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "72726305", "Animal_Strain_used": "C57BL/6 mice- KRAS-mutant Lewis lung carcinoma (LLC)", "Cell_line_used_to_induce_tumor_in_mice": "LLC", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2096", "Drug": "CKI27 + anti-GITR (DTA-1) + anti-CTLA-4 (9D9)", "Drug_category": "others/combination", "Drugbank_ID": "DB14779", "Target/s_or_mechanism_of_action": "KI27 inhibits MEK1/2–ERK signaling; DTA-1 agonizes GITR/TNFRSF18 and provides T-cell costimulation; 9D9 blocks CTLA-4-mediated inhibitory signaling and promotes T-cell activation/Treg depletion", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C)N1C2=NC=NC(=C2C(=N1)C3=CC4=C(C=C3)OC(=N4)N)N", "Single/Combination": "Combination", "PMID": "38885362", "Cancer_Type": "Colon Cancer; Lung Cancer", "Cancer_Type_Description": "Lung cancer / colon cancer", "System": null, "Dose": "CT26: 2 mg/kg orally, 4-on/3-off; Anti-GITR -1 mg/mouse, i.p., single dose on day 1, Anti-CTLA-4-100 µg/mouse, i.p., twice weekly", "Technique": "low cytometry TIL profiling", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "CD8⁺ T-cell, CD4⁺ effector T-cell, CD8⁺/CD4⁺ effector-memory and memory phenotypes,  cytotoxic T-cell function, CD8:Treg ratio, cytotoxic/effector genes including Gzma, Gzmm, Tbx21 and Eomes", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; Regulatory T cells / Tregs; T cells", "Immune_System-Function_inhibited/numbers_decreased": "Intratumoral Tregs, MDSCs, CTLA-4/CD25 expression on Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD25 / IL2RA; CTLA-4; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "72726305", "Animal_Strain_used": "BALB/cJ mice-KRAS-mutant CT26 colon carcinoma", "Cell_line_used_to_induce_tumor_in_mice": "CT26", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2097", "Drug": "JQ1", "Drug_category": "others/combination", "Drugbank_ID": "DB17021", "Target/s_or_mechanism_of_action": "BRD4 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=C(SC2=C1C(=N[C@H](C3=NN=C(N32)C)CC(=O)OC(C)(C)C)C4=CC=C(C=C4)Cl)C", "Single/Combination": "Single", "PMID": "35517410", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": null, "Dose": "50 mg/kg i.p. daily", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "infiltrating Foxp3+ Treg cells", "Controlled_Terms_Function_inhibited_Number_decreased": "FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "46907787", "Animal_Strain_used": "C57BL/6 mice", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2103", "Drug": "Doxorubicin (DOX) + indocyanine green (ICG) + anti-PD-L1 antibody (αPD-L1)", "Drug_category": "others/combination", "Drugbank_ID": "DB00997+DB09374", "Target/s_or_mechanism_of_action": "DOX causes DNA damage; ICG generates ROS upon ultrasound exposure, promoting mitochondrial DNA oxidation and cGAS–STING activation; αPD-L1 blocks PD-L1-mediated immune suppression.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COC1=CC=CC2=C1C(=O)C1=C(O)C3=C(C[C@](O)(C[C@@H]3O[C@H]3C[C@H](N)[C@H](O)[C@H](C)O3)C(=O)CO)C(O)=C1C2= and CC1(C)C(=CC=CC=CC=CC2=[N+](CCCCS([O-])(=O)=O)C3=CC=C4=CC=CC=C4C=C3C2(C)C)N(CCCCS(O)(=O)=O)C2=CC=C3C=CC=CC3=C12", "Single/Combination": "Combination", "PMID": "37391428", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": null, "Dose": "DOX 0.5 mg/kg + ICG 4 mg/kg intravenously; treatment on days 10 and 13, ultrasound on days 11 and 14", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "CD8⁺ T-cell infiltration; antitumor T-cell immunity", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1-mediated immune suppression", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1-mediated immunosuppression was blocked", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": "D03899+D01342", "Drug_Pubchem": "31703+11967809", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2104", "Drug": "Luminespib + Emricasan + anti-PD-L1", "Drug_category": "others/combination", "Drugbank_ID": "DB05408", "Target/s_or_mechanism_of_action": "Hsp90 inhibition+Inhibits caspases, including caspase-associated apoptotic signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C and C[C@@H](C(=O)N[C@@H](CC(=O)O)C(=O)COC1=C(C(=CC(=C1F)F)F)F)NC(=O)C(=O)NC2=CC=CC=C2C(C)(C)C", "Single/Combination": "Combination", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": null, "Dose": "Luminespib 75 mg/kg every 2 days; emricasan 10 mg/kg daily; anti-PD-L1 100 µg/mouse every 4 days", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "Antitumor immune response and sensitivity to PD-L1 blockade", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274", "Immune_System-Function_inhibited/numbers_decreased": "Caspase activity inhibited by emricasan; PD-L1-mediated immune suppression blocked by anti-PD-L1", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1-mediated adaptive immune resistance is the therapeutic target; B16 model was used to assess whether the combination could overcome resistance", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": null, "Drug_Pubchem": "135539077 + 12000240", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "B16", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2105", "Drug": "Venetoclax + anti-PD-L1", "Drug_category": "others/combination", "Drugbank_ID": "DB11581", "Target/s_or_mechanism_of_action": "D10679", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1(CCC(=C(C1)C2=CC=C(C=C2)Cl)CN3CCN(CC3)C4=CC(=C(C=C4)C(=O)NS(=O)(=O)C5=CC(=C(C=C5)NCC6CCOCC6)[N+](=O)[O-])OC7=CN=C8C(=C7)C=CN8)C", "Single/Combination": "Combination", "PMID": "40300857", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer", "System": null, "Dose": "Venetoclax 100 mg/kg orally daily + anti-PD-L1 10 mg/kg intravenously twice weekly", "Technique": "Flow cytometry, ELISA, qRT-PCR", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA); Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD3+ and CD8+ T cells; IFN-γ, IL-2 and TNF-α increased; mRNA expression of Ccl5, Cxcl10, and Ifnβ( STING signaling pathway)", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-2; TNF-α / TNF; CCL5 / RANTES; CXCL10 / IP-10; CD8; CD3; T cells; cGAS–STING signaling", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression increased", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": "49846579", "Drug_Pubchem": "40300857", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2106", "Drug": "Venetoclax + anti-PD-L1", "Drug_category": "others/combination", "Drugbank_ID": "DB11581", "Target/s_or_mechanism_of_action": "D10679", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1(CCC(=C(C1)C2=CC=C(C=C2)Cl)CN3CCN(CC3)C4=CC(=C(C=C4)C(=O)NS(=O)(=O)C5=CC(=C(C=C5)NCC6CCOCC6)[N+](=O)[O-])OC7=CN=C8C(=C7)C=CN8)C", "Single/Combination": "Combination", "PMID": "40300857", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer", "System": null, "Dose": "Venetoclax 100 mg/kg orally daily + anti-PD-L1 10 mg/kg intravenously twice weekly", "Technique": "Flow cytometry, ELISA, qRT-PCR", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA); Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD3+ and CD8+ T cells; IFN-γ, IL-2 and TNF-α increased; mRNA expression of Ccl5, Cxcl10, and Ifnβ( STING signaling pathway)", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-2; TNF-α / TNF; CCL5 / RANTES; CXCL10 / IP-10; CD8; CD3; T cells; cGAS–STING signaling", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression increased", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": "49846579", "Drug_Pubchem": "40300857", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2107", "Drug": "Venetoclax + anti-PD-L1", "Drug_category": "others/combination", "Drugbank_ID": "DB11581", "Target/s_or_mechanism_of_action": "D10679", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1(CCC(=C(C1)C2=CC=C(C=C2)Cl)CN3CCN(CC3)C4=CC(=C(C=C4)C(=O)NS(=O)(=O)C5=CC(=C(C=C5)NCC6CCOCC6)[N+](=O)[O-])OC7=CN=C8C(=C7)C=CN8)C", "Single/Combination": "Combination", "PMID": "40300857", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer", "System": null, "Dose": "Venetoclax 100 mg/kg orally daily + anti-PD-L1 10 mg/kg intravenously twice weekly", "Technique": "Flow cytometry, ELISA, qRT-PCR", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA); Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD3+ and CD8+ T cells; IFN-γ, IL-2 and TNF-α increased; mRNA expression of Ccl5, Cxcl10, and Ifnβ( STING signaling pathway)", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-2; TNF-α / TNF; CCL5 / RANTES; CXCL10 / IP-10; CD8; CD3; T cells; cGAS–STING signaling", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression increased", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": "49846579", "Drug_Pubchem": "40300857", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "EMT6", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2108", "Drug": "Doxorubicin (DOX)+ indocyanine green +Ultrasound", "Drug_category": "others/combination", "Drugbank_ID": "DB00997+DB09374", "Target/s_or_mechanism_of_action": "DOX inhibits topoisomerase II and intercalates DNA. ICG acts as a sonosensitizer under ultrasound exposure, promoting reactive oxygen species (ROS) generation and mitochondrial DNA oxidation/release, activating the cGAS–STING–TBK1–IRF3 pathway and type I interferon responses", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COC1=CC=CC2=C1C(=O)C1=C(O)C3=C(C[C@](O)(C[C@@H]3O[C@H]3C[C@H](N)[C@H](O)[C@H](C)O3)C(=O)CO)C(O)=C1C2= and CC1(C)C(=CC=CC=CC=CC2=[N+](CCCCS([O-])(=O)=O)C3=CC=C4=CC=CC=C4C=C3C2(C)C)N(CCCCS(O)(=O)=O)C2=CC=C3C=CC=CC3=C12", "Single/Combination": "Combination", "PMID": "37391428", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal/colon cancer", "System": null, "Dose": "DOX 0.5 mg/kg + ICG 4 mg/kg intravenously; treatment on days 10 and 13, ultrasound on days 11 and 14", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "Dendritic-cell activation (CD80 + DC,CD86 + DC, SIINFEKL/H-2Kb); antigen presentation, type I interferon signaling, intratumoral CD8⁺ T-cell infiltration, and antitumor immune responses", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; CD80; CD86; Dendritic cells; T cells; MHC class I; Immune-cell infiltration; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03899+D01342", "Drug_Pubchem": "31703+11967809", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2109", "Drug": "JQ1", "Drug_category": "others/combination", "Drugbank_ID": "DB17021", "Target/s_or_mechanism_of_action": "BRD4 inhibition", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=C(SC2=C1C(=N[C@H](C3=NN=C(N32)C)CC(=O)OC(C)(C)C)C4=CC=C(C=C4)Cl)C", "Single/Combination": "Combination", "PMID": "35517410", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": null, "Dose": "50 mg/kg i.p. daily", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "infiltrating Foxp3+ Treg cells", "Controlled_Terms_Function_inhibited_Number_decreased": "FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "46907787", "Animal_Strain_used": "C57BL/6 mice", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2110", "Drug": "Luminespib + Emricasan + anti-PD-L1", "Drug_category": "others/combination", "Drugbank_ID": "DB05408", "Target/s_or_mechanism_of_action": "Hsp90 inhibition+Inhibits caspases, including caspase-associated apoptotic signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C and C[C@@H](C(=O)N[C@@H](CC(=O)O)C(=O)COC1=C(C(=CC(=C1F)F)F)F)NC(=O)C(=O)NC2=CC=CC=C2C(C)(C)C", "Single/Combination": "Combination", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": null, "Dose": "Luminespib 75 mg/kg every 2 days; emricasan 10 mg/kg daily; anti-PD-L1 100 µg/mouse every 4 days", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "Type I interferon signaling; CD45⁺ immune-cell infiltration; CD8⁺ T-cell infiltration and activation; granzyme B expression; antitumor immune response", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; CD45; T cells; Granzyme B / GZMB; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1-mediated immune checkpoint suppression blocked by anti-PD-L1", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression induced by the luminespib–emricasan combination, contributing to adaptive immune resistance; anti-PD-L1 blocks this pathway", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": null, "Drug_Pubchem": "135539077 + 12000240", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2111", "Drug": "FK228 (Romidepsin)", "Drug_category": "others/combination", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "HDAC inhibitor; reported to directly inhibit HDAC1, HDAC2, HDAC4 and HDAC6. In this study, FK228 induces ER-stress-associated necroptosis in tumor cells, producing immunogenic cell death and remodeling the tumor immune microenvironment.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C/C=C\\1/C(=O)N[C@H](C(=O)O[C@H]\\2CC(=O)N[C@@H](C(=O)N[C@H](CSSCC/C=C2)C(=O)N1)C(C)C)C(C)C", "Single/Combination": "Combination", "PMID": "40940553", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "colorectal cancer", "System": null, "Dose": "anti-PD-L1 and FK228", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "Greatest infiltration of anticancer immune cells, such as proinflammatory Mφ, dendritic cell (DC), neutrophil, and CD8+ T cells, as well the modest accumulation of anticancer natural killer (NK)\ncells. Highest frequency of GZMB-positive CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Macrophages; Dendritic cells; NK cells; T cells; Neutrophils / granulocytes; Granzyme B / GZMB; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "remarkable decrease in anti-inflammatory Mφs", "Controlled_Terms_Function_inhibited_Number_decreased": "Macrophages", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06637", "Drug_Pubchem": "5352062", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2112", "Drug": "FK228 (Romidepsin)", "Drug_category": "others/combination", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "HDAC inhibitor; reported to directly inhibit HDAC1, HDAC2, HDAC4 and HDAC6. In this study, FK228 induces ER-stress-associated necroptosis in tumor cells, producing immunogenic cell death and remodeling the tumor immune microenvironment.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C/C=C\\1/C(=O)N[C@H](C(=O)O[C@H]\\2CC(=O)N[C@@H](C(=O)N[C@H](CSSCC/C=C2)C(=O)N1)C(C)C)C(C)C", "Single/Combination": "Combination", "PMID": "40940553", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "colorectal cancer", "System": null, "Dose": "anti-PD-L1 and FK228", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "Greatest infiltration of anticancer immune cells, such as proinflammatory Mφ, dendritic cell (DC), neutrophil, and CD8+ T cells, as well the modest accumulation of anticancer natural killer (NK)\ncells. Highest frequency of GZMB-positive CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Macrophages; Dendritic cells; NK cells; T cells; Neutrophils / granulocytes; Granzyme B / GZMB; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "remarkable decrease in anti-inflammatory Mφs", "Controlled_Terms_Function_inhibited_Number_decreased": "Macrophages", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06637", "Drug_Pubchem": "5352062", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2113", "Drug": "Irinotecan (IRIN)+Radiotherapy", "Drug_category": "others/combination", "Drugbank_ID": "DB00762", "Target/s_or_mechanism_of_action": "DNA damage; cGAS–STING pathway activation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCC1=C2CN3C(=CC4=C(C3=O)COC(=O)[C@@]4(CC)O)C2=NC5=C1C=C(C=C5)OC(=O)N6CCC(CC6)N7CCCCC7", "Single/Combination": "Combination", "PMID": "37779919", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": null, "Dose": "IRIN silicasome 40 mg/kg IV every 3 days for 4 administrations; radiation 2 Gy × 4 fractions", "Technique": "Western blot, flow cytometry, immunofluorescence", "Controlled_Technique": "Western blot/immunoblot analysis; Flow cytometry; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "Increased tumor-infiltrating CD4⁺ T cells, CD8⁺ T cells and CD11c⁺ dendritic cells; increased IFN-γ expression", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; CD11c / ITGAX; Dendritic cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08086", "Drug_Pubchem": "60838", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2115", "Drug": "Luminespib + Emricasan", "Drug_category": "others/combination", "Drugbank_ID": "DB05408", "Target/s_or_mechanism_of_action": "Hsp90 inhibition+Inhibits caspases, including caspase-associated apoptotic signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCNC(=O)C1=NOC(=C1C2=CC=C(C=C2)CN3CCOCC3)C4=CC(=C(C=C4O)O)C(C)C and C[C@@H](C(=O)N[C@@H](CC(=O)O)C(=O)COC1=C(C(=CC(=C1F)F)F)F)NC(=O)C(=O)NC2=CC=CC=C2C(C)(C)C", "Single/Combination": "Combination", "PMID": "38056894", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Murine colorectal cancer", "System": null, "Dose": "Luminespib 75 mg/kg every 2 days; emricasan 10 mg/kg daily", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "ype I IFN/IFN-β production; CD8⁺ T-cell-dependent antitumor immunity", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression can increase following combination treatment, contributing to adaptive immune resistance", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": null, "Drug_Pubchem": "135539077 + 12000240", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2119", "Drug": "FK228 (Romidepsin)", "Drug_category": "others/combination", "Drugbank_ID": "DB06176", "Target/s_or_mechanism_of_action": "HDAC inhibitor; reported to directly inhibit HDAC1, HDAC2, HDAC4 and HDAC6. In this study, FK228 induces ER-stress-associated necroptosis in tumor cells, producing immunogenic cell death and remodeling the tumor immune microenvironment.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C/C=C\\1/C(=O)N[C@H](C(=O)O[C@H]\\2CC(=O)N[C@@H](C(=O)N[C@H](CSSCC/C=C2)C(=O)N1)C(C)C)C(C)C", "Single/Combination": "Combination", "PMID": "40940553", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": null, "System": null, "Dose": "FK228 (0.5 mg/kg) via the tail vein every 2 days (5 times\nin total) and FK228 treated dead MC38 cells", "Technique": "In-vivo vaccination assay, immunohistochemistry/immunofluorescence, flow cytometry, single-cell RNA sequencing (scRNA-seq), pySCENIC transcription-factor analysis.", "Controlled_Technique": "In-vivo/in-vitro immunological assay; Immunohistochemistry (IHC); Immunofluorescence assay; Flow cytometry; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "CD8⁺ T-cell infiltration increased,CD8⁺ T-cell activation increased, GZMB- and IFN-γ-expressing CD8⁺ T cells increased, NK-cell infiltration increased, macrophages shifted toward a pro-inflammatory phenotype, neutrophils increased in the combination-treatment tumor microenvironment.", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; Macrophages; NK cells; T cells; Neutrophils / granulocytes; Granzyme B / GZMB; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression increased on cancer cells and macrophages; PD-1 expression increased on total T cells and CD8⁺ T cells following FK228 treatment. Tregs also increased", "Controlled_Terms_Negative_Regulation": "CD8; PD-L1 / CD274; PD-1 / PDCD1; Regulatory T cells / Tregs; Macrophages; T cells", "KEGG_Drug_ID": "D06637", "Drug_Pubchem": "5352062", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2120", "Drug": "Melarsoprol (MEL)", "Drug_category": "others/combination", "Drugbank_ID": "DB12864", "Target/s_or_mechanism_of_action": "DNA damage; activates cGAS–STING–TBK1–IRF3 signaling, promoting IFN-β production", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1C(S[As](S1)C2=CC=C(C=C2)NC3=NC(=NC(=N3)N)N)CO", "Single/Combination": "Single", "PMID": "40528981", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "mouse HCC cell line", "System": null, "Dose": "1 and 2.5 mg/kg in vivo", "Technique": "Western blot, RT-qPCR, ELISA, cGAS–STING signaling", "Controlled_Technique": "Western blot/immunoblot analysis; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "TNF-α production through NF-κB signaling increases; potentially pro-tumorigenic", "Controlled_Terms_Function_enhanced_Number_increased": "TNF-α / TNF", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00832", "Drug_Pubchem": "10311", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Hepa1–6", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2121", "Drug": "Melarsoprol (MEL)+Lenalidomide (LEN)", "Drug_category": "others/combination", "Drugbank_ID": "DB12864+DB00480", "Target/s_or_mechanism_of_action": "DNA damage; activates cGAS–STING–TBK1–IRF3 signaling, promoting IFN-β production", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1C(S[As](S1)C2=CC=C(C=C2)NC3=NC(=NC(=N3)N)N)CO and C1CC(=O)NC(=O)C1N2CC3=C(C2=O)C=CC=C3N", "Single/Combination": "Combination", "PMID": "40528981", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "mouse HCC cell line", "System": null, "Dose": "2 mg/kg MEL + 2.5 mg/kg LEN; intravenous", "Technique": "flow cytometry; RT-qPCR; ELISA", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Activated dendritic cells, CD8⁺ cytotoxic T cells, CD4⁺ helper T cells, CD4⁺ and CD8⁺ memory T cells; IFN-β, IL-12, IFN-γ, CXCL9 and CXCL10 increased", "Controlled_Terms_Function_inhibited_Number_decreased": "IFN-γ; IL-12; CXCL9; CXCL10 / IP-10; CD4; CD8; Dendritic cells; T cells", "Immune_System_function_unaffected": "Tregs, IL-10, TGF-β and TNF-α decreased", "Controlled_Terms_Unaffected": "IL-10; TNF-α / TNF; TGF-β; Regulatory T cells / Tregs", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00832+\t\nD04687", "Drug_Pubchem": "10311+216326", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Hepa1–6", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2122", "Drug": "Lycorine hydrochloride", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Inhibits viability; induces cell-cycle arrest and reduces cyclin D1, cyclin D3 and CDK2 expression", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "28416753", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renca murine renal carcinoma cell line; Renca-Luc used in mouse tumor model", "System": null, "Dose": "lycorine 5 mg/kg/day for 7 days", "Technique": "flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ CD44+ CD62L− effector T cells increased in combination-treated mice; 42.89 ± 0.49%", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; T cells", "Immune_System-Function_inhibited/numbers_decreased": "CD4+ Foxp3+ regulatory T cells decreased in combination-treated mice; 13.88 ± 0.75%", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; FOXP3; Regulatory T cells / Tregs; T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "164943", "Animal_Strain_used": "BALB/c mice", "Cell_line_used_to_induce_tumor_in_mice": "RENCA", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2124", "Drug": "Lycorine hydrochloride Anti-mouse CTLA-4 monoclonal antibody (clone 9H10)", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Inhibits viability; induces cell-cycle arrest and reduces cyclin D1, cyclin D3 and CDK2 expression", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "28416753", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renca murine renal carcinoma cell line; Renca-Luc used in mouse tumor model", "System": null, "Dose": "lycorine 5 mg/kg/day for 7 days; anti-CTLA-4 100 μg/mouse on treatment days 0 and 7", "Technique": "flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ CD44+ CD62L− effector T cells increased in combination-treated mice; 52.95 ± 3.40%", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; T cells", "Immune_System-Function_inhibited/numbers_decreased": "CD4+ Foxp3+ regulatory T cells decreased in combination-treated mice; 3.70 ± 0.23%", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; FOXP3; Regulatory T cells / Tregs; T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "CTLA-4 blockade reduces inhibitory checkpoint signaling; combination treatment decreases immunosuppressive Tregs", "Controlled_Terms_Negative_Regulation": "CTLA-4; Regulatory T cells / Tregs", "KEGG_Drug_ID": null, "Drug_Pubchem": "164943", "Animal_Strain_used": "BALB/c mice", "Cell_line_used_to_induce_tumor_in_mice": "RENCA", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2125", "Drug": "OBP-801 + anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "DB12279", "Target/s_or_mechanism_of_action": "Potent class-I HDAC inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C)[C@H]1NC(=O)[C@H]2CSSCC/C=C/[C@H](CC(=O)N[C@H](C)C(=O)N2)OC(=O)C[C@@H]1O", "Single/Combination": "Combination", "PMID": "39682244", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Clear cell renal cell carcinoma", "System": null, "Dose": "OBP-801 10 mg/kg IV + anti-PD-1 10 mg/kg IP; days 1,4,7 for immune-analysis experiment", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "LMP2, MHC-I presentation, CD45⁺CD3e⁺ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD3; CD45; T cells; MHC class I; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "PD-1 inhibitory signaling blocked", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-1 / PDCD1", "Immune_System_function_unaffected": "CD8a⁺CD8b⁺ T cells", "Controlled_Terms_Unaffected": "CD8; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-1/PD-L1 negative immune regulation inhibited", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; PD-1 / PDCD1", "KEGG_Drug_ID": null, "Drug_Pubchem": "11178958", "Animal_Strain_used": "BALB/c mice", "Cell_line_used_to_induce_tumor_in_mice": "RENCA", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2127", "Drug": "NHS-IL12", "Drug_category": "others/combination", "Drugbank_ID": "DB17585", "Target/s_or_mechanism_of_action": "NHS76 antibody targets exposed DNA/histones in necrotic tumor regions; IL-12 activates NK/T cells and induces IFN-γ", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "35764364", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "MHC-I-deficient, IFN-γ-responsive lung tumor", "System": null, "Dose": "2 µg s.c., alternate days ×3", "Technique": "Flow cytometry; immunofluorescence; cytokine/chemokine analysis; RNA-seq", "Controlled_Technique": "Flow cytometry; Immunofluorescence assay; Cytokine/chemokine analysis; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T-cell frequency, NK-cell proliferation, increased IFN-γ/IL-12-associated responses", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-12; CD8; NK cells; T cells; Cell proliferation / Ki-67", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "Treg tumor infiltration in TC-1/a9; CD8+ TIL absolute number in TC-1/a9", "Controlled_Terms_Unaffected": "CD8; Regulatory T cells / Tregs; Immune-cell infiltration", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "Female C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "TC-1/a9", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2128", "Drug": "NHS-IL12", "Drug_category": "others/combination", "Drugbank_ID": "DB17585", "Target/s_or_mechanism_of_action": "Tumor-localized IL-12 → activation of NK/T cells, IFN-γ production, antigen presentation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "35764364", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "MHC-I/APM-deficient, IFN-γ-response-defective lung tumor", "System": null, "Dose": "2 µg s.c., alternate days ×3", "Technique": "Flow cytometry; immunofluorescence; cytokine/chemokine analysis", "Controlled_Technique": "Flow cytometry; Immunofluorescence assay; Cytokine/chemokine analysis", "Immune_System-Function_enhanced/numbers_increased": "H-2Kb expression, CD8+ TIL frequency, M1-like macrophages, cDC1; increased IFN-γ/TNFα; increased chemokines including CCL5/CXCL10/CXCL13", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; TNF-α / TNF; CCL5 / RANTES; CXCL10 / IP-10; CXCL13; CD8; Macrophages; MHC class I; Immune-cell infiltration; Chemokines", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "Female C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "CMT.64", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2028", "Drug": "Oxaliplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00526", "Target/s_or_mechanism_of_action": "Inhibiting DNA synthesis and transcription", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "[H][N]1([H])[C@@H]2CCCC[C@H]2[N]([H])([H])[Pt]11OC(=O)C(=O)O1", "Single/Combination": "Single Drug", "PMID": "32079180", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "2.5 mg/kg", "Technique": "Immunoblotting,Immunohistochemistry", "Controlled_Technique": "Western blot/immunoblot analysis; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "tumor programmed cell death 1 ligand 1 (PD-L1) level", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01790", "Drug_Pubchem": "6857599", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2134", "Drug": "Doxorubicin + Celecoxib", "Drug_category": "others/combination", "Drugbank_ID": "DB00997 + DB00482", "Target/s_or_mechanism_of_action": "DNA damage and ICD induction combined with COX-2/IDO1 pathway suppression", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COC1=CC=CC2=C1C(=O)C1=C(O)C3=C(C[C@](O)(C[C@@H]3O[C@H]3C[C@H](N)[C@H](O)[C@H](C)O3)C(=O)CO)C(O)=C1C2=O and CC1=CC(=NN1C2=CC=C(C=C2)S(=O)(=O)N)C3=CC=C(C=C3)C(F)(F)F", "Single/Combination": "Combination", "PMID": "38988937", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "LLC tumor-bearing mice", "System": null, "Dose": "25 mg/kg; 50 mg/kg", "Technique": "Flow cytometery", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "increased mature DCs reported in the DOX + celecoxib treatment comparison", "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD8+ T-cell depletion reduces the antitumor effect", "Controlled_Terms_Function_inhibited_Number_decreased": "CD8; T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "COX-2/IDO1-associated immunosuppression is a proposed mechanism", "Controlled_Terms_Negative_Regulation": "IDO1; COX-2", "KEGG_Drug_ID": "D03899+D00567", "Drug_Pubchem": "31703 + 2662", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "LLC", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2135", "Drug": "Gemcitabine + Celecoxib + Anti-PD-1 (GCP)", "Drug_category": "others/combination", "Drugbank_ID": "DB00441 + DB00482 + NR", "Target/s_or_mechanism_of_action": "GEM-induced ICD plus celecoxib-mediated IDO1 suppression and anti-PD-1 checkpoint blockade", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F and CC1=CC(=NN1C2=CC=C(C=C2)S(=O)(=O)N)C3=CC=C(C=C3)C(F)(F)F", "Single/Combination": "Combination", "PMID": "38988937", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "LLC tumor-bearing C57BL/6J mice", "System": null, "Dose": "GEM 25 mg/kg IV; celecoxib 50 mg/kg oral gavage; aPD-1 100 µg/mouse IV", "Technique": "Tumor growth and survival monitoring; flow cytometry; immunohistochemistry; ELISA", "Controlled_Technique": "Tumor growth/survival analysis; Flow cytometry; Immunohistochemistry (IHC); Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "Enhanced antitumor efficacy; increased tumor CD8 staining; reduced MDSCs; improved tumor control and survival", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Myeloid-derived suppressor cells / MDSCs; Tumor growth / burden outcome; Survival outcome", "Immune_System-Function_inhibited/numbers_decreased": "Reduced IDO1 and COX-2 expression; reduced MDSC numbers", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs; IDO1; COX-2", "Immune_System_function_unaffected": "No significant difference in IL-2; no significant difference in CD4+ T cells or CD8+IFN-γ+ cells among groups", "Controlled_Terms_Unaffected": "IFN-γ; IL-2; CD4; CD8; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Reduced IDO1-associated immunosuppression and PD-1 checkpoint-mediated inhibition", "Controlled_Terms_Negative_Regulation": "PD-1 / PDCD1; IDO1", "KEGG_Drug_ID": "D02368+D00567", "Drug_Pubchem": "60750 + 2662", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "LLC", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2136", "Drug": "Entinostat + anti-PD-1 + anti-CTLA-4", "Drug_category": "others/combination", "Drugbank_ID": "DB11842", "Target/s_or_mechanism_of_action": "HDAC1/HDAC3 inhibition; systemic immune modulation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C4", "Single/Combination": "Combination", "PMID": "42515717", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Syngeneic murine NSCLC", "System": null, "Dose": "Entinostat 7.5 mg/kg p.o., 5×/week, 8 doses + anti-PD-1 200 µg i.p. twice weekly ×3 + anti-CTLA-4 200 µg i.p. twice weekly ×3", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD4⁺ and CD8⁺ T cells, effector CD8⁺ T cells, antigen-specific CD8⁺ response, IFN-γ production by gp33-specific CD8⁺ cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD4⁺ IFN-γ response not significantly altered by gp33/gp66 stimulation", "Controlled_Terms_Unaffected": "IFN-γ; CD4", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09339", "Drug_Pubchem": "4261", "Animal_Strain_used": "C57BL/6 mice", "Cell_line_used_to_induce_tumor_in_mice": "KPN1.1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2137", "Drug": "Entinostat + NHS-IL12", "Drug_category": "others/combination", "Drugbank_ID": "DB11841 + DB17585", "Target/s_or_mechanism_of_action": "Synergistic enhancement of MHC-I/APM, cytotoxic lymphocyte activation, IFN-γ/JAK-STAT signaling and antigen presentation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3", "Single/Combination": "Combination", "PMID": "35764364", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "MHC-I-deficient CMT.64 lung tumor", "System": null, "Dose": "Entinostat 6 mg/kg/day p.o.; NHS-IL12 2 µg s.c., alternate days ×3", "Technique": "Flow cytometry; immunofluorescence; cytokine/chemokine assays", "Controlled_Technique": "Flow cytometry; Immunofluorescence assay; Cytokine/chemokine analysis", "Immune_System-Function_enhanced/numbers_increased": "CD8+ TILs, cytolytic GzmB, increased CD8+ proliferation, increased NK proliferation, increased M1-like TAMs, increased DC activation, increased cDC1, increased IFN-γ/TNFα/IL-12p70/CXCL9, increased CD8+/Treg ratio", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; TNF-α / TNF; CXCL9; CD8; Regulatory T cells / Tregs; Macrophages; Dendritic cells; NK cells; Granzyme B / GZMB; Cell proliferation / Ki-67", "Immune_System-Function_inhibited/numbers_decreased": "Dampened Treg TILs, M2-like macrophage phenotype", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs; Macrophages", "Immune_System_function_unaffected": "Activated splenic DC frequency remained unchanged", "Controlled_Terms_Unaffected": "Dendritic cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "Female C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "CMT.64", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2138", "Drug": "Entinostat + anti-PD-1 + anti-CTLA-4", "Drug_category": "others/combination", "Drugbank_ID": "DB11843", "Target/s_or_mechanism_of_action": "HDAC1/HDAC3 inhibition; systemic immune modulation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C5", "Single/Combination": "Combination", "PMID": "42515717", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Orthotopic syngeneic murine NSCLC", "System": null, "Dose": "Entinostat 7.5 mg/kg p.o., 5×/week for 2 weeks + dual ICI", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Effector T-cell phenotype particularly CD8⁺ effector T cells, antigen-specific CD8⁺ immune response", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells", "Immune_System-Function_inhibited/numbers_decreased": "—", "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "—", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "—", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09340", "Drug_Pubchem": "4261", "Animal_Strain_used": "C57BL/6 mice", "Cell_line_used_to_induce_tumor_in_mice": "KPN1.1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2139", "Drug": "Citarinostat + Oxaliplatin", "Drug_category": "others/combination", "Drugbank_ID": "DB15449 + DB00526", "Target/s_or_mechanism_of_action": "HDAC6 inhibition/immunomodulation + platinum-mediated DNA damage", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "35223194", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC / lung adenocarcinoma", "System": null, "Dose": "ACY241 3×/week + oxaliplatin 10 mg/kg 1×/week for 6 weeks", "Technique": "Flow cytometery, transcriptomics", "Controlled_Technique": "Flow cytometry; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "CD8:Treg ratio, CD8+ T-cell expressing IL-2, TNF-α, IFN-γ, CD4+ T-cell", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-2; TNF-α / TNF; CD4; CD8; Regulatory T cells / Tregs; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10918 + D01790", "Drug_Pubchem": "53340426 + 9887054", "Animal_Strain_used": "Kras+/LSL-G12D; Trp53L/L (KP) mice", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2140", "Drug": "Vinblastine (VBL)", "Drug_category": "others/combination", "Drugbank_ID": "DB00570", "Target/s_or_mechanism_of_action": "Binds tubulin/microtubules and inhibits microtubule polymerization.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC[C@]1(O)C[C@@H]2CN(CCc3c([nH]c4ccccc34)[C@@](C(=O)OC)(c3cc4c(cc3OC)N(C)[C@H]3[C@@](O)(C(=O)OC)[C@H](OC(C)=O)[C]5(CC)C=CCN6CC[C@]43[C@@H]65)C2)C1", "Single/Combination": "Combination", "PMID": "37652576", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Pulmonary/lung cancer", "System": null, "Dose": "VBL 1.25 mg/kg + anti-PD-1 100 µg/mouse", "Technique": "macrophage reprogramming and T-cell activity", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "M2-like phenotype", "Controlled_Terms_Function_enhanced_Number_increased": "Macrophages", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08675", "Drug_Pubchem": "241903", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "LLC (Lewis lung carcinoma)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2141", "Drug": "Gemcitabine + Celecoxib", "Drug_category": "others/combination", "Drugbank_ID": "DB00441 + DB00482", "Target/s_or_mechanism_of_action": "Enhances ICD and antitumor immunity; celecoxib suppresses COX-2/PGE2-associated PI3K/AKT/IDO1 signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F and CC1=CC(=NN1C2=CC=C(C=C2)S(=O)(=O)N)C3=CC=C(C=C3)C(F)(F)F", "Single/Combination": "Combination", "PMID": "38988937", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "LLC tumor-bearing C57BL/6J mice", "System": null, "Dose": "GEM 25 mg/kg IV; celecoxib 50 mg/kg oral gavage; frequency per study protocol", "Technique": "Tumor-volume monitoring; flow cytometry; immunohistochemistry", "Controlled_Technique": "Tumor growth/survival analysis; Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "Increased CD8+ T-cell proportion and mature DC proportion reported for GC-related treatment comparisons", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Dendritic cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": "Reduced COX-2/IDO1-associated immunosuppressive signaling", "Controlled_Terms_Function_inhibited_Number_decreased": "IDO1; COX-2", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Reduced IDO1-associated immunosuppression", "Controlled_Terms_Negative_Regulation": "IDO1", "KEGG_Drug_ID": "D02368+D00567", "Drug_Pubchem": "60750 + 2662", "Animal_Strain_used": "C57BL/6J mice", "Cell_line_used_to_induce_tumor_in_mice": "LLC", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2143", "Drug": "Entinostat + NHS-IL12", "Drug_category": "others/combination", "Drugbank_ID": "DB11841 + DB17585", "Target/s_or_mechanism_of_action": "HDAC inhibition increases tumor immune recognition/MHC-I/APM while tumor-targeted IL-12 activates cytotoxic lymphocytes and IFN-γ pathways", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3", "Single/Combination": "Combination", "PMID": "35764364", "Cancer_Type": "Lung Cancer; Hpv16-Expressing Tumors", "Cancer_Type_Description": "MHC-I-deficient, HPV16 E6/E7+ lung tumor", "System": null, "Dose": "Entinostat 6 mg/kg/day p.o.; NHS-IL12 2 µg s.c., alternate days ×3", "Technique": "Flow cytometry; immunofluorescence; RNA-seq; GSEA; cytokine/chemokine assays", "Controlled_Technique": "Flow cytometry; Immunofluorescence assay; Gene expression/sequencing analysis; Cytokine/chemokine analysis", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T-cell infiltration, activation and proliferation, GzmB, NK-cell proliferation, M1-like macrophages, activated APC/DCs, increased MHC-I/APM, increased IFN-γ, IL-12, CXCL9/CXCL13", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-12; CXCL9; CXCL13; CD8; Macrophages; Dendritic cells; NK cells; T cells; Granzyme B / GZMB; MHC class I; Cell proliferation / Ki-67; Immune-cell infiltration; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "M2-like macrophages, Treg activity/infiltration in tumor-dependent manner", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs; Macrophages; Immune-cell infiltration", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "Female C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "TC-1/a9", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1876", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "28282575", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Breast Tumor", "System": null, "Dose": "(30 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD4+ and CD8+ T lymphocytes, induction of T cell memory.", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "FVB/N", "Cell_line_used_to_induce_tumor_in_mice": "NT2.5 tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2144", "Drug": "Belantamab mafodotin (GSK2857916)", "Drug_category": "others/combination", "Drugbank_ID": "DB15719", "Target/s_or_mechanism_of_action": "Binds BCMA (TNFRSF17) on multiple myeloma cells; delivers MMAF, inducing apoptosis. Promotes immunogenic cell death (ICD), DAMP release, and dendritic-cell maturation.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "34253590", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma", "System": null, "Dose": "15 mg/kg", "Technique": "Flow cytometry; immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "activation markers including CD25, CD69, and inducible T-cell costimulator (ICOS), CD8+PD-1+ cells and CD8+ granzyme B (GrzB)+ cytotoxic cells ;CD4+ T-cells, regulatory T cells (Treg: CD4+CD25+FoxP3+) in tumor, NK cell (CD49+) and DC infiltration (CD11c+), and expression of the costimulatory molecule CD86", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD11c / ITGAX; CD25 / IL2RA; CD69; CD86; PD-1 / PDCD1; FOXP3; Regulatory T cells / Tregs; Dendritic cells; NK cells; T cells; Granzyme B / GZMB; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "CD8+ T-cell depletion reduced or abrogated antitumor efficacy", "Controlled_Terms_Function_inhibited_Number_decreased": "CD8; T cells", "Immune_System_function_unaffected": "No specific immune function conclusively established as unaffected", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "No direct evidence of enhanced regulatory T-cell activity or other negative immune-regulatory functions reported", "Controlled_Terms_Negative_Regulation": "Regulatory T cells / Tregs; T cells", "KEGG_Drug_ID": "D11595", "Drug_Pubchem": null, "Animal_Strain_used": "Female C57BL/6 mice", "Cell_line_used_to_induce_tumor_in_mice": "EL4-hBCMA", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2147", "Drug": "Glaucocalyxin A", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Inhibits STAT3 phosphorylation; reduces STAT3-associated survival signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C[C@@]12CCC(=O)C([C@H]1C[C@H]([C@]34[C@H]2CC[C@H]([C@H]3O)C(=C)C4=O)O)(C)C", "Single/Combination": "Single", "PMID": "34923957", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple myeloma", "System": null, "Dose": "30 mg/kg body weight", "Technique": "Western blotting, and immunohistochemistry (IHC)", "Controlled_Technique": "Western blot/immunoblot analysis; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "Cleaved PARP and cleaved caspase-3 increased", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis / caspase activation", "Immune_System-Function_inhibited/numbers_decreased": "phosphorylated STAT3 (p-STAT3) decreased,  Ki-67 and PCNA expression significantly decreased", "Controlled_Terms_Function_inhibited_Number_decreased": "STAT3 signaling; Cell proliferation / Ki-67", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "10471963", "Animal_Strain_used": "Nude mice", "Cell_line_used_to_induce_tumor_in_mice": "RPMI-8226", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2148", "Drug": "Pomalidomide+ CAR T cells", "Drug_category": "others/combination", "Drugbank_ID": "DB08910", "Target/s_or_mechanism_of_action": "Enhances BCMA CAR-T-cell activity, effector cytokine production and tumor infiltration; supports T-cell-mediated antitumor responses through immunomodulation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1CC(=O)NC(=O)C1N2C(=O)C3=C(C2=O)C(=CC=C3)N", "Single/Combination": "Combination", "PMID": "41410870", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Human U266 multiple myeloma xenograft model", "System": null, "Dose": "U266 cells: 1 × 10^7 cells/mouse; pomalidomide: 2.5 mg/kg intraperitoneally, 5 times/week for 21 days; BCMA CAR-T cells: 1 × 10^7 cells/mouse intravenously", "Technique": "ELISA; flow cytometry, qPCR", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "Increased intratumoral CD3+ T-cell infiltration; increased IL-2, IFN-γ and increased tumor-tissue expression of IL-2, IFNG and CXCL9–CXCL11", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-2; CXCL9; CXCL11 / I-TAC; CD3; T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "TNF-α, IL-10 and IL-6 were not further increased by pomalidomide in the CAR-T combination", "Controlled_Terms_Unaffected": "IL-6; IL-10; TNF-α / TNF", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04690", "Drug_Pubchem": "9826528", "Animal_Strain_used": "Female NOD-SCID mice", "Cell_line_used_to_induce_tumor_in_mice": "U266", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2149", "Drug": "Dendritic cell vaccine + pomalidomide + dexamethasone", "Drug_category": "others/combination", "Drugbank_ID": "DB08910+DB01234", "Target/s_or_mechanism_of_action": "Pomalidomide binds CRBN and promotes IKZF1/IKZF3 degradation; dexamethasone activates the glucocorticoid receptor and has anti-inflammatory and antimyeloma effects", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1CC(=O)NC(=O)C1N2C(=O)C3=C(C2=O)C(=CC=C3)N and C[C@@H]1C[C@H]2[C@@H]3CCC4=CC(=O)C=C[C@@]4([C@]3([C@H](C[C@@]2([C@]1(C(=O)CO)O)C)O)F)C", "Single/Combination": "Combination", "PMID": "30123221", "Cancer_Type": "Plasmacytoma", "Cancer_Type_Description": "Murine MOPC-315 plasmacytoma model", "System": null, "Dose": "Pomalidomide: 0.06 mg/kg/day orally; dexamethasone: 0.6 mg/kg intravenously on scheduled days; DC vaccine: 1×1061×106 cells/mouse per dose", "Technique": "flow cytometry; IFN-γ ELISPOT; ELISA", "Controlled_Technique": "Flow cytometry; ELISpot/FluoroSpot assay; Cytokine/chemokine analysis; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "CD4⁺ effector T cells, CD8⁺ effector T cells, Effector memory T cells, Natural killer (NK) cells, M1 macrophages, IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; Macrophages; NK cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": "Myeloid-derived suppressor cells (MDSCs; CD11b⁺Gr-1⁺), Regulatory T cells (Tregs; CD4⁺CD25⁺FoxP3⁺), M2 macrophages (CD11b⁺F4/80⁺CD206⁺)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD11b / ITGAM; CD25 / IL2RA; CD206 / MRC1; FOXP3; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; Macrophages; T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08976+D00292", "Drug_Pubchem": "134780+5743", "Animal_Strain_used": "Female BALB/c mice", "Cell_line_used_to_induce_tumor_in_mice": "MOPC-315", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2151", "Drug": "CN133 + anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "NR", "Target/s_or_mechanism_of_action": "Potent class-I HDAC inhibitor; inhibits HDAC1, HDAC2 and HDAC3", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN(Cc1ccc(/C=C/C(=O)NO)cc1)CC12CC3CC(CC(C3)C1)C2", "Single/Combination": "Combination", "PMID": "37880708", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Subcutaneous prostate-cancer allograft; combination therapy tested for enhancement of anti-PD-1 response", "System": null, "Dose": "CN133 1 mg/kg IP twice/week + anti-PD-1 10 mg/kg IP twice/week", "Technique": "flow cytometry; immunofluorescence", "Controlled_Technique": "Flow cytometry; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "CD8⁺ TIL infiltration, CD4⁺ and CD8⁺ T cells, CD8⁺ T-cell granzyme B, perforin", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; T cells; Granzyme B / GZMB; Perforin / PRF1; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "PMN-MDSCs(CD11b⁺Ly6G⁺),PMN-MDSC (Arg-1, iNOS)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs; PMN-MDSCs / G-MDSCs; Arginase-1 / ARG1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "NR", "Drug_Pubchem": "NR", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "RM1 prostate cancer cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2152", "Drug": "CN133 + anti-PD-1", "Drug_category": "others/combination", "Drugbank_ID": "NR", "Target/s_or_mechanism_of_action": "Potent class-I HDAC inhibitor; inhibits HDAC1, HDAC2 and HDAC3", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN(Cc1ccc(/C=C/C(=O)NO)cc1)CC12CC3CC(CC(C3)C1)C2", "Single/Combination": "Combination", "PMID": "37880708", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Subcutaneous MyC-CaP prostate-cancer model", "System": null, "Dose": "CN133 1 mg/kg IP twice/week + anti-PD-1 10 mg/kg IP twice/week", "Technique": "flow cytometry; immunofluorescence", "Controlled_Technique": "Flow cytometry; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "CD8⁺ TIL infiltration, CD4⁺ and CD8⁺ T cells, CD8⁺ T-cell granzyme B, perforin", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; T cells; Granzyme B / GZMB; Perforin / PRF1; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "PMN-MDSCs(CD11b⁺Ly6G⁺),PMN-MDSC (Arg-1, iNOS)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs; PMN-MDSCs / G-MDSCs; Arginase-1 / ARG1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "NR", "Drug_Pubchem": "NR", "Animal_Strain_used": "FVB", "Cell_line_used_to_induce_tumor_in_mice": "MyC-CaP", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2153", "Drug": "Trabectedin + oHSV 107107", "Drug_category": "others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "Binds DNA minor groove; interferes with transcription and DNA repair", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39492947", "Cancer_Type": "Rhabdomyosarcoma", "Cancer_Type_Description": "Human rhabdomyosarcoma PDX", "System": null, "Dose": "0.15 mg/kg IV on days 0 and 7; HSV1716 intratumorally on days 0 and 2", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "Increased granzyme expression in tumor-infiltrating T cells and NK cells; oHSV-associated increase in tumor-infiltrating GP70+ CD8 T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; NK cells; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "decrease in immunosuppressive cells, including CD206hi tumor-associated macrophages (TAM), T regulatory cells, and CTLA4+ CD4 T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD206 / MRC1; CTLA-4; Regulatory T cells / Tregs; Macrophages; Tumor-associated macrophages / TAMs; T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06199", "Drug_Pubchem": "108150", "Animal_Strain_used": "CB17 SCID", "Cell_line_used_to_induce_tumor_in_mice": "PDX-0027", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2154", "Drug": "NHS-IL12", "Drug_category": "others/combination", "Drugbank_ID": "DB17585", "Target/s_or_mechanism_of_action": "Tumor-targeted IL-12; activation of innate/adaptive immunity and IFN-γ pathways", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NR", "Single/Combination": "Single", "PMID": "35764364", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "MHC-I-deficient, IFN-γ-resistant RVP3 sarcoma", "System": null, "Dose": "2 µg s.c., alternate days ×3", "Technique": "Flow cytometry; cytokine/chemokine analysis", "Controlled_Technique": "Flow cytometry; Cytokine/chemokine analysis", "Immune_System-Function_enhanced/numbers_increased": "Increased M1-like TAMs; decreased M2-like TAMs; increased M1:M2 ratio", "Controlled_Terms_Function_enhanced_Number_increased": "Macrophages", "Immune_System-Function_inhibited/numbers_decreased": "M2-like TAMs decreased", "Controlled_Terms_Function_inhibited_Number_decreased": "Macrophages", "Immune_System_function_unaffected": "NK TIL number remained unchanged", "Controlled_Terms_Unaffected": "NK cells; Immune-cell infiltration", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "NR", "Drug_Pubchem": "NR", "Animal_Strain_used": "Female C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "RVP3", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2166", "Drug": "Palbociclib", "Drug_category": "others/combination", "Drugbank_ID": "DB09073", "Target/s_or_mechanism_of_action": "Inhibits CDK4/6, reducing RB1 phosphorylation and cell-cycle progression", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single", "PMID": "32661093", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "BRAF V600E-mutant, PTEN-loss melanoma", "System": null, "Dose": "429 ppm in chow", "Technique": "Flow cytometry; Western blot", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "Increased tumor immunogenicity and CD8⁺ T-cell infiltration , CD137L (4-1BBL) expression is implicated in the immune response to treatment", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD137 / 4-1BB; T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "No significant changes reported in CD4⁺ T cells, FOXP3⁺ regulatory T cells or NK cells in the reported comparison", "Controlled_Terms_Unaffected": "CD4; FOXP3; Regulatory T cells / Tregs; NK cells; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10372", "Drug_Pubchem": "5330286", "Animal_Strain_used": "C57BL/6; NSG", "Cell_line_used_to_induce_tumor_in_mice": "D4M3.A", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2157", "Drug": "Trabectedin + rRp450 oHSV", "Drug_category": "others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "Binds DNA minor groove; interferes with transcription and DNA repair", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39492947", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Human Ewing sarcoma xenograft", "System": null, "Dose": "0.15 mg/kg IV on days 0 and 7; oHSV 107107 PFU intratumorally on days 0 and 2", "Technique": "RNA-seq, flow cytometry", "Controlled_Technique": "Gene expression/sequencing analysis; Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Increased granzyme expression in tumor-infiltrating T cells and NK cells; oHSV-associated increase in tumor-infiltrating GP70+ CD8 T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; NK cells; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "decrease in immunosuppressive cells, including CD206hi tumor-associated macrophages (TAM), T regulatory cells, and CTLA4+ CD4 T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD206 / MRC1; CTLA-4; Regulatory T cells / Tregs; Macrophages; Tumor-associated macrophages / TAMs; T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06199", "Drug_Pubchem": "108150", "Animal_Strain_used": "Athymic nude", "Cell_line_used_to_induce_tumor_in_mice": "A673", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2158", "Drug": "Trabectedin + rRp450 oHSV", "Drug_category": "others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "Binds DNA minor groove; interferes with transcription and DNA repair", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39492947", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Human Ewing sarcoma PDX", "System": null, "Dose": "0.15 mg/kg IV on days 0 and 7; oHSV 107107 PFU intratumorally on days 0 and 2", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "Increased granzyme expression in tumor-infiltrating T cells and NK cells; oHSV-associated increase in tumor-infiltrating GP70+ CD8 T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; NK cells; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "decrease in immunosuppressive cells, including CD206hi tumor-associated macrophages (TAM), T regulatory cells, and CTLA4+ CD4 T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD206 / MRC1; CTLA-4; Regulatory T cells / Tregs; Macrophages; Tumor-associated macrophages / TAMs; T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06199", "Drug_Pubchem": "108150", "Animal_Strain_used": "Athymic nude", "Cell_line_used_to_induce_tumor_in_mice": "CHLA258 (PDX)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2159", "Drug": "Trabectedin + oHSV 107107", "Drug_category": "others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "Binds DNA minor groove; interferes with transcription and DNA repair", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39492947", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Human Ewing sarcoma PDX", "System": null, "Dose": "0.15 mg/kg IV on days 0 and 7; oHSV 107107 PFU intratumorally on days 0 and 2", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "Increased granzyme expression in tumor-infiltrating T cells and NK cells; oHSV-associated increase in tumor-infiltrating GP70+ CD8 T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; NK cells; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "decrease in immunosuppressive cells, including CD206hi tumor-associated macrophages (TAM), T regulatory cells, and CTLA4+ CD4 T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD206 / MRC1; CTLA-4; Regulatory T cells / Tregs; Macrophages; Tumor-associated macrophages / TAMs; T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06199", "Drug_Pubchem": "108150", "Animal_Strain_used": "Athymic nude", "Cell_line_used_to_induce_tumor_in_mice": "EW5 (PDX)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2160", "Drug": "Trabectedin + oHSV 107107", "Drug_category": "others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "Binds DNA minor groove; interferes with transcription and DNA repair", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39492947", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Human Ewing sarcoma xenograft in NK-deficient mice", "System": null, "Dose": "0.15 mg/kg IV on days 0 and 7; HSV1716 intratumorally on days 0 and 2", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "Increased granzyme expression in tumor-infiltrating T cells and NK cells; oHSV-associated increase in tumor-infiltrating GP70+ CD8 T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; NK cells; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "decrease in immunosuppressive cells, including CD206hi tumor-associated macrophages (TAM), T regulatory cells, and CTLA4+ CD4 T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD206 / MRC1; CTLA-4; Regulatory T cells / Tregs; Macrophages; Tumor-associated macrophages / TAMs; T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06199", "Drug_Pubchem": "108150", "Animal_Strain_used": "NSG-SGM3", "Cell_line_used_to_induce_tumor_in_mice": "A673", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2161", "Drug": "Trabectedin + oHSV 107107", "Drug_category": "others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "Binds DNA minor groove; interferes with transcription and DNA repair", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39492947", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Syngeneic murine osteosarcoma", "System": null, "Dose": "0.15 mg/kg IV on day 0 for immune profiling; HSV1716 108108 PFU/mL intratumorally on days 0, 2 and 4", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "Increased granzyme expression in tumor-infiltrating T cells and NK cells; oHSV-associated increase in tumor-infiltrating GP70+ CD8 T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; NK cells; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "decrease in immunosuppressive cells, including CD206hi tumor-associated macrophages (TAM), T regulatory cells, and CTLA4+ CD4 T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD206 / MRC1; CTLA-4; Regulatory T cells / Tregs; Macrophages; Tumor-associated macrophages / TAMs; T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06199", "Drug_Pubchem": "108150", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "K7M2", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2162", "Drug": "Trabectedin + rRp450 oHSV", "Drug_category": "others/combination", "Drugbank_ID": "DB05109", "Target/s_or_mechanism_of_action": "Binds DNA minor groove; interferes with transcription and DNA repair", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=CC2=C([C@@H]3[C@@H]4[C@H]5C6=C(C(=C7C(=C6[C@@H](N4[C@H]([C@H](C2)N3C)O)COC(=O)[C@@]8(CS5)C9=CC(=C(C=C9CCN8)O)OC)OCO7)C)OC(=O)C)C(=C1OC)O", "Single/Combination": "Combination", "PMID": "39492947", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Syngeneic murine osteosarcoma", "System": null, "Dose": "0.15 mg/kg IV in initial regimen; dose alterations were investigated due to toxicity; oHSV intratumorally", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "Increased granzyme expression in tumor-infiltrating T cells and NK cells; oHSV-associated increase in tumor-infiltrating GP70+ CD8 T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; NK cells; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "decrease in immunosuppressive cells, including CD206hi tumor-associated macrophages (TAM), T regulatory cells, and CTLA4+ CD4 T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD206 / MRC1; CTLA-4; Regulatory T cells / Tregs; Macrophages; Tumor-associated macrophages / TAMs; T cells; CD4+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06199", "Drug_Pubchem": "108150", "Animal_Strain_used": "B6-albino; C57BL/6 background", "Cell_line_used_to_induce_tumor_in_mice": "F420", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2163", "Drug": "All-trans-retinoic acid (ATRA), or Retinoic acid/ Tretinoin", "Drug_category": "others/combination", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Combination", "PMID": "12907617", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Fibrosarcoma", "System": null, "Dose": "ATRA pellets (21-day release, 5 mg)", "Technique": "ELISPOT assay", "Controlled_Technique": "ELISpot/FluoroSpot assay; Cytokine/chemokine analysis", "Immune_System-Function_enhanced/numbers_increased": "antigenspecific IFN-γ -producing T cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00094", "Drug_Pubchem": "5538", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "C3", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2164", "Drug": "All-trans-retinoic acid (ATRA), or Retinoic acid/ Tretinoin", "Drug_category": "others/combination", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Combination", "PMID": "12907617", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma", "System": null, "Dose": "ATRA pellets (21-day release, 5 mg)", "Technique": "ELISPOT assay, Flow cytometry", "Controlled_Technique": "ELISpot/FluoroSpot assay; Cytokine/chemokine analysis; Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "antigenspecific T cells", "Controlled_Terms_Function_enhanced_Number_increased": "T cells", "Immune_System-Function_inhibited/numbers_decreased": "Gr-1+CD11b+ ImCs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00094", "Drug_Pubchem": "5538", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "MethA sarcoma", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2165", "Drug": "Entinostat + NHS-IL12", "Drug_category": "others/combination", "Drugbank_ID": "DB11841 + DB17585", "Target/s_or_mechanism_of_action": "Combined epigenetic and cytokine immunostimulation; activation of CD8+ T/NK cells, APCs and M1-like macrophages", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "Entinostat SMILES + NHS-IL12 NR", "Single/Combination": "Combination", "PMID": "35764364", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "MHC-I-deficient, IFN-γ-resistant RVP3 sarcoma", "System": null, "Dose": "Entinostat 6 mg/kg/day p.o.; NHS-IL12 2 µg s.c., alternate days ×3", "Technique": "Flow cytometry; cytokine/chemokine analysis; immunophenotyping", "Controlled_Technique": "Flow cytometry; Cytokine/chemokine analysis; Immune-cell profiling/phenotyping", "Immune_System-Function_enhanced/numbers_increased": "cytolytic/proliferative CD8+ TILs, NK cells,  M1-like TAMs, increased B-cell activity, increased DC MHC-II/PD-L1,  CXCL9/CXCL13/CCL20/CXCL5", "Controlled_Terms_Function_enhanced_Number_increased": "CCL2 / MCP-1; CXCL9; CXCL13; CD8; PD-L1 / CD274; Macrophages; Dendritic cells; NK cells; B cells; MHC class II; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "Decreased M2-like TAMs; M1:M2 ratio increased", "Controlled_Terms_Function_inhibited_Number_decreased": "Macrophages", "Immune_System_function_unaffected": "NK TIL absolute number unchanged", "Controlled_Terms_Unaffected": "NK cells; Immune-cell infiltration", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338 + NR", "Drug_Pubchem": "4261 + NR", "Animal_Strain_used": "Female C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "RVP3", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1887", "Drug": "UNC2025", "Drug_category": "Tyrosine Kinase inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "28605477", "Cancer_Type": "Brain cancer", "Cancer_Type_Description": "Glioblastoma", "System": null, "Dose": "UNC2025 (65 mg/kg via oral gavage daily starting day 7", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "F4-80+ cells", "Controlled_Terms_Unaffected": "F4-80+ cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57Bl/6", "Cell_line_used_to_induce_tumor_in_mice": "TRP-MSCV-luc cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2170", "Drug": "AZD0156 + RT + anti-PD-L1", "Drug_category": "others/combination", "Drugbank_ID": "AZD0156", "Target/s_or_mechanism_of_action": "ATM inhibition and RT promote interferon signaling; anti-PD-L1 blocks PD-1/PD-L1 immune-checkpoint signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "37730275", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Murine melanoma model", "System": null, "Dose": "AZD0156: 10 mg/kg orally; RT: 12 Gy; anti-PD-L1: 200 µg intraperitoneally on days 0, 4, 8 and 12", "Technique": "flow cytometry; qPCR; ELISA", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "Improved antitumor response and survival; enhanced antitumor immune activity", "Controlled_Terms_Function_enhanced_Number_increased": "Survival outcome", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1-mediated immune inhibition targeted pharmacologically", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274", "Immune_System_function_unaffected": "NR", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression induced by IFN-β provides a rationale for checkpoint blockade", "Controlled_Terms_Negative_Regulation": "IFN-γ; PD-L1 / CD274", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "B78-D14 (B78)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2171", "Drug": "AZD0156 + RT", "Drug_category": "others/combination", "Drugbank_ID": "AZD0156", "Target/s_or_mechanism_of_action": "ATM inhibition increases radiation-associated cytosolic DNA and STING-dependent IFN-β signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "37730275", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Murine melanoma model", "System": null, "Dose": "AZD0156: 10 mg/kg orally daily for 5 days; RT: 12 Gy", "Technique": "flow cytometry; qPCR; ELISA", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "increased the proportion of CD45+tumor-infiltrating cells composed of CD4+, CD8+, and natural killer (NK)1.1+ cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD45; NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Increased PD-L1 expression", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "B78-D14 (B78)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2172", "Drug": "NextA + anti-SIRPα", "Drug_category": "others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "NextA promotes M1 macrophage polarization; anti-SIRPα blocks SIRPα-mediated immunosuppressive signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "38414061", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Murine melanoma", "System": null, "Dose": "20 mg/kg every other day", "Technique": "In vivo melanoma model; immune-cell analysis", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "M1 Macrophages, CD4⁺ T cells, CD4⁺ and CD8⁺ effector-memory T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; Macrophages; T cells", "Immune_System-Function_inhibited/numbers_decreased": "M2 macrophages", "Controlled_Terms_Function_inhibited_Number_decreased": "Macrophages", "Immune_System_function_unaffected": "Total CD45⁺ immune cells, CD8⁺ T cells, T-regs, CD4⁺/CD8⁺ central-memory T cells", "Controlled_Terms_Unaffected": "CD4; CD8; CD45; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "M2 macrophage-mediated immunosuppression decreased", "Controlled_Terms_Negative_Regulation": "Macrophages", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57BL/6 mice", "Cell_line_used_to_induce_tumor_in_mice": "SM1 melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2173", "Drug": "PD0325901 + Palbociclib", "Drug_category": "others/combination", "Drugbank_ID": "DB09073", "Target/s_or_mechanism_of_action": "Combined MEK and CDK4/6 inhibition; reduces ERK1/2 and RB1 phosphorylation and enhances tumor antigen presentation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "32661093", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "BRAF V600E-mutant, PTEN-loss melanoma", "System": null, "Dose": "7 ppm PD0325901 + 429 ppm palbociclib in chow", "Technique": "Flow cytometry; Western blot, CD8⁺ T-cell depletion; CD137L-receptor blockade", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "Increased MHC-I/MHC-II expression and intratumoral CD8⁺ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; MHC class I; MHC class II; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "CD8⁺ T-cell depletion or CD137L-receptor blockade reduced the duration of tumor control", "Controlled_Terms_Function_inhibited_Number_decreased": "CD8; CD137 / 4-1BB; T cells; Tumor growth / burden outcome", "Immune_System_function_unaffected": "No significant changes reported in CD4⁺ T cells, FOXP3⁺ regulatory T cells or NK cells in the reported profiling experiment", "Controlled_Terms_Unaffected": "CD4; FOXP3; Regulatory T cells / Tregs; NK cells; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10372", "Drug_Pubchem": "5330286", "Animal_Strain_used": "C57BL/6; NSG", "Cell_line_used_to_induce_tumor_in_mice": "D4M3.A", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2175", "Drug": "AZD0156 + RT", "Drug_category": "others/combination", "Drugbank_ID": "AZD0156", "Target/s_or_mechanism_of_action": "ATM inhibition increases radiation-associated cytosolic DNA and STING-dependent IFN-β signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "37730275", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Murine HNSCC model", "System": null, "Dose": "AZD0156: 10 mg/kg orally daily for 5 days; RT: 8 Gy", "Technique": "flow cytometry; qPCR; ELISA", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "Increased CD8+ T-cell infiltration and activation; increased IFN-β and MHC-I expression, upregulated CD69 and the cytotoxic enzyme GZMB in CD8+T cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-β; CD8; CD69; T cells; CD8+ T cells; Granzyme B / GZMB; MHC class I; Immune-cell infiltration; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD4+ T-cell and NK-cell infiltration did not significantly increase in this model", "Controlled_Terms_Unaffected": "CD4; NK cells; T cells; Immune-cell infiltration", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Increased PD-L1 expression", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MOC2", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2176", "Drug": "AZD0156 + RT + anti-PD-L1", "Drug_category": "others/combination", "Drugbank_ID": "AZD0156", "Target/s_or_mechanism_of_action": "ATM inhibition and RT promote interferon signaling; anti-PD-L1 blocks PD-1/PD-L1 immune-checkpoint signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "37730275", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Murine HNSCC model", "System": null, "Dose": "AZD0156: 10 mg/kg orally; RT: 8 Gy; anti-PD-L1: 200 µg intraperitoneally on days 0, 4, 8 and 12", "Technique": "flow cytometry; qPCR; ELISA", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "Increased functional antitumor T-cell responses", "Controlled_Terms_Function_enhanced_Number_increased": "T cells", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1-mediated immune inhibition targeted pharmacologically", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression induced by IFN-β provides a rationale for checkpoint blockade", "Controlled_Terms_Negative_Regulation": "IFN-γ; PD-L1 / CD274", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MOC2", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2177", "Drug": "Entinostat (MS-275) + ERAP1 silencing", "Drug_category": "others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "HDAC inhibition + loss/silencing of ERAP1, altering antigen processing/presentation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3", "Single/Combination": "Combination", "PMID": "39438988", "Cancer_Type": "Brain Cancer", "Cancer_Type_Description": "9464D murine neuroblastoma", "System": null, "Dose": "Entinostat 5 mg/kg/day i.p. ×14 days, ERAP1 genetically silenced", "Technique": "Flow cytometry, IHC, immunofluorescence, immunopeptidomics", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC); Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "CD8⁺ and CD4⁺ TILs, CD8⁺ T-cell activation, IFN-γ/granzyme-B-positive T cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; T cells; Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "Female C57BL/6 mice, 6–8 weeks", "Cell_line_used_to_induce_tumor_in_mice": "9464D", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2178", "Drug": "Entinostat + anti-PD-1 antibody + ERAP1 silencing", "Drug_category": "others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "HDAC inhibition + PD-1 blockade + altered antigen processing/presentation through ERAP1 silencing", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC(=O)OCC3=CN=CC=C3", "Single/Combination": "Combination", "PMID": "39438988", "Cancer_Type": "Brain Cancer", "Cancer_Type_Description": "9464D murine neuroblastoma", "System": null, "Dose": "Entinostat 10 mg/kg oral gavage ×21 days + anti-PD-1 300 mg/mouse i.p. 3 times per week ×21 days + ERAP1 silencing", "Technique": "Flow cytometry, IHC, immunofluorescence", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC); Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "CD8⁺ T-cell infiltration increased", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "PD-1 inhibitory signaling blocked", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-1 / PDCD1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-1 negative regulation inhibited", "Controlled_Terms_Negative_Regulation": "PD-1 / PDCD1", "KEGG_Drug_ID": "D09338", "Drug_Pubchem": "4261", "Animal_Strain_used": "Female C57BL/6 mice, 6–8 weeks", "Cell_line_used_to_induce_tumor_in_mice": "9464D", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1956", "Drug": "Plerixafor (AMD3100)", "Drug_category": "Phenylmethylamines", "Drugbank_ID": "DB06809", "Target/s_or_mechanism_of_action": "Plerixafor inhibits the CXCR4 chemokine receptors on CD34+ cells and reversibly blocks binding of the ligand, stromal cell-derived factor-1-alpha (SDF-1α). By blocking the interaction between SDF-1α and CXCR4 with plerixafor, mobilization of progenitor cells is triggered.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C(N1CCCNCCNCCCNCC1)C1=CC=C(CN2CCCNCCNCCCNCC2)C=C1", "Single/Combination": "Single Drug", "PMID": "30700545", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Metastatic Breast Cancer", "System": null, "Dose": "AMD3100 10 mg/kg/day", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "αSMA+ cells", "Controlled_Terms_Function_inhibited_Number_decreased": "Alpha-smooth muscle actin (α-SMA)-positive cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08971", "Drug_Pubchem": "65015", "Animal_Strain_used": "wild-type FVB", "Cell_line_used_to_induce_tumor_in_mice": "CFP-labeled MCa-M3C cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1957", "Drug": "Plerixafor (AMD3100)", "Drug_category": "Phenylmethylamines", "Drugbank_ID": "DB06809", "Target/s_or_mechanism_of_action": "Plerixafor inhibits the CXCR4 chemokine receptors on CD34+ cells and reversibly blocks binding of the ligand, stromal cell-derived factor-1-alpha (SDF-1α). By blocking the interaction between SDF-1α and CXCR4 with plerixafor, mobilization of progenitor cells is triggered.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C(N1CCCNCCNCCCNCC1)C1=CC=C(CN2CCCNCCNCCCNCC2)C=C1", "Single/Combination": "Single Drug", "PMID": "30700545", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Metastatic Breast Cancer", "System": null, "Dose": "AMD3100 10 mg/kg/day", "Technique": "QRT-PCR array", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "Ifng and Gzmb", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": "Cxcl5 and Cxcr2", "Controlled_Terms_Function_inhibited_Number_decreased": "CXCL5", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08971", "Drug_Pubchem": "65015", "Animal_Strain_used": "αSMA-dsRed", "Cell_line_used_to_induce_tumor_in_mice": "CFP-labeled MCa-M3C cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1958", "Drug": "Plerixafor (AMD3100)", "Drug_category": "Phenylmethylamines", "Drugbank_ID": "DB06809", "Target/s_or_mechanism_of_action": "Plerixafor inhibits the CXCR4 chemokine receptors on CD34+ cells and reversibly blocks binding of the ligand, stromal cell-derived factor-1-alpha (SDF-1α). By blocking the interaction between SDF-1α and CXCR4 with plerixafor, mobilization of progenitor cells is triggered.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C(N1CCCNCCNCCCNCC1)C1=CC=C(CN2CCCNCCNCCCNCC2)C=C1", "Single/Combination": "Single Drug", "PMID": "30700545", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Metastatic Breast Cancer", "System": null, "Dose": "AMD3100 10 mg/kg/day", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "cytotoxic T lymphocytes (CTLs) infilteration", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; Cytotoxic T lymphocytes / CTLs", "Immune_System-Function_inhibited/numbers_decreased": "cancer-associated fibroblasts (CAFs), αSMA+ cells at both the center and periphery of the tumors, infiltration of FoxP3+ regulatory T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "FOXP3; Regulatory T cells / Tregs; T cells; Immune-cell infiltration", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08971", "Drug_Pubchem": "65015", "Animal_Strain_used": "αSMA-dsRed", "Cell_line_used_to_induce_tumor_in_mice": "CFP-labeled MCa-M3C cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1959", "Drug": "Plerixafor (AMD3100)", "Drug_category": "Phenylmethylamines", "Drugbank_ID": "DB06809", "Target/s_or_mechanism_of_action": "Plerixafor inhibits the CXCR4 chemokine receptors on CD34+ cells and reversibly blocks binding of the ligand, stromal cell-derived factor-1-alpha (SDF-1α). By blocking the interaction between SDF-1α and CXCR4 with plerixafor, mobilization of progenitor cells is triggered.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C(N1CCCNCCNCCCNCC1)C1=CC=C(CN2CCCNCCNCCCNCC2)C=C1", "Single/Combination": "Single Drug", "PMID": "30700545", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Metastatic Breast Cancer", "System": null, "Dose": "AMD3100 10 mg/kg/day", "Technique": "Flow cytometry, Q-PCR", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "cytotoxic CD8+ CTLs", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Cytotoxic T lymphocytes / CTLs", "Immune_System-Function_inhibited/numbers_decreased": "Treg cell fractions, 50% reduction in CD11b+ Gr1+ Ly6G+ neutrophils , CD11b+ F4/80+ macrophages CXCR4 in αSMA+ cell populations in the tumors , Cxcr4 and Cxcl12 in the tumors", "Controlled_Terms_Function_inhibited_Number_decreased": "CXCL12 / SDF-1; CD11b / ITGAM; Regulatory T cells / Tregs; Macrophages; Neutrophils / granulocytes; CXCR4", "Immune_System_function_unaffected": "CD45+CD11b+Gr1+ myeloid-derived suppressor cells", "Controlled_Terms_Unaffected": "CD11b / ITGAM; CD45; Myeloid-derived suppressor cells / MDSCs", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08971", "Drug_Pubchem": "65015", "Animal_Strain_used": "αSMA-Cre-ERT2/Cxcr4flox/flox", "Cell_line_used_to_induce_tumor_in_mice": "E0771 breast tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1967", "Drug": "CXCR4 inhibitor AMD 3100 /\n Plerixafor", "Drug_category": "Phenylmethylamines", "Drugbank_ID": "DB06809", "Target/s_or_mechanism_of_action": "Plerixafor inhibits the CXCR4 chemokine receptors on CD34+ cells and reversibly blocks binding of the ligand, stromal cell-derived factor-1-alpha (SDF-1α). By blocking the interaction between SDF-1α and CXCR4 with plerixafor, mobilization of progenitor cells is triggered.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C(N1CCCNCCNCCCNCC1)C1=CC=C(CN2CCCNCCNCCCNCC2)C=C1", "Single/Combination": "Single Drug", "PMID": "30802149", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": null, "Dose": "AMD3100 (3 mg/kg of mouse body weight) 10 times every other day from d 20 post–tumor implantation", "Technique": "ELISA, Flow cytometery", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ and CD4+ T cells intratumoral filteration, FN-γ expressing on CD8+ and CD4+ T cells, forkhead box P3 (FoxP3)+CD25−CD4+ T cells in the tumor, IL-2+CD40L+FoxP3+CD25− cells , PD-L1+ CD38− cells IL-2", "Controlled_Terms_Function_enhanced_Number_increased": "IL-2; CD4; CD8; CD25 / IL2RA; CD40L / CD154; PD-L1 / CD274; FOXP3; T cells; CD4+ T cells; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": "CD4+FoxP3+CD25+ Treg cells in tumor CXCL12", "Controlled_Terms_Function_inhibited_Number_decreased": "CXCL12 / SDF-1; CD4; CD25 / IL2RA; FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08971", "Drug_Pubchem": "65015", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "luciferase-expressing syngeneic ID8-luc cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2009", "Drug": "Domatinostat (4SC-202)", "Drug_category": "phenylpyrazoles", "Drugbank_ID": "DB13101", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C=C(C=N1)C1=CC=C(C=C1)S(=O)(=O)N1C=CC(\\C=C\\C(=O)NC2=CC=CC=C2N)=C1", "Single/Combination": "Single Drug", "PMID": "31703604", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "domatinostat (20 mg/kg twice daily)", "Technique": "Flow cytometry and IHC, gene expression by RNA-seq", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC); Gene expression/sequencing analysis; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "CTLs within the tumor core, CD4+ T cells Ifng and IFN-γ APM and MHC-I and -II genes", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; MHC class I; T cells; CD4+ T cells; Cytotoxic T lymphocytes / CTLs; Antigen processing and presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "15985904", "Animal_Strain_used": "BALB/c nude ( irradiated with a γ-source (whole-body irradiation, 2 Gy, 60Co) 24 h) and BALB/c immunocompetent", "Cell_line_used_to_induce_tumor_in_mice": "CT26 cell", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2010", "Drug": "Domatinostat (4SC-202)", "Drug_category": "phenylpyrazoles", "Drugbank_ID": "DB13101", "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1C=C(C=N1)C1=CC=C(C=C1)S(=O)(=O)N1C=CC(\\C=C\\C(=O)NC2=CC=CC=C2N)=C1", "Single/Combination": "Single Drug", "PMID": "31703604", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "20 mg/kg domatinostat", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CTLs within the tumors (CTLs - effector memory (EM) phenotype (CD44+CD62L−) and expressed the activation markers CD69 and GITR as well as the inhibitory marker PD-1, LAG3 or both ) MHC-I and -II molecules on C38 tumor cells and of MHC-II molecules on M1 macrophages", "Controlled_Terms_Function_enhanced_Number_increased": "CD69; PD-1 / PDCD1; LAG-3; MHC class II; MHC class I; Macrophages; Cytotoxic T lymphocytes / CTLs; M1 macrophage phenotype", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "15985904", "Animal_Strain_used": "C57BL/6 J", "Cell_line_used_to_induce_tumor_in_mice": "C38 tumor fragments", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1668", "Drug": "Oxaliplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00526", "Target/s_or_mechanism_of_action": "Inhibiting DNA synthesis and transcription", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "[H][N]1([H])[C@@H]2CCCC[C@H]2[N]([H])([H])[Pt]11OC(=O)C(=O)O1", "Single/Combination": null, "PMID": "19881547", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": null, "Dose": "(250 mg/kg)", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "pre-apoptotic exposure of calreticulin (CRT)", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis / caspase activation; Calreticulin / CRT", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01790", "Drug_Pubchem": "6857599", "Animal_Strain_used": "BALB/c (H-2d)", "Cell_line_used_to_induce_tumor_in_mice": "CT26 colon", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1825", "Drug": "Cisplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": "Single Drug", "PMID": "26590944", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - A Murine B16 Melanoma Model", "System": null, "Dose": "2.5 - 7.5 mg/kg", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "IFN-g CD 80, CD 86", "Controlled_Terms_Function_enhanced_Number_increased": "Interferon gamma (IFN-γ); CD80 (B7-1); CD86 (B7-2)", "Immune_System-Function_inhibited/numbers_decreased": "the frequency of MDSC decreased remarkably in regional tumor and spleen in given doses. granzyme 1 expression on MDSC decreased", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": "CD11b and CD3+, CD4+, CD8+ T cells and B cells MHC II", "Controlled_Terms_Unaffected": "CD4; CD8; CD3; CD11b / ITGAM; MHC class II; B cells; T cells; CD8+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00275", "Drug_Pubchem": "5702198", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1855", "Drug": "Cisplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": "Single Drug", "PMID": "27569212", "Cancer_Type": "Hpv16-Expressing Tumors", "Cancer_Type_Description": "Human Papillomavirus (Hpv)-Associated Cancer", "System": null, "Dose": "Maximum tolerated dose of 10 mg/kg", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "tumor-specific effector and memory CD8+ T cells, and intratumoral phagocytic APCs (cd 11b+) IFNg and TNF, monocyte chemotactic protein 1 (MCP-1/\n CCL2) CD70, CD80, and CD86 b HMGB1 release of tumor cells", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; TNF-α / TNF; CCL2 / MCP-1; CD8; CD80; CD86; Monocytes; T cells; CD8+ T cells; HMGB1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD4+CD25+Foxp3+ T cells and MDSCs OX40L, 4-1BBL, and ICOSL", "Controlled_Terms_Unaffected": "CD4; CD25 / IL2RA; FOXP3; Myeloid-derived suppressor cells / MDSCs; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00275", "Drug_Pubchem": "5702198", "Animal_Strain_used": "C57/BL6", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1986", "Drug": "Cisplatin-based NAC", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": null, "PMID": "31404614", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC", "System": null, "Dose": null, "Technique": "RT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression on tumor AKT ACTIVATION", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; Immune checkpoint pathway; AKT signaling", "KEGG_Drug_ID": "D00275", "Drug_Pubchem": "5702198", "Animal_Strain_used": "athymic NMRI-Foxn1 nu/nu (Janvier™)", "Cell_line_used_to_induce_tumor_in_mice": "human lung adenocarcinoma cell line (A549)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2027", "Drug": "Oxaliplatin", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00526", "Target/s_or_mechanism_of_action": "Inhibiting DNA synthesis and transcription", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "[H][N]1([H])[C@@H]2CCCC[C@H]2[N]([H])([H])[Pt]11OC(=O)C(=O)O1", "Single/Combination": "Single Drug", "PMID": "32079180", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "6 mg/kg,", "Technique": "Immunoblotting,immunohistochemistry,qRT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Western blot/immunoblot analysis; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "Ifng, Ifngr1 Cd274 (Pdl1) and Pdcd1lg2 (Pdl2) tumor programmed cell death 1 ligand 1 (PD-L1) level, phosphorylation of STAT1 and its downstream transcription factor IRF1", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; PD-L1 / CD274; PD-L2 / PDCD1LG2; Immune checkpoint pathway; STAT1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01790", "Drug_Pubchem": "6857599", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1987", "Drug": "Teniposide", "Drug_category": "Podophyllotoxins", "Drugbank_ID": "DB00444", "Target/s_or_mechanism_of_action": "Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "[H][C@]12COC(=O)[C@]1([H])[C@H](C1=CC(OC)=C(O)C(OC)=C1)C1=C(C=C3OCOC3=C1)[C@H]2O[C@]1([H])O[C@]2([H])CO[C@H](O[C@@]2([H])[C@H](O)[C@H]1O)C1=CC=CS1", "Single/Combination": "Single Drug", "PMID": "31408442", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Adenocarcinoma", "System": null, "Dose": "50 μM teniposide (For the immunization study)", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "MHC-I, MHC-II, and antigen presentation machinery gene expression Immunogenic cell death", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class II; MHC class I; Immunogenic cell death; Antigen processing and presentation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02698", "Drug_Pubchem": "452548", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1993", "Drug": "AST 487", "Drug_category": "RET kinase inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31540894", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Papillary Thyroid Carcinoma", "System": null, "Dose": "AST 487(10mg/kg-35mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "HLA-A,B,C", "Controlled_Terms_Function_enhanced_Number_increased": "HLA class I antigen", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "PD-L1", "Controlled_Terms_Unaffected": "PD-L1 / CD274; Immune checkpoint pathway", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "immunodeficient NRG (NOD-Rag1null IL2rgnull)", "Cell_line_used_to_induce_tumor_in_mice": "TPC1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1645", "Drug": "All-trans-retinoic acid (ATRA), or Retinoic acid/ Tretinoin", "Drug_category": "Retinoids", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Single Drug", "PMID": "12907617", "Cancer_Type": "Adenocarcinoma", "Cancer_Type_Description": "Mammalian Adenocarcinoma", "System": null, "Dose": "ATRA pellets (21-day release, 5 mg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Gr-1+CD11b+ ImCs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00094", "Drug_Pubchem": "5538", "Animal_Strain_used": "C57BL/6 and BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "DA3-HA", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1647", "Drug": "All-trans-retinoic acid (ATRA), or Retinoic acid/ Tretinoin", "Drug_category": "Retinoids", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Single Drug", "PMID": "12907617", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Fibrosarcoma", "System": null, "Dose": "ATRA pellets (21-day release, 5 mg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Gr-1+CD11b+ ImCs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00094", "Drug_Pubchem": "5538", "Animal_Strain_used": "C57BL/6 and BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "C3", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1885", "Drug": "All-trans-retinoic acid (ATRA), or Retinoic acid/ Tretinoin", "Drug_category": "Retinoids", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Single Drug", "PMID": "28515123", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Osteosarcoma", "System": null, "Dose": "a daily treatment of 40 mg/kg ATRA (i.g.) for 1 to 2 consecutive weeks (intravenous injection) or 4 consecutive weeks (intrafemural injection)", "Technique": "Immunohistochemical Staining", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "F4/80+CD209+ (M2-like) TAMs secretion of MMP12 in M2 macrophages", "Controlled_Terms_Function_inhibited_Number_decreased": "Tumor-associated macrophages / TAMs; Macrophages; M2 macrophage phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00094", "Drug_Pubchem": "5538", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "K7M2 WT cells,", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1984", "Drug": "All-trans-retinoic acid (ATRA), or Retinoic acid/ Tretinoin", "Drug_category": "Retinoids", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Single Drug", "PMID": "31296953", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Osteosarcoma", "System": null, "Dose": "Daily for 7 days with 20 mg/kg ATRA before K7M2 WT cell injection; after inoculation, the mice were treated i.g. daily for 7 days for 4 consecutive weeks with 40 mg/kg ATRA", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "F4/80+CD209+ cells", "Controlled_Terms_Function_inhibited_Number_decreased": "F4/80-positive CD209-positive cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00094", "Drug_Pubchem": "5538", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "K7M2 WT osteosarcoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2054", "Drug": "All-trans-retinoic acid (ATRA), or Retinoic acid/ Tretinoin", "Drug_category": "Retinoids", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Single", "PMID": "12907617", "Cancer_Type": "Adenocarcinoma", "Cancer_Type_Description": "Mammalian Adenocarcinoma", "System": null, "Dose": "ATRA pellets (21-day release, 5 mg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Gr-1+CD11b+ ImCs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00094", "Drug_Pubchem": "5538", "Animal_Strain_used": "C57BL/6 and BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "DA3-HA", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2074", "Drug": "MSU-42011", "Drug_category": "Retinoids", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "Activates retinoid X receptor (RXR), particularly RXRα", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC(C)CN(C1=NC=C(C=C1)C(=O)O)C2=CC(=CC(=C2)C(C)(C)C)C(C)(C)C", "Single/Combination": "Single", "PMID": "36901727", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "HER2-positive mammary tumors", "System": null, "Dose": "100 mg/kg/day in diet (approximately 25 mg/kg/day body weight) for 10 days", "Technique": "RNA-seq, qPCR, immunohistochemistry, flow cytometry", "Controlled_Technique": "Gene expression/sequencing analysis; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunohistochemistry (IHC); Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "increased IL-18, increased H2-AA/MHC-II expression, increased pro-inflammatory CCL6 evidence of macrophage polarization toward an anti-tumor phenotype (M1), Tlr9 and Irf1, Col6a3 and Map9", "Controlled_Terms_Function_enhanced_Number_increased": "IL-18; Macrophages; MHC class II; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "Decreased F4/80⁺CD206⁺ macrophages, decreased IL-13 (immunosuppressive cytokine)", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-13; CD206 / MRC1; Macrophages; Cytokines", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "154656181", "Animal_Strain_used": "MMTV-Neu transgenic mice", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2075", "Drug": "Bexarotene", "Drug_category": "Retinoids", "Drugbank_ID": "DB00307", "Target/s_or_mechanism_of_action": "Selectively binds and activates RXRα, RXRβ and RXRγ", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=CC2=C(C=C1C(=C)C3=CC=C(C=C3)C(=O)O)C(CCC2(C)C)(C)C", "Single/Combination": "Single", "PMID": "36901727", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "HER2-positive mammary tumors", "System": null, "Dose": "100 mg/kg/day in diet (approximately 25 mg/kg/day body weight) for 10 days", "Technique": "RNA-seq, qPCR, immunohistochemistry, flow cytometry", "Controlled_Technique": "Gene expression/sequencing analysis; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunohistochemistry (IHC); Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "IL-13 expression decreased in BMDMs treated with bexarotene; however, no significant reduction in F4/80⁺CD206⁺ macrophage proportion was observed", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-13; CD206 / MRC1; Macrophages", "Immune_System_function_unaffected": "F4/80⁺CD206⁺ macrophage proportion, IL-18", "Controlled_Terms_Unaffected": "IL-18; CD206 / MRC1; Macrophages", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03106", "Drug_Pubchem": "82146", "Animal_Strain_used": "MMTV-Neu transgenic mice", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2156", "Drug": "All-trans-retinoic acid (ATRA), or Retinoic acid/ Tretinoin", "Drug_category": "Retinoids", "Drugbank_ID": "DB00755", "Target/s_or_mechanism_of_action": "Tretinoin promotes cornified cell detachment and enhances shedding", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C\\C(\\C=C\\C1=C(C)CCCC1(C)C)=C/C=C/C(/C)=C/C(O)=O", "Single/Combination": "Single", "PMID": "12907617", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma - Fibrosarcoma", "System": null, "Dose": "ATRA pellets (21-day release, 5 mg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Gr-1+CD11b+ ImCs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00094", "Drug_Pubchem": "5538", "Animal_Strain_used": "C57BL/6 and BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "C3", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1878", "Drug": "RK20449", "Drug_category": "Src family kinase Inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "28399411", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Human Colon Adenocarcinoma", "System": null, "Dose": "RK20449 (30mg/kg) for 10 days", "Technique": "Quantitative RT-PCR, Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD206-expressing CD45+CD11b+F4/80+ macrophages TAMs and Ki67+ proliferating cells AAM genes Il4, Il10, Il13, Arg1, and Ym1", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-4; IL-10; IL-13; CD11b / ITGAM; CD45; CD206 / MRC1; Tumor-associated macrophages / TAMs; Macrophages; Arginase-1 / ARG1; Cell proliferation / Ki-67", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "Rag1KO", "Cell_line_used_to_induce_tumor_in_mice": "DLD1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1879", "Drug": "RK20449", "Drug_category": "Src family kinase Inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "28399411", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Human Colon Adenocarcinoma", "System": null, "Dose": "RK20449 (30mg/kg) for 10 days", "Technique": "Quantitative RT-PCR, Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD206-expressing CD45+CD11b+F4/80+ macrophages TAMs and Ki67+ proliferating cells AAM genes Il4, Il10, Il13, Arg1, and Ym1", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-4; IL-10; IL-13; CD11b / ITGAM; CD45; CD206 / MRC1; Tumor-associated macrophages / TAMs; Macrophages; Arginase-1 / ARG1; Cell proliferation / Ki-67", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "Rag1KO", "Cell_line_used_to_induce_tumor_in_mice": "HCT116", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1880", "Drug": "RK20449", "Drug_category": "Src family kinase Inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "28399411", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Human Colon Adenocarcinoma", "System": null, "Dose": "RK20449 (30mg/kg) for 10 days", "Technique": "Quantitative RT-PCR, Flow cytometry", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD206-expressing CD45+CD11b+F4/80+ macrophages TAMs and Ki67+ proliferating cells AAM genes Il4, Il10, Il13, Arg1, and Ym1", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-4; IL-10; IL-13; CD11b / ITGAM; CD45; CD206 / MRC1; Tumor-associated macrophages / TAMs; Macrophages; Arginase-1 / ARG1; Cell proliferation / Ki-67", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": "Rag1KO", "Cell_line_used_to_induce_tumor_in_mice": "SW480", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1678", "Drug": "Docetaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01248 (APRD00932)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "[H][C@@]12C[C@H](O)[C@@]3(C)C(=O)[C@H](O)C4=C(C)[C@H](C[C@@](O)([C@@H](OC(=O)C5=CC=CC=C5)[C@]3([H])[C@@]1(CO2)OC(C)=O)C4(C)C)OC(=O)[C@H](O)[C@@H](NC(=O)OC(C)(C)C)C1=CC=CC=C2", "Single/Combination": "Single Drug", "PMID": "20702612", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Mammary Tumor", "System": null, "Dose": "33 mg/kg body weight", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Gr-1+CD11b+ MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; 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Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "CSF1", "Controlled_Terms_Negative_Regulation": "CSF1 / M-CSF", "KEGG_Drug_ID": null, "Drug_Pubchem": "36314", "Animal_Strain_used": "MMTV-PyMT", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1720", "Drug": "Paclitaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01229 (APRD00259, DB05261, DB05927, DB05526, DB05281)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "[H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Single Drug", "PMID": "23359505", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "(1 mg/kg)", "Technique": "Flow cytometry, ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "CD8 T cell effector", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "CD11b+Gr1+ MDSCs TGF-β, GM-CSF, IL-1β, IL-10, IL-5, IL-13, TNF-α and IFN-γ in the primary skin tumor microenvironment p38 MAPK, S100A8/A9", "Controlled_Terms_Function_inhibited_Number_decreased": "IFN-γ; IL-1 family; IL-5; IL-10; IL-13; TNF-α / TNF; GM-CSF / CSF2; TGF-β; CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs; MAPK signaling", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00491", "Drug_Pubchem": "36314", "Animal_Strain_used": "ret transgenic", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1924", "Drug": "Docetaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01248 (APRD00932)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "[H][C@@]12C[C@H](O)[C@@]3(C)C(=O)[C@H](O)C4=C(C)[C@H](C[C@@](O)([C@@H](OC(=O)C5=CC=CC=C5)[C@]3([H])[C@@]1(CO2)OC(C)=O)C4(C)C)OC(=O)[C@H](O)[C@@H](NC(=O)OC(C)(C)C)C1=CC=CC=C0", "Single/Combination": "Single Drug", "PMID": "29500278", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "(DTX; 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It works by inhibiting DNA topoisomerases, type I.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC[C@@]1(O)C(=O)OCC2=C1C=C1N(CC3=CC4=C(C=CC(O)=C4CN(C)C)N=C13)C2=O", "Single/Combination": "Single Drug", "PMID": "28069806", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "20 mg/kg TPT was administered i.p. to the mice every 4 d after the tumor volume reached 100 mm3 (day 0", "Technique": "Flow Cytometry, Immunostaining", "Controlled_Technique": "Flow cytometry; Immunostaining/image analysis", "Immune_System-Function_enhanced/numbers_increased": "CD3+ T cells, CD8+ T cells, neutrophils (Ly-6G+ F4/802), and DCs (I-A/I-E+ CD11c+ )", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD3; CD11c / ITGAX; Neutrophils / granulocytes; Dendritic cells; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08618", "Drug_Pubchem": "60700", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "E0771 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1928", "Drug": "Antibody-Drug Conjugate, Trastuzumab Deruxtecan (DS-8201a)", "Drug_category": "Topoisomerase I Inhibitor", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29703841", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "DS-8201a (10 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells (CD45+CD3+CD8+ cells) and Granzyme B+ CD8+ T cells , ratio of DCs (CD45+CD11c+MHC class II+ cells) to lymphocytes (CD45+ cells) significantly increased , CD86+ cells in DCs CD86 expression on DC , PD-L1 and MHC class I on hHER2+ cells was higher in DS-8201a–treated tumors", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; 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Immunostaining/image analysis", "Immune_System-Function_enhanced/numbers_increased": "MHC class I expression but also PD-L1 expression", "Controlled_Terms_Function_enhanced_Number_increased": "PD-L1 / CD274; MHC class I; Immune checkpoint pathway", "Immune_System-Function_inhibited/numbers_decreased": "Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08086", "Drug_Pubchem": "60838", "Animal_Strain_used": "C3H/HeN", "Cell_line_used_to_induce_tumor_in_mice": "FM3A tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1665", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "19244102", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma (RCC)", "System": null, "Dose": "10–40 mg/kg daily", "Technique": "Fluorescent Immunohistochemistry And Confocal Laser Scanning Microscopy Of Frozen Tumor Sections, Western Blot", "Controlled_Technique": "Western blot/immunoblot analysis; Immunohistochemistry (IHC); Immunofluorescence assay; Microscopy; Confocal microscopy", "Immune_System-Function_enhanced/numbers_increased": "tumor cell apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis / caspase activation", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs , tumor-infiltrating Tregs p-Stat3 inhibition,Cyclin E and Survivin protein expression ,Stat3 activity in MDSCs and macrophages", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; Macrophages; STAT3 signaling; Immune-cell infiltration", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "Renca cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1666", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "19276342", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Tumor", "System": null, "Dose": "0.015 mg", "Technique": "Flow cytometry,RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "T-cell-CD4+ and CD8+ T cells IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD4; CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "CD4+CD25+Foxp3+ Treg, MDSC IL-10, TGF-β PD-1, CTLA4, and BAFF Foxp3", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-10; TGF-β; CD4; CD25 / IL2RA; PD-1 / PDCD1; CTLA-4; FOXP3; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "MCA26", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1674", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "20406969", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Mammary", "System": null, "Dose": "sunitinib (40mg/kg)", "Technique": "Flow cytometry, BrdU assay", "Controlled_Technique": "Flow cytometry; Cell viability/proliferation assay; Cell proliferation assay", "Immune_System-Function_enhanced/numbers_increased": "T-cells", "Controlled_Terms_Function_enhanced_Number_increased": "T cells", "Immune_System-Function_inhibited/numbers_decreased": "CD11b+Gr1+ MDSC, intrasplenic proliferation of m-MDSC", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Myeloid-derived suppressor cells / MDSCs; Monocytic MDSCs / M-MDSCs; Cell proliferation / Ki-67", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "4T1-mammary", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1675", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "20406969", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": null, "Dose": "sunitinib (40mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "T-cells", "Controlled_Terms_Function_enhanced_Number_increased": "T cells", "Immune_System-Function_inhibited/numbers_decreased": "CD11b+Gr1+ MDSC", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; 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Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": "CD4+ and CD8+ cell", "Controlled_Terms_Unaffected": "CD4; CD8", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "murine cell line 1MEA", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1695", "Drug": "Gefitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00317", "Target/s_or_mechanism_of_action": "Gefitinib is an inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase that binds to the adenosine triphosphate (ATP)-binding site of the enzyme.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single Drug", "PMID": "21680779", "Cancer_Type": "Adenocarcinoma", "Cancer_Type_Description": "Adenocarcinoma", "System": null, "Dose": "twice weekly i.p. injections of gemcitabine at a dose of 75µg/g of body weight", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "IFN-γ P-STAT1", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; STAT1", "Immune_System-Function_inhibited/numbers_decreased": "MDSC", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02368", "Drug_Pubchem": "60750", "Animal_Strain_used": "BALB/c X DBA/2F1 (CD2F1)", "Cell_line_used_to_induce_tumor_in_mice": "Colon 26 (C26) tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1696", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "21873989", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastrointestinal Stromal Tumor (GIST)", "System": null, "Dose": "1.12 mg i.p. twice daily based on an established dose of 45 mg kg−1", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "T reg apoptosis selectively within the tumor", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs; Apoptosis / caspase activation", "Immune_System_function_unaffected": "myeloid cells, B cells, NK, or NKT cells IL-4, IL-17, or IFN-γ by CD4+ T cells", "Controlled_Terms_Unaffected": "IFN-γ; IL-4; IL-17 / IL-17A; CD4; NKT cells; B cells; T cells; CD4+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": "5291", "Animal_Strain_used": "(KitV558Δ/+)", "Cell_line_used_to_induce_tumor_in_mice": "spontaneous", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1708", "Drug": "Axitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB06626", "Target/s_or_mechanism_of_action": "Axitinib selectively blocks the tyrosine kinase receptors VEGFR-1 (vascular endothelial growth factor receptor), VEGFR-2, and VEGFR-3.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=C(SC2=CC=C3C(NN=C3\\C=C\\C3=CC=CC=N3)=C2)C=CC=C1", "Single/Combination": "Single Drug", "PMID": "22504156", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "axitinib alone (0.5 mg/day provided via oral gavage on days 7–13)", "Technique": "Flow Cytometry, Rt-Pcr And Fluorescence Microscopy", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Microscopy", "Immune_System-Function_enhanced/numbers_increased": "bulk CD8+ T cells IFN-γ,CXCR3,CXCL10 CD31+ Tbet", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CXCL10 / IP-10; CD8; CD31 / PECAM-1; T cells; CD8+ T cells; CXCR3", "Immune_System-Function_inhibited/numbers_decreased": "Treg (CD4+Foxp3+) phenotypes in the TME", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; FOXP3; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03218", "Drug_Pubchem": "6450551", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MO5 (B16.OVA) tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1718", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "23108136", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": null, "Dose": "40 mg/kg", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Treg", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1721", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "23409093", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "30 mg·kg−1·day−1 sorafenib -60 mg·kg−1·day−1 sorafenib", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "NK cells (CD3− and NK1.1+) CD69", "Controlled_Terms_Negative_Regulation": "CD3; CD69; NK cells", "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Hepa1-6", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1722", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "23424039", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "(25 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "hepatic NK cells", "Controlled_Terms_Function_inhibited_Number_decreased": "NK cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "HBV-tg", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1723", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "23424039", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "(25 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "hepatic NK cells", "Controlled_Terms_Function_inhibited_Number_decreased": "NK cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "LTa/b-tg", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1737", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "23818246", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "(30 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "tumor-infiltrating CD8 T cells IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; T cells; CD8+ T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "PD-1-expressing CD8(+) T cells and regulatory T cells (Tregs)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD8; PD-1 / PDCD1; Regulatory T cells / Tregs; T cells; CD8+ T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "BNL cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1738", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "23818246", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "(30 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "tumor-infiltrating CD8 T cells IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD8; T cells; CD8+ T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "ML-1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1742", "Drug": "Axitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB06626", "Target/s_or_mechanism_of_action": "Axitinib selectively blocks the tyrosine kinase receptors VEGFR-1 (vascular endothelial growth factor receptor), VEGFR-2, and VEGFR-3.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=C(SC2=CC=C3C(NN=C3\\C=C\\C3=CC=CC=N3)=C2)C=CC=C1", "Single/Combination": "Single Drug", "PMID": "24135499", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "axitinib (25 mg/kg, twice a day)", "Technique": "Hematoxylin and eosin staining,TUNEL assay, Q-PCR, Flow cytometry", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR); Apoptosis/cell viability assay; Hematoxylin and eosin (H&E)/histology", "Immune_System-Function_enhanced/numbers_increased": "tumor-infiltrating CD8 +, CD45.2 + cells induced the apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD45; Apoptosis / caspase activation; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs IL-6, TNF-a, and IFN-g", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6; TNF-α / TNF; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": "CD4 + T cells or Treg cells", "Controlled_Terms_Unaffected": "CD4; Regulatory T cells / Tregs; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03218", "Drug_Pubchem": "6450551", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "B16F1 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1747", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "24323358", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastrointestinal Stromal Tumor (GIST)", "System": null, "Dose": "600 mg/liter", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "TAMs and TAMs to become M2-like CD11c, MHC class II, CD80, and CD86 were reduced in TAMs", "Controlled_Terms_Function_inhibited_Number_decreased": "CD80; CD86; CD11c / ITGAX; MHC class II; Tumor-associated macrophages / TAMs; M2 macrophage phenotype", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": "5291", "Animal_Strain_used": "GIST (KITΔV558/+ on a C57BL/6 (B6) background", "Cell_line_used_to_induce_tumor_in_mice": "spontaneous", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1751", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "24734217", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "0.01–1 mg/day", "Technique": "Immunofluorescence Staining And Fluorescence Microscopy", "Controlled_Technique": "Immunofluorescence assay; Microscopy; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "CD8+ TIL", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; Tumor-infiltrating lymphocytes / TILs", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": "3062316", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "M05 melanoma cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1765", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "24994118", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid Cancer - (Anaplastic)", "System": null, "Dose": "orally gavaged with 50 mg/kg dasatinib five days per week", "Technique": "Immunohistochemial Analysis", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD8+ T cells and F4/80+ cells infilateration to tumor tissue, B220+ B cells is observed in tumors, Caspase 3", "Controlled_Terms_Unaffected": "CD8; B cells; T cells; CD8+ T cells; Apoptosis / caspase activation", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": "3062316", "Animal_Strain_used": "B6129SF1/J syngeneic", "Cell_line_used_to_induce_tumor_in_mice": "105 TBP-3743 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1771", "Drug": "Axitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB06626", "Target/s_or_mechanism_of_action": "Axitinib selectively blocks the tyrosine kinase receptors VEGFR-1 (vascular endothelial growth factor receptor), VEGFR-2, and VEGFR-3.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=C(SC2=CC=C3C(NN=C3\\C=C\\C3=CC=CC=N3)=C2)C=CC=C1", "Single/Combination": "Single Drug", "PMID": "25081318", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal - Metastatic Renal Cell Cancer", "System": null, "Dose": "25 mg/ kg daily via oral administration", "Technique": "Tunel Assay,Flow Cytometry,Western Blotting, Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Immunohistochemistry (IHC); Apoptosis/cell viability assay", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T-cells in TME apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; T cells; Apoptosis / caspase activation", "Immune_System-Function_inhibited/numbers_decreased": "MDSC p-STAT3", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells / MDSCs; STAT3 signaling", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03218", "Drug_Pubchem": "6450551", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "Renca", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1779", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "25388653", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Adenocarcinoma", "System": null, "Dose": "cabozantinib-containing diet for 10 or 35 days", "Technique": "Immunohistochemical Analysis, Flow Cytometry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells,increased infiltration of CD3+ lymphocytes", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD3; T cells; CD8+ T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "T regulatory cells (Tregs), myeloid-derived suppressor cells (MDSCs), infiltration of MDSCs,infiltrating tumor-associated macrophages vascular density of MC38-CEA tumors", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; Tumor-associated macrophages / TAMs; Macrophages; Immune-cell infiltration", "Immune_System_function_unaffected": "CD4+ T cells in the spleen", "Controlled_Terms_Unaffected": "CD4; T cells; CD4+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10062", "Drug_Pubchem": "25102847", "Animal_Strain_used": "CEA-Tg C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1780", "Drug": "Golvatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB11977", "Target/s_or_mechanism_of_action": "An orally bioavailable dual kinase inhibitor of c-Met (hepatocyte growth factor receptor) and VEGFR-2 (vascular endothelial growth factor receptor-2) tyrosine kinases with potential antineoplastic activity. Golvatinib binds to and inhibits the activities of both c-Met and VEGFR-2, which may inhibit tumor cell growth and survival of tumor cells that overexpress these receptor tyrosine kinases. c-Met and VEGFR-2 are upregulated in a variety of various tumor cell types and play important roles in tumor cell growth, migration and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC1)C1CCN(CC1)C(=O)NC1=CC(OC2=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C(F)=C2)=CC=N1", "Single/Combination": "Single Drug", "PMID": "25458359", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid -Human Thyroid Cancer", "System": null, "Dose": "golvatinib 100 mg/kg", "Technique": "Immunohistochemical Analysis, Flow Cytometry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "myeloid cells (CD11b+), macrophages (F4/80+ in Flow cytometry, CD11b+F4/80+ in immunohistochemistry)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; Macrophages", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "16118392", "Animal_Strain_used": "Nude (CAnN.Cg-Foxn1nu/CrlCrlj; female, 5–6 weeks old)", "Cell_line_used_to_induce_tumor_in_mice": "K1/angiopoietin-2 (Ang2)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1782", "Drug": "Lenvatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB09078", "Target/s_or_mechanism_of_action": "Lenvatinib is a receptor tyrosine kinase (RTK) inhibitor that inhibits the kinase activities of vascular endothelial growth factor (VEGF) receptors VEGFR1 (FLT1), VEGFR2 (KDR), and VEGFR3 (FLT4). Lenvatinib also inhibits other RTKs that have been implicated in pathogenic angiogenesis, tumor growth, and cancer progression in addition to their normal cellular functions, including fibroblast growth factor (FGF) receptors FGFR1, 2, 3, and 4; the platelet derived growth factor receptor alpha (PDGFRα), KIT, and RET", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COC1=C(C=C2C(OC3=CC=C(NC(=O)NC4CC4)C(Cl)=C3)=CC=NC2=C1)C(N)=O", "Single/Combination": "Single Drug", "PMID": "25458359", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Thyroid -Human Thyroid Cancer", "System": null, "Dose": "lenvatinib 10 mg/kg", "Technique": "Immunohistochemical Analysis, Flow Cytometry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "myeloid cells (CD11b+)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09919", "Drug_Pubchem": "9823820", "Animal_Strain_used": "Nude (CAnN.Cg-Foxn1nu/CrlCrlj; female, 5–6 weeks old)", "Cell_line_used_to_induce_tumor_in_mice": "K1/angiopoietin-2 (Ang2)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1783", "Drug": "Golvatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB11977", "Target/s_or_mechanism_of_action": "An orally bioavailable dual kinase inhibitor of c-Met (hepatocyte growth factor receptor) and VEGFR-2 (vascular endothelial growth factor receptor-2) tyrosine kinases with potential antineoplastic activity. Golvatinib binds to and inhibits the activities of both c-Met and VEGFR-2, which may inhibit tumor cell growth and survival of tumor cells that overexpress these receptor tyrosine kinases. c-Met and VEGFR-2 are upregulated in a variety of various tumor cell types and play important roles in tumor cell growth, migration and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC1)C1CCN(CC1)C(=O)NC1=CC(OC2=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C(F)=C2)=CC=N1", "Single/Combination": "Single Drug", "PMID": "25458359", "Cancer_Type": "Uterus", "Cancer_Type_Description": "Endometrial - Human Endometrial Cancer", "System": null, "Dose": "golvatinib 100 mg/kg", "Technique": "Immunohistochemical Analysis, Flow Cytometry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "macrophage population", "Controlled_Terms_Function_inhibited_Number_decreased": "Macrophages", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "16118392", "Animal_Strain_used": "Nude (CAnN.Cg-Foxn1nu/CrlCrlj; female, 5–6 weeks old)", "Cell_line_used_to_induce_tumor_in_mice": "AN3CA tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1785", "Drug": "Lenvatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB09078", "Target/s_or_mechanism_of_action": "Lenvatinib is a receptor tyrosine kinase (RTK) inhibitor that inhibits the kinase activities of vascular endothelial growth factor (VEGF) receptors VEGFR1 (FLT1), VEGFR2 (KDR), and VEGFR3 (FLT4). Lenvatinib also inhibits other RTKs that have been implicated in pathogenic angiogenesis, tumor growth, and cancer progression in addition to their normal cellular functions, including fibroblast growth factor (FGF) receptors FGFR1, 2, 3, and 4; the platelet derived growth factor receptor alpha (PDGFRα), KIT, and RET", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COC1=C(C=C2C(OC3=CC=C(NC(=O)NC4CC4)C(Cl)=C3)=CC=NC2=C1)C(N)=O", "Single/Combination": "Single Drug", "PMID": "25458359", "Cancer_Type": "Uterus", "Cancer_Type_Description": "Endometrial - Human Endometrial Cancer", "System": null, "Dose": "lenvatinib 10 mg/kg", "Technique": "Immunohistochemical Analysis, Flow Cytometry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "TEM infiltration", "Controlled_Terms_Function_enhanced_Number_increased": "Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09919", "Drug_Pubchem": "9823820", "Animal_Strain_used": "Nude (CAnN.Cg-Foxn1nu/CrlCrlj; female, 5–6 weeks old)", "Cell_line_used_to_induce_tumor_in_mice": "AN3CA tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1786", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "25529917", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "sorafenib at a dose of 50mg/kg", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "F4/80+ TAMs, and CD11b+Gr-1+ and CD45+CXCR4+ myeloid cells,", "Controlled_Terms_Negative_Regulation": "CD11b / ITGAM; CD45; Tumor-associated macrophages / TAMs; CXCR4", "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "nude", "Cell_line_used_to_induce_tumor_in_mice": "JHH-7 HCC", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1787", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "25529917", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "sorafenib at a dose of 50mg/kg", "Technique": "Flow Cytometry, Immunofluorescence Analysis, Western Blot Analysis", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis; Immunofluorescence assay; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "F4/80+ TAMs, and CD11b+Gr-1+ and CD45+CXCR4+ myeloid cells, CD4+CD25+FoxP3+ Tregs in HCA-1 tumors PD-L1 expression, PD-L1 on multiple hematopoietic cells, including on a fraction of Gr-1+ cells, TAMs, dendritic cells and lymphocytes", "Controlled_Terms_Negative_Regulation": "CD4; CD25 / IL2RA; CD11b / ITGAM; CD45; PD-L1 / CD274; FOXP3; Regulatory T cells / Tregs; Tumor-associated macrophages / TAMs; Dendritic cells; Immune checkpoint pathway; CXCR4", "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "C3H", "Cell_line_used_to_induce_tumor_in_mice": "HCA-1 tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1808", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "25949902", "Cancer_Type": "Cervical Cancer", "Cancer_Type_Description": "Cervical Cancer", "System": null, "Dose": "20, 40 and 60 mg/kg body weight", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells CD69 on the surface of intratumoral and intrasplenic CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD69; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "MDSCs,Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "TC-1 tumor cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1813", "Drug": "Gefitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00317", "Target/s_or_mechanism_of_action": "Gefitinib is an inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase that binds to the adenosine triphosphate (ATP)-binding site of the enzyme.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COC1=C(OCCCN2CCOCC2)C=C2C(NC3=CC(Cl)=C(F)C=C3)=NC=NC2=C1", "Single/Combination": "Single Drug", "PMID": "25998384", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": null, "Dose": "(20 mg/kg, i.g.) every other day", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-L1 expression and NF-κB in tumor cells,", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; Immune checkpoint pathway; NF-κB signaling", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01977", "Drug_Pubchem": "123631", "Animal_Strain_used": "nude", "Cell_line_used_to_induce_tumor_in_mice": "PC-9 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1816", "Drug": "Axitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB06626", "Target/s_or_mechanism_of_action": "Axitinib selectively blocks the tyrosine kinase receptors VEGFR-1 (vascular endothelial growth factor receptor), VEGFR-2, and VEGFR-3.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=C(SC2=CC=C3C(NN=C3\\C=C\\C3=CC=CC=N3)=C2)C=CC=C1", "Single/Combination": "Single Drug", "PMID": "26137411", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Subcutaneous And Intracranial Mouse Melanoma", "System": null, "Dose": "axitinib (25 mg/kg)", "Technique": "Flow Cytometry, Histochemistry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD45+ cells in the spleen of axitinib-treated mice,CD3+ cells, CD8+ T cells,CD4+ T-cell, immune cells within subcutaneous and intracranial tumors, which is mainly due to an increase of CD11b+ cells and more specifically of CD11b+ Ly6ChighLy6G- moMDSCs. CD80 expression on the CD11c+ cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD3; CD80; CD11b / ITGAM; CD11c / ITGAX; CD45; Monocytic MDSCs / M-MDSCs; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD4+CD25+ cells (Tregs), CD11c+ cells (DCs) and CD11b+ cells, MDSC populations", "Controlled_Terms_Unaffected": "CD4; CD25 / IL2RA; CD11b / ITGAM; CD11c / ITGAX; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs; Dendritic cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03218", "Drug_Pubchem": "6450551", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MO4 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1839", "Drug": "Cediranib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB04849", "Target/s_or_mechanism_of_action": "Cediranib inhibits vacular endothelial growth factor (VEGF) receptor tyrosine kinase (RTK).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OCCCN1CCCC1)N=CN=C2OC1=C(F)C2=C(NC(C)=C2)C=C1", "Single/Combination": "Single Drug", "PMID": "27044097", "Cancer_Type": "Brain cancer", "Cancer_Type_Description": "Glioblastoma", "System": null, "Dose": "cediranib (6 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "TAMs", "Controlled_Terms_Function_inhibited_Number_decreased": "Tumor-associated macrophages / TAMs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08881", "Drug_Pubchem": "9933475", "Animal_Strain_used": "nude or C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Gl261 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1874", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "28274958", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": null, "Dose": "100 mg/kg in water", "Technique": "Flow cytometry,histopathologic evaluation,Quantitative RT-PCR analysis,RNA in situ hybridization (RISH)", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); RNA in situ hybridization (RISH); Hematoxylin and eosin (H&E)/histology", "Immune_System-Function_enhanced/numbers_increased": "Ly6G+, myeloperoxidase+ (MPO+) neutrophil infiltration into the tumor within 24–48 hours,CD11b+GR1+ tumor-infiltrating immune cells , CD11b+CD86+ cells CXCL12 and its receptor CXCR4 within the tumor microenvironment perivascular ICAM-1, intratumoral CD86 expression caspase-3", "Controlled_Terms_Function_enhanced_Number_increased": "CXCL12 / SDF-1; CD86; CD11b / ITGAM; Neutrophils / granulocytes; Apoptosis / caspase activation; ICAM-1 / CD54; CXCR4; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "gene expression of CD3, CD4, CD8 (T cell markers) or NKG2D (NK and activated CD8 T cell marker)", "Controlled_Terms_Unaffected": "CD4; CD8; CD3; T cells; CD8+ T cells; NKG2D ligand / receptor pathway", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10062", "Drug_Pubchem": "25102847", "Animal_Strain_used": "Probasin Cre-driven conditional prostate-specific knockout of PTEN and p53 genes (Pb-Cre; PTENfl/lflp53fl/fl)", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1875", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "28274958", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": null, "Dose": "100 mg/kg in water", "Technique": "Immunohistochemistry, Flow cytometry, qPCR-based RNA profiling,RISH", "Controlled_Technique": "Flow cytometry; Polymerase chain reaction (PCR/qPCR); Immunohistochemistry (IHC); RNA in situ hybridization (RISH)", "Immune_System-Function_enhanced/numbers_increased": "neutrophil infiltration into the tumor, CD11b+GR1+ tumor-infiltrating immune cells- Ly6GhiLy6Clo, consistent with a granulocytic (and not monocytic) predominance of tumor-infiltrating immune cells, CD11b+CD86+ cells chemokine CXCL12 and its receptor CXCR4 within the tumor microenvironment ICAM-1,CD86 expression caspase-3", "Controlled_Terms_Function_enhanced_Number_increased": "CXCL12 / SDF-1; CD86; CD11b / ITGAM; Neutrophils / granulocytes; Apoptosis / caspase activation; ICAM-1 / CD54; CXCR4; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10062", "Drug_Pubchem": "25102847", "Animal_Strain_used": "(Pb-Cre; PTENfl/lflp53fl/fl)", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1893", "Drug": "Regorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08896", "Target/s_or_mechanism_of_action": "Regorafenib is a small molecule inhibitor of multiple membrane-bound and intracellular kinases involved in normal cellular functions and in pathologic processes such as oncogenesis, tumor angiogenesis, and maintenance of the tumor microenvironment.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=CC(OC2=CC(F)=C(NC(=O)NC3=CC=C(Cl)C(=C3)C(F)(F)F)C=C2)=CC=N1", "Single/Combination": "Single Drug", "PMID": "28775208", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "Reg (8 mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "intratumoral CD45+ leukocytes and CD8+ T cells MHC-I", "Controlled_Terms_Function_enhanced_Number_increased": "CD8; CD45; MHC class I; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "CD155, semaphorin 4D, CEACAM1, and galectin-9", "Controlled_Terms_Function_inhibited_Number_decreased": "CD155 / PVR", "Immune_System_function_unaffected": "intratumoral dendritic cells, macrophages, myeloid-derived suppressor cells, or natural killer cells", "Controlled_Terms_Unaffected": "Myeloid-derived suppressor cells / MDSCs; Macrophages; Dendritic cells; NK cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10138", "Drug_Pubchem": "11167602", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "B16-F1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1895", "Drug": "Regorafenib+ anti-CD40 + 50 μg c-di-GMP", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08896", "Target/s_or_mechanism_of_action": "Regorafenib is a small molecule inhibitor of multiple membrane-bound and intracellular kinases involved in normal cellular functions and in pathologic processes such as oncogenesis, tumor angiogenesis, and maintenance of the tumor microenvironment.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=CC(OC2=CC(F)=C(NC(=O)NC3=CC=C(Cl)C(=C3)C(F)(F)F)C=C2)=CC=N1", "Single/Combination": "Single Drug", "PMID": "28775208", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "Reg (4 mg/kg), 100 μg of anti-CD40, 50 μg c-di-GMP", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "intratumoral CD45+ leukocytes, CD4+ T cells, and CD8+ T cells, but did not increase CD4+ T cells within the CD45+ population", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; CD8; CD45; T cells; CD8+ T cells; CD4+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10138", "Drug_Pubchem": "11167602", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "B16-F1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1909", "Drug": "AG1478", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": "AG1478 tyrosine kinase inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COC1=C(C=C2C(=C1)C(=NC=N2)NC3=CC(=CC=C3)Cl)OC", "Single/Combination": "Single Drug", "PMID": "29056908", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung", "System": null, "Dose": "AG1478 (1 mg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "a strong induction of H-2Kb and H-2Db expression, MHC-I expression", "Controlled_Terms_Function_enhanced_Number_increased": "MHC class I", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": "2051", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "D122", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1916", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "29152128", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": null, "Dose": null, "Technique": "FACS", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "M1 macrophage population (F4/80+, MHCII+)", "Controlled_Terms_Function_inhibited_Number_decreased": "MHC class II; Macrophages; M1 macrophage phenotype", "Immune_System_function_unaffected": "M2 macrophages (F4/80+, CD206+)", "Controlled_Terms_Unaffected": "CD206 / MRC1; Macrophages; M2 macrophage phenotype", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10062", "Drug_Pubchem": "25102847", "Animal_Strain_used": "severe combined immuno-deficient (beige SCID) male (4- to 10-week-old male )", "Cell_line_used_to_induce_tumor_in_mice": "ARCaPM cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1917", "Drug": "Sunitinib+immunization with B6/WT-19 cells", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "29296523", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Cancer (HCC)", "System": null, "Dose": "(40 mg/kg body weight)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells producing IFN-γ and TNF-α IFN-γ and TNF-α", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; TNF-α / TNF; CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": "Treg TGF-β and IL-10", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-10; TGF-β; Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1920", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "29413757", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "50 mg/kg", "Technique": "Flow Cytometry, Immunohistochemistry And ELISA, RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Enzyme-linked immunosorbent assay (ELISA); Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "CD4+CD25+Foxp3+ Tregs,expression of PD-L1 in tumor tissue IL-10 and TGF-β", "Controlled_Terms_Negative_Regulation": "IL-10; TGF-β; CD4; CD25 / IL2RA; PD-L1 / CD274; FOXP3; Regulatory T cells / Tregs; Immune checkpoint pathway", "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "hepa1-6 cell", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1923", "Drug": "Axitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB06626", "Target/s_or_mechanism_of_action": "Axitinib selectively blocks the tyrosine kinase receptors VEGFR-1 (vascular endothelial growth factor receptor), VEGFR-2, and VEGFR-3.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=C(SC2=CC=C3C(NN=C3\\C=C\\C3=CC=CC=N3)=C2)C=CC=C1", "Single/Combination": "Single Drug", "PMID": "29487979", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Carcinoma", "System": null, "Dose": "25 mg/kg/day", "Technique": "Flow Cytometry, Depleting Studies By Neutralizing Antibodies", "Controlled_Technique": "Flow cytometry; Immune suppression/blocking/depletion assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "intratumoral innate immune cells- tumor-promoting differentiated mast cells\n (CD45+, C117+, FcεR1α+) and TAMs (CD45+, CD11b+,\n F4/80+) , regulatory T cells, monocytes (CD45+,\n CD11b+, Ly-6G−, Ly6C+) and granulocytes (CD45+,\n CD11b+, Ly-6G+, Ly6C−) , HSCs determined as CD45+\n Lin−, CD117+, Sca-1+ cells IN Spleen.", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; CD45; Regulatory T cells / Tregs; Tumor-associated macrophages / TAMs; Monocytes; Neutrophils / granulocytes; T cells", "Immune_System_function_unaffected": "Intratumoral T cells and CD8 T cells", "Controlled_Terms_Unaffected": "CD8; T cells; CD8+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03218", "Drug_Pubchem": "6450551", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MC38 tumors", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1936", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "30123861", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "30 mg/ml", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD4+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4; T cells; CD4+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD8+ T cells", "Controlled_Terms_Unaffected": "CD8; T cells; CD8+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MTD2", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1937", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "30123861", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "40 mg/kg", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Tregs (CD4+CD25+FoxP3+) , and MDSCs (CD11b+Gr-1+)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4; CD25 / IL2RA; CD11b / ITGAM; FOXP3; Regulatory T cells / Tregs; Myeloid-derived suppressor cells / MDSCs", "Immune_System_function_unaffected": "CD8+ T cells", "Controlled_Terms_Unaffected": "CD8; T cells; CD8+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MTD2", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1938", "Drug": "Sunitinib + immunized with 3 × 107 of B6/WT-19 cells", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "30123861", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "40 mg/kg", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells producing IFN-γ and TNF-α IFN-γ and TNF-α", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; TNF-α / TNF; CD8; T cells; CD8+ T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": "5329102", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "MTD2", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1976", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "31078430", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "7.5 mg/kg sorafenib for 5 days after eight days of Hepa1-6-chGPC3 tumor implantation", "Technique": "QPCR, ELISA", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IL12 mRNA in TAMs", "Controlled_Terms_Function_enhanced_Number_increased": "IL-12; Tumor-associated macrophages / TAMs", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": "216239", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "Hepa1-6-chGPC3 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1983", "Drug": "Erlotinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00530", "Target/s_or_mechanism_of_action": "Erlotinib inhibits the intracellular phosphorylation of tyrosine kinase associated with the epidermal growth factor receptor (EGFR).", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "COCCOC1=CC2=C(C=C1OCCOC)C(NC1=CC(=CC=C1)C#C)=NC=N2", "Single/Combination": "Single Drug", "PMID": "31291990", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer", "System": null, "Dose": "25 mg/kg, 5 days a week", "Technique": "Flow Cytometry,Bio-Plex Cytokine Assay", "Controlled_Technique": "Flow cytometry; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "CD45+ immune cells and the absolute number of CD4+ and CD8+ T cells,infiltration of T cells into the lungs,CD103+ dendritic cells CCL2 and CCL5 ,IFN-γ, IL-12p40, Irf5 expression CD86 on Aleveolar macrophages-inflammatory response in AMs.", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-12; CCL2 / MCP-1; CCL5 / RANTES; CD4; CD8; CD86; CD45; Macrophages; Dendritic cells; T cells; CD8+ T cells; Immune-cell infiltration", "Immune_System-Function_inhibited/numbers_decreased": "CCL3 and chemokine CXCL1", "Controlled_Terms_Function_inhibited_Number_decreased": "CCL3 / MIP-1α; CXCL1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "increased Cd274 (the gene encoding Pd-l1) expression and Pd-l1 protein on AMs", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274; Immune checkpoint pathway", "KEGG_Drug_ID": "D07907", "Drug_Pubchem": "176870", "Animal_Strain_used": "CCSP-rtTA; TetO-EGFRL858R bitransgenic", "Cell_line_used_to_induce_tumor_in_mice": "doxycycline diet", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/1994", "Drug": "Alectinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB11363", "Target/s_or_mechanism_of_action": "Alectinib is a second generation oral drug that selectively inhibits the activity of anaplastic lymphoma kinase (ALK) tyrosine kinase.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CCC1=CC2=C(C=C1N1CCC(CC1)N1CCOCC1)C(C)(C)C1=C(C3=CC=C(C=C3N1)C#N)C2=O", "Single/Combination": "Single Drug", "PMID": "31540894", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Anaplastic Large Cell Lymphoma (ALCL)", "System": null, "Dose": "alectinib ((20mg/kg -35mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "HLA-A,B,C", "Controlled_Terms_Function_enhanced_Number_increased": "HLA class I antigen", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; 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More specifically, it inhibits anaplastic lymphoma kinase (ALK), hepatocyte growth factor receptor (HGFR, c-MET), and Recepteur d'Origine Nantais (RON). Abnormalities in the ALK gene caused by mutations or translocations may lead to expression of oncogenic fusion proteins. In patients with NSCLC, they have the EML4-ALK gene. Crizotinib inhibits ALK tyrosine kinase which ultimately results in decreased proliferation of cells that carry the genetic mutation and tumour survivability.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "C[C@@H]OC1=CC(=CN=C1N)C1=CN(N=C1)C1CCNCC1)C1=C(Cl)C=CC(F)=C1Cl", "Single/Combination": "Single Drug", "PMID": "31540894", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Anaplastic Large Cell Lymphoma (ALCL)", "System": null, "Dose": "crizotinib(10mg/kg -25mg/kg)", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "HLA-A,B,C", "Controlled_Terms_Function_enhanced_Number_increased": "HLA class I antigen", "Immune_System-Function_inhibited/numbers_decreased": "PD-L1", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-L1 / CD274; Immune checkpoint pathway", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09731", "Drug_Pubchem": "11626560", "Animal_Strain_used": "NSG", "Cell_line_used_to_induce_tumor_in_mice": "Karpas 299 cells", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2015", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "31704808", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Tumor", "System": null, "Dose": "Imatinib (0, 10, or 50 mg/kg)", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "T reg cells", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells / Tregs", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": "5291", "Animal_Strain_used": "BALB/c", "Cell_line_used_to_induce_tumor_in_mice": "CT26", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2050", "Drug": "Axitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB06626", "Target/s_or_mechanism_of_action": "Axitinib selectively blocks the tyrosine kinase receptors VEGFR-1 (vascular endothelial growth factor receptor), VEGFR-2, and VEGFR-3.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CNC(=O)C1=C(SC2=CC=C3C(NN=C3\\C=C\\C3=CC=CC=N3)=C2)C=CC=C1", "Single/Combination": "Single Drug", "PMID": null, "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung - Lewis Lung Carcinoma", "System": null, "Dose": "25 mg/kg/day", "Technique": "Flow Cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "intratumoral innate immune cells- tumor-promoting differentiated mast cells\n (CD45+, C117+, FcεR1α+) and TAMs (CD45+, CD11b+,\n F4/80+) , regulatory T cells,Monocytes and\n granulocytes", "Controlled_Terms_Function_inhibited_Number_decreased": "CD11b / ITGAM; CD45; Regulatory T cells / Tregs; Tumor-associated macrophages / TAMs; Monocytes; Neutrophils / granulocytes; T cells", "Immune_System_function_unaffected": "Intratumoral T cells and CD8 T cells", "Controlled_Terms_Unaffected": "CD8; T cells; CD8+ T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03218", "Drug_Pubchem": "6450551", "Animal_Strain_used": "C57BL/6", "Cell_line_used_to_induce_tumor_in_mice": "LLC1", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2102", "Drug": "Vinblastine (VBL)", "Drug_category": "Vinca alkaloids", "Drugbank_ID": "DB00570", "Target/s_or_mechanism_of_action": "Binds tubulin/microtubules and inhibits microtubule polymerization.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC[C@]1(O)C[C@@H]2CN(CCc3c([nH]c4ccccc34)[C@@](C(=O)OC)(c3cc4c(cc3OC)N(C)[C@H]3[C@@](O)(C(=O)OC)[C@H](OC(C)=O)[C]5(CC)C=CCN6CC[C@]43[C@@H]65)C2)C1", "Single/Combination": "Single", "PMID": "37652576", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal cancer", "System": null, "Dose": "VBL 1.25 mg/kg", "Technique": "M1-like TAM polarization, macrophage phagocytosis, CD8⁺ T-cell activation/infiltration", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "M2-like TAM phenotype/function; TAM-mediated immunosuppression", "Controlled_Terms_Function_enhanced_Number_increased": "Macrophages; Tumor-associated macrophages / TAMs", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08675", "Drug_Pubchem": "241903", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "MC38", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "animal_studies", "ID": "CANIMM/2133", "Drug": "Vinblastine (VBL)", "Drug_category": "Vinca alkaloids", "Drugbank_ID": "DB00570", "Target/s_or_mechanism_of_action": "Binds tubulin/microtubules and inhibits microtubule polymerization.", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": "CC[C@]1(O)C[C@@H]2CN(CCc3c([nH]c4ccccc34)[C@@](C(=O)OC)(c3cc4c(cc3OC)N(C)[C@H]3[C@@](O)(C(=O)OC)[C@H](OC(C)=O)[C]5(CC)C=CCN6CC[C@]43[C@@H]65)C2)C1", "Single/Combination": "Single", "PMID": "37652576", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Pulmonary/lung cancer", "System": null, "Dose": "VBL 1.25 mg/kg", "Technique": "M1-like TAM polarization", "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "M2-like TAM-associated immunosuppression", "Controlled_Terms_Function_enhanced_Number_increased": "Macrophages; Tumor-associated macrophages / TAMs", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08675", "Drug_Pubchem": "241903", "Animal_Strain_used": "C57BL/6J", "Cell_line_used_to_induce_tumor_in_mice": "LLC (Lewis lung carcinoma)", "Patient_Sample": null, "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2224", "Drug": "Cyclophosphamide", "Drug_category": "Alkylating agents", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": "2907", "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Single Drug", "PMID": "16960692", "Cancer_Type": "Adenocarcinoma", "Cancer_Type_Description": "Adenocarcinoma", "System": null, "Dose": "CTX 50 mg orally, twice a day 1 week on and 1 week oV for 1 month or more", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "T cells and NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": "T regs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": "T lymphocyte, CD3+ T cell, CD8+ T cell, and CD3,CD56 and NK cells", "Controlled_Terms_Unaffected": "NK cells; CD8+ T cells; T cells; Lymphocytes; CD56 / NCAM1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "3", "Male/Female": "2024-01-02 00:00:00", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2225", "Drug": "Cyclophosphamide", "Drug_category": "Alkylating agents", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": "2907", "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Single Drug", "PMID": "16960692", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Carcinoma", "System": null, "Dose": "CTX 50 mg orally, twice a day 1 week on and 1 week oV for 1 month or more", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "T cells and NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": "T regs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": "T lymphocyte, CD3+ T cell, CD8+ T cell, and CD3,CD56 and NK cells", "Controlled_Terms_Unaffected": "NK cells; CD8+ T cells; T cells; Lymphocytes; CD56 / NCAM1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "2", "Male/Female": "2024-01-01 00:00:00", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2226", "Drug": "Cyclophosphamide", "Drug_category": "Alkylating agents", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": "2907", "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Single Drug", "PMID": "16960692", "Cancer_Type": "Mesothelioma", "Cancer_Type_Description": "Pleural Mesothelioma", "System": null, "Dose": "CTX 50 mg orally, twice a day 1 week on and 1 week oV for 1 month or more", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "T cells and NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": "T regs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": "T lymphocyte, CD3+ T cell, CD8+ T cell, and CD3,CD56 and NK cells", "Controlled_Terms_Unaffected": "NK cells; CD8+ T cells; T cells; Lymphocytes; CD56 / NCAM1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "1", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2227", "Drug": "Cyclophosphamide", "Drug_category": "Alkylating agents", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": "2907", "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Single Drug", "PMID": "16960692", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer -Clear Cell Ovarian Cancer", "System": null, "Dose": "CTX 50 mg orally, twice a day 1 week on and 1 week oV for 1 month or more", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "T cells and NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": "T regs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": "T lymphocyte, CD3+ T cell, CD8+ T cell, and CD3,CD56 and NK cells", "Controlled_Terms_Unaffected": "NK cells; CD8+ T cells; T cells; Lymphocytes; CD56 / NCAM1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "1", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2230", "Drug": "Cyclophosphamide", "Drug_category": "Alkylating agents", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": "2907", "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Single Drug", "PMID": "16960692", "Cancer_Type": "Sarcoma", "Cancer_Type_Description": "Sarcoma", "System": null, "Dose": "CTX 50 mg orally, twice a day 1 week on and 1 week oV for 1 month or more", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "T cells and NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": "T regs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": "T lymphocyte, CD3+ T cell, CD8+ T cell, and CD3,CD56 and NK cells", "Controlled_Terms_Unaffected": "NK cells; CD8+ T cells; T cells; Lymphocytes; CD56 / NCAM1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "1", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2231", "Drug": "Cyclophosphamide", "Drug_category": "Alkylating agents", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": "2907", "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Single Drug", "PMID": "16960692", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "CTX 50 mg orally, twice a day 1 week on and 1 week oV for 1 month or more", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "T cells and NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": "T regs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": "T lymphocyte, CD3+ T cell, CD8+ T cell, and CD3,CD56 and NK cells", "Controlled_Terms_Unaffected": "NK cells; CD8+ T cells; T cells; Lymphocytes; CD56 / NCAM1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "1", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2256", "Drug": "Cyclophosphamide", "Drug_category": "Alkylating agents", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": "2907", "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Single Drug", "PMID": "28855352", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Metastatic Colorectal Cancer", "System": null, "Dose": "2-week-long courses of low-dose (50 mg twice a day)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+CD8+ T-cells IFNγ intracellular perforin and granzyme B", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; Perforin / PRF1; Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": "CD4+ T cells expressing CD25hi/Foxp3-T regs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); CD4+ T cells; T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "(n = 27)", "Male/Female": "2024-09-18 00:00:00", "Median_age/Range": "65.2"}, {"study_type": "patient_studies", "ID": "CANIMM/2270", "Drug": "Cyclophosphamide", "Drug_category": "Alkylating agents", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": "2907", "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Single Drug", "PMID": "21148486", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Advanced Cancer Including Melanoma", "System": null, "Dose": "50 mg/d", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "CD4 T cells as the major source of IL-17A", "Controlled_Terms_Function_enhanced_Number_increased": "CD4+ T cells; T cells; IL-17", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "21", "Male/Female": "2024-12-09 00:00:00", "Median_age/Range": "51 (27–74)"}, {"study_type": "patient_studies", "ID": "CANIMM/2179", "Drug": "Vemurafenib", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": null, "Pubchem_ID": "42611257", "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Single Drug", "PMID": "29721378", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "oral vemurafenib (960 mg twice daily) for\n 2 weeks", "Technique": "IHC, Flow cytometry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells, CD4+ FoxP3+ regulatory T cells\n and CD11b+ myeloid cells", "Controlled_Terms_Function_enhanced_Number_increased": "Regulatory T cells (Tregs); CD4+ T cells; CD8+ T cells; T cells; CD11b / ITGAM", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09996", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "N=6", "Male/Female": "3M/3F", "Median_age/Range": "42 (range 23–58)"}, {"study_type": "patient_studies", "ID": "CANIMM/2181", "Drug": "BRAF-targeted therapies-BRAFi (vemurafenib)/ (dabrafenib + trametinib)", "Drug_category": "BRAF inhibitor", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "24251082", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": null, "Technique": "CDR3 sequencing", "Controlled_Technique": "Gene expression/sequencing analysis; CDR3 sequencing", "Immune_System-Function_enhanced/numbers_increased": "TIL clonality,influx of T cells", "Controlled_Terms_Function_enhanced_Number_increased": "Tumor-infiltrating lymphocytes (TILs); T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "serial biopsies collected before treatment and 10–14 d after the initiation of BRAF-targeted therapy from 8 metastatic melanoma patients harboring BRAF mutations", "Male/Female": null, "Median_age/Range": "25 - 72 y"}, {"study_type": "patient_studies", "ID": "CANIMM/2194", "Drug": "BRAF inhibitor (vemurafenib)", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": null, "Pubchem_ID": "42611257", "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Single Drug", "PMID": "23307859", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": null, "Technique": "immunohistochemistry and immunofluorescence, Quantitative PCR", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Immunohistochemistry (IHC); Immunofluorescence assay; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cell infiltrate   MART, TYRP-1. TYRP-2, and GP100- Melanoma antigen expression", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells; MART antigen; gp100 antigen; TYRP-1; TYRP-2", "Immune_System-Function_inhibited/numbers_decreased": "immunosuppressive cytokines IL-6 and IL-8 markers of T cell cytotoxicity (perforin, granzyme B)", "Controlled_Terms_Function_inhibited_Number_decreased": "T cells; IL-6; IL-8 / CXCL8; Perforin / PRF1; Granzyme B / GZMB; Cytotoxicity / cytolysis", "Immune_System_function_unaffected": "CD4+ T cell infiltrate TGF-beta and IL-10 HLA expression", "Controlled_Terms_Unaffected": "CD4+ T cells; T cells; IL-10; TGF-β", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "T cell exhaustion markers TIM3 and PD1, immunosuppressive ligand PDL1", "Controlled_Terms_Negative_Regulation": "T cells; PD-1 / PDCD1; PD-L1 / CD274; TIM-3", "KEGG_Drug_ID": "D09996", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "patients 1-5", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2195", "Drug": "Vemurafenib", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": null, "Pubchem_ID": "42611257", "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Single Drug", "PMID": "25256614", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": null, "Technique": "qPCR analysis,histology", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Hematoxylin and eosin (H&E)/histology", "Immune_System-Function_enhanced/numbers_increased": "CD68, M1 marker CD86 and the M2 marker CD163-indicating an accumulation of M1 and M2 polarized macrophages", "Controlled_Terms_Function_enhanced_Number_increased": "Macrophages; CD86; CD68; CD163", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "TNFα expression  MITF expression", "Controlled_Terms_Negative_Regulation": "TNF-α / TNF; MITF", "KEGG_Drug_ID": "D09996", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "paired BRAFV600E positive tumor biopsies from patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2209", "Drug": "Dabrafenib", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB08912", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene.", "KEGG_Drug__ID": null, "Pubchem_ID": "44462760", "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1", "Single/Combination": "Single Drug", "PMID": "28123875", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "150 mg orally, twice daily", "Technique": "Flow cytometry, immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cell infiltrates", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Melanoma biopsies from patients treated at the Melanoma Institute Australia Sydney and the Netherlands Cancer Institute", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/17", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase", "KEGG_Drug__ID": null, "Pubchem_ID": "60750", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": null, "PMID": "19797418", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": null, "Dose": "gemcitabine 1000 mg/m(2) for 3 weeks, followed by 1 week of rest", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD14(+) monocytes and CD11c(+) (myeloid) DC, CD123(+) (plasmacytoid) DC", "Controlled_Terms_Function_enhanced_Number_increased": "Monocytes; Dendritic cells; CD14; CD11c / ITGAX", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02368", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "28 patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2210", "Drug": "Vemurafenib", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": null, "Pubchem_ID": "42611257", "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Single Drug", "PMID": "28123875", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "960 mg orally twice daily", "Technique": "Flow cytometry, immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cell infiltrates", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09996", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Melanoma biopsies from patients treated at the Melanoma Institute Australia Sydney and the Netherlands Cancer Institute", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2279", "Drug": "Vemurafenib", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": null, "Pubchem_ID": "42611257", "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Single Drug", "PMID": "24504444", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "Flow cytometry", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "NK cells, CCR7(+)CD45RA(+) (naïve)", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; CCR7; CD45RA", "Immune_System-Function_inhibited/numbers_decreased": "a significant decrease in peripheral lymphocytes within the first 12 weeks of treatment, neutrophil counts, CD4+ T cell compartment, CD8+ T cells , , CD4+ T cells with a central memory phenotype, T cells (Th1), loss of peripheral lymphocytes interferon-γ and interleukin-9 by CD4(+) T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4+ T cells; CD8+ T cells; T cells; Neutrophils; Lymphocytes; IFN-γ; IL-9; Th1 cells; Central memory T cells", "Immune_System_function_unaffected": "B cells IL-2, IL-4, IL-10 and IL-17A", "Controlled_Terms_Unaffected": "B cells; IL-2; IL-4; IL-10; IL-17", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09996", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "(n = 277)", "Male/Female": "164/113", "Median_age/Range": "56 (21–84)"}, {"study_type": "patient_studies", "ID": "CANIMM/2280", "Drug": "Dabrafenib", "Drug_category": "BRAF inhibitor", "Drugbank_ID": "DB08912", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene.", "KEGG_Drug__ID": null, "Pubchem_ID": "44462760", "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1", "Single/Combination": "Single Drug", "PMID": "24504444", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "Flow cytometry", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "neutrophil counts", "Controlled_Terms_Function_inhibited_Number_decreased": "Neutrophils", "Immune_System_function_unaffected": "peripheral lymphocytes", "Controlled_Terms_Unaffected": "Lymphocytes", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "(n = 65)", "Male/Female": "41/24", "Median_age/Range": "51 (20–79)"}, {"study_type": "patient_studies", "ID": "CANIMM/2183", "Drug": "Vorinostat (SAHA)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": null, "Pubchem_ID": "5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "16297208", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphomas - Cutaneous T Cell Lymphomas (CTCL)", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "apoptosis", "Controlled_Terms_Function_enhanced_Number_increased": "Apoptosis", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06320", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "n=11", "Male/Female": "2024-07-04 00:00:00", "Median_age/Range": "44-81"}, {"study_type": "patient_studies", "ID": "CANIMM/2185", "Drug": "Benzamide-derived MS-275, Entinostat", "Drug_category": "Histone deacetylase inhibitors", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": "4261", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "19759901", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia  - Chronic Lymphocytic Leukaemia (CLL)", "System": null, "Dose": "ibrutinib 420 mg orally once daily until disease progression or the occurrence of intolerable side effects", "Technique": "Luminex 200 instrument (Luminex) for determination of individual cytokine concentrations,immunohistochemistry, Flow cytometry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC); Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "Eotaxin", "Controlled_Terms_Function_enhanced_Number_increased": "Eotaxin / CCL11", "Immune_System-Function_inhibited/numbers_decreased": "circulating T cells, CD4+ T cells that expressed HLA-DR or CD39, CD8+ cells expressing HLA-DR , PD-1 expression on T cells, CD4+ Th17 T cells (CXCR3neg, CCR6+),Macrophage-CLL cell interactions CCL22, IL-8, CXCL10, CCL2, CCL3, CCL4, and CCL7, IL-10, IL-1ra, TNFα, IFNα,IFNγ, IL-4", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4+ T cells; CD8+ T cells; T cells; Macrophages; IFN-γ; IFN-α; IL-4; IL-8 / CXCL8; IL-10; TNF-α / TNF; CCL2 / MCP-1; CCL3 / MIP-1α; CCL4 / MIP-1β; CCL7; CXCL10 / IP-10; PD-1 / PDCD1; HLA-DR; IL-1Ra; Th17 cells; CCL22; CD39", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "80 CLL patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2273", "Drug": "SAHA/Vorinostat", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB02546", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM)", "KEGG_Drug__ID": null, "Pubchem_ID": "5311", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1", "Single/Combination": "Single Drug", "PMID": "19759901", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": null, "Dose": "Lenalidomide:2.5-5 mg/day daily for first 4 weeks; week 5 to week 12: 30 mg (thrice in a week); then lenalidomide escalted stepwise upto 15mg/day upto 16 weeks", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "Ki67+CD8+, HLA-DR+ cells; effector memory CD8+ cells;", "Controlled_Terms_Function_enhanced_Number_increased": "HLA-DR; Ki-67; Effector memory T cells", "Immune_System-Function_inhibited/numbers_decreased": "effector cells (CD4+ and CD8+)", "Controlled_Terms_Function_inhibited_Number_decreased": "Effector CD4-positive T cells; Effector CD8-positive T cells", "Immune_System_function_unaffected": "CD4+ T cells, CD8+ T cells, NK cells and NKT cells; Ki67+CD4+", "Controlled_Terms_Unaffected": "Natural killer T cells (NKT cells); NK cells; CD4+ T cells; CD8+ T cells; T cells; Ki-67", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06320", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "23", "Male/Female": "14M/9F", "Median_age/Range": "Median 69 (61–85)"}, {"study_type": "patient_studies", "ID": "CANIMM/2274", "Drug": "Trichostatin A (TSA)", "Drug_category": "Histone Deacetylase Inhibitors", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": "444732", "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Single Drug", "PMID": "19759901", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": null, "Dose": "Lenalidomide:2.5-5 mg/day daily for first 4 weeks; week 5 to week 12: 30 mg (thrice in a week); then lenalidomide escalted stepwise upto 15mg/day upto 16 weeks", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "CD52− T cells, HLA-DR+ cells; effector memory CD4+ and CD8+ cells", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; HLA-DR; Effector memory T cells; CD52", "Immune_System-Function_inhibited/numbers_decreased": "CD4+ T cells, CD8+ T cells, NK cells and NKT cells; naïve CD4+ and CD8+ T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "Natural killer T cells (NKT cells); NK cells; CD4+ T cells; CD8+ T cells; T cells", "Immune_System_function_unaffected": "Central memory T cells, PD-1+ cells CTLA-4", "Controlled_Terms_Unaffected": "T cells; PD-1 / PDCD1; CTLA-4; Central memory T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "23", "Male/Female": "14M/9F", "Median_age/Range": "Median 69 (61–85)"}, {"study_type": "patient_studies", "ID": "CANIMM/2182", "Drug": "Thalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB01041", "Target/s_or_mechanism_of_action": "Previous research indicate that thalidomide binds to cerebron, a component of the E3 ubiquitin ligase complex, to selectively degrade the transcription factor IKZF3 and IKZF1. These 2 transcription factors are vital for the proliferation and survival of malignant myeloma cells", "KEGG_Drug__ID": null, "Pubchem_ID": "5426", "STR_LINK_(SMILES)": "O=C1N(C2CCC(=O)NC2=O)C(=O)C2=CC=CC=C12", "Single/Combination": "Single Drug", "PMID": "11418482", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": null, "Dose": "Thal 200 to 800 mg/day", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "The 3 patients responding to treatment showed an increase in the percentage of CD561 NK cells (fold increases of 5.6, 2.7, and 2.1) compared to patients who failed to respond (fold increases of 0.5 and 1.2 IL-2 and IFN-γ (in patient having good partial response)", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; IFN-γ; IL-2", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00754", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "5 patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2192", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "21748755", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate - Recurrent Prostate Cancer", "System": null, "Dose": "5mg or 25mg of lenalidomide", "Technique": "High Throughput Immunoblot Analysis, multiplexed bead-based immunoassay for cytokine detection", "Controlled_Technique": "Western blot/immunoblot analysis; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "IL-2, IL-4, IL-5, IL-10, IL-13, and G-CSF  immunoreactivity to prostate-associated antigens", "Controlled_Terms_Function_enhanced_Number_increased": "IL-2; IL-4; IL-5; IL-10; IL-13; G-CSF / CSF3; Cancer-testis antigens", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "49 of the 51 available patient samples", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2205", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "16569772", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "MDS", "System": null, "Dose": "10 mg/day", "Technique": "Flow cytometry,real-time RT-PCR (TaqMan) analysis", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "NKT cells expansion IFN-y", "Controlled_Terms_Function_enhanced_Number_increased": "Natural killer T cells (NKT cells); IFN-γ; NKT cells; Cell proliferation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "5(el5q MDS)", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2207", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "30104242", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Relapsed Chronic Lymphocytic Leukemia (CLL)", "System": null, "Dose": "lenalidomide at 10 mg or 20 mg daily for 3 weeks followed by 3 weeks off for up to 8 cycles", "Technique": "gene expression profiling ( on circulating CD19+-selected cells from 11 patients ), Flow cytometry, Immunohistochemistry, Deep sequencing", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC); Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "IFNγ+ CD4+ and CD8+ T cells chemokines (CCL3, CCL4), cytokines or cytokine receptors (IL13RA1, TNF, TNFSF13B), signal transduction molecules (STK3, RCAN1, KSR2) and molecules involved in the regulation of apoptosis (DDIT4, PAPRP9, CFLAR), IFNγ signaling pathway  TBX21 encoding T-bet( in the LN biopsies of responders compared to non-responders)", "Controlled_Terms_Function_enhanced_Number_increased": "CD4+ T cells; CD8+ T cells; T cells; IFN-γ; TNF-α / TNF; CCL3 / MIP-1α; CCL4 / MIP-1β; Apoptosis; TNFSF13B / BAFF; IL13RA1", "Immune_System-Function_inhibited/numbers_decreased": "decreasing diversity of the T-cell repertoire and an expansion of select clonotypes in responders", "Controlled_Terms_Function_inhibited_Number_decreased": "decreasing diversity of the T-cell repertoire and an expansion of select clonotypes in responders", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Thirty-three patients with relapsed CLL", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2215", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "27467960", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": null, "Dose": "a consolidation therapy with two cycles of lenalidomide (25 mg on day 1–21, cycle duration 28 d). Half of the study population continued treatment with lenalidomide maintenance therapy for 2 y (10 mg daily for 3 mo, if tolerable dose escalation to 15 mg/d from the 4th mo), while the other patients received lenalidomide maintenance therapy until complete remission", "Technique": "IFNγ ELISpot-assays, IFNγ-, Granzyme B and Perforin-ELISAs, Flow cytometry", "Controlled_Technique": "Flow cytometry; ELISpot/FluoroSpot assay", "Immune_System-Function_enhanced/numbers_increased": "HM1.24aa22-30 specific T-cell responses IFNγ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": "CD57 on CD8+ T-cells (n = 19)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD57", "Immune_System_function_unaffected": "CD28 (n = 37), CCR7 (n = 37), PD-1 (n = 39) CD38 (n = 19), CD154 (n = 19) and HLA-DR (n = 19)", "Controlled_Terms_Unaffected": "PD-1 / PDCD1; CD28; HLA-DR; CCR7; CD154 / CD40 ligand; CD38", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "CD4+CD127dimCD25highFoxp3+regulatory T-cells of CD4+ T cells ((n = 18)", "Controlled_Terms_Negative_Regulation": "Regulatory T cells (Tregs); CD4+ T cells; T cells", "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "58 patients with (n = 30) or without (n = 28) lenalidomide therapy and 12 patients refractory to lenalidomide", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2217", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "29755666", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": null, "Dose": null, "Technique": "Flow cytometry , bioplex", "Controlled_Technique": "Flow cytometry; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "naïve CD8+ T cells,stem\n cell memory CD8+ T cells, central memory CD4+ and CD8+ T cells, transitional memory T\n cells (both CD4+ and CD8+), effector memory T cells, NKT cells, CD4+ CD25high CD127low Foxp3high Tregs, CD28+ CD4+ cells, CD28+ CD8+ cells,CD137+ CD4+ cells, CD137+ CD28+ CD8+ cells, ICOS+ CD4+ cells, ICOS+ CD8+ cells, TIGIT on both CD4+ and CD8+ T-cell IL-8, IFN-γ, MIP-1β, TNF-α CD28, CD137/4-1BB and ICOS", "Controlled_Terms_Function_enhanced_Number_increased": "Regulatory T cells (Tregs); Natural killer T cells (NKT cells); CD4+ T cells; CD8+ T cells; T cells; IFN-γ; IL-8 / CXCL8; TNF-α / TNF; CCL4 / MIP-1β; 4-1BB / CD137; CD28; Central memory T cells; Effector memory T cells; ICOS / CD278", "Immune_System-Function_inhibited/numbers_decreased": "effector memory CD4+ T cells, terminal effector T cells, monocytic MDSCs (CD33+ CD11b+\n CD14+ HLA-DRlow), CD45RA+ Tregs, PD-1,\n TIM-3 and LAG-3 on T cells,", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); Myeloid-derived suppressor cells (MDSCs); Monocytic myeloid-derived suppressor cells (M-MDSCs); CD4+ T cells; T cells; PD-1 / PDCD1; TIM-3; LAG-3; CD14; Effector memory T cells; CD45RA; CD11b / ITGAM; CD33", "Immune_System_function_unaffected": "naïve CD4+ T cells, stem cell memory\n CD4+ T cells, NK cell", "Controlled_Terms_Unaffected": "NK cells; CD4+ T cells; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "17", "Male/Female": "8M/9F", "Median_age/Range": "51.7-66 (median 59.2)"}, {"study_type": "patient_studies", "ID": "CANIMM/2223", "Drug": "Thalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB01041", "Target/s_or_mechanism_of_action": "Previous research indicate that thalidomide binds to cerebron, a component of the E3 ubiquitin ligase complex, to selectively degrade the transcription factor IKZF3 and IKZF1. These 2 transcription factors are vital for the proliferation and survival of malignant myeloma cells", "KEGG_Drug__ID": null, "Pubchem_ID": "5426", "STR_LINK_(SMILES)": "O=C1N(C2CCC(=O)NC2=O)C(=O)C2=CC=CC=C12", "Single/Combination": "Single Drug", "PMID": "16569772", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Myeloma", "System": null, "Dose": "50 mg/d to 100 mg/d", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NKT cells expansion", "Controlled_Terms_Function_enhanced_Number_increased": "Natural killer T cells (NKT cells); NKT cells; Cell proliferation", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00754", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "2 (myeloma )", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2235", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "21149673", "Cancer_Type": "Myelodysplastic Syndrome", "Cancer_Type_Description": "Recurrent Or Refractory Solid Tumors Or Myelodysplastic Syndrome (MDS)", "System": null, "Dose": "5mg/day", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK (CD3-/\n 16+/56+) cells, granzyme B, LAMP-1, IL-2, IL-15, GM-CSF KIR3DL1 (CD158b+) receptor, KIR2DS4 receptor, Nkp46, CD107a", "Controlled_Terms_Function_enhanced_Number_increased": "IL-2; IL-15; GM-CSF / CSF2; CD107a / LAMP1; Granzyme B / GZMB; KIR3DL1; KIR2DS4; NKp46 / NCR1", "Immune_System-Function_inhibited/numbers_decreased": "Treg cells (CD4+/CD25+)", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); CD25 / IL2RA", "Immune_System_function_unaffected": "IL-8 CD94/NKG2a", "Controlled_Terms_Unaffected": "IL-8 / CXCL8; NKG2A", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "N=49", "Male/Female": "26M/23F", "Median_age/Range": "median 16 (1-21)"}, {"study_type": "patient_studies", "ID": "CANIMM/2240", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "24244687", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer - Kras-Mutant Metastatic Colorectal Cancer", "System": null, "Dose": "Lenalidomide", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cells, T regulatory cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": "B cells , T helper cells, Absolute T cells , Absolute lymphocytes", "Controlled_Terms_Function_inhibited_Number_decreased": "T cells; B cells; Lymphocytes", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "N=21", "Male/Female": "12 M, 9F", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2246", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "25313353", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia", "System": null, "Dose": "70 mg twice daily and dose reductions were made in case of toxicity", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "lymphocytosis-cytotoxic T-cell and NK-cell", "Controlled_Terms_Function_enhanced_Number_increased": "Lymphocytes", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "22", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2277", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "24032527", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": null, "Dose": null, "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "NKT cell frequency  CD25", "Controlled_Terms_Unaffected": "Natural killer T cells (NKT cells); CD25 / IL2RA", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "n=11", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2278", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "24032527", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Relapsed/Refractory Myeloma", "System": null, "Dose": null, "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "NKT cells", "Controlled_Terms_Function_inhibited_Number_decreased": "Natural killer T cells (NKT cells)", "Immune_System_function_unaffected": "CD4+, CD4− and CD8+", "Controlled_Terms_Unaffected": "CD4-positive T cells; CD4-negative T cells; CD8-positive T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "n=23", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2281", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "25748683", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": null, "Dose": "5 to 15 mg/day.", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "IP-10, IL-8, MIP-1b", "Controlled_Terms_Function_enhanced_Number_increased": "IL-8 / CXCL8; CXCL10 / IP-10", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "10", "Male/Female": null, "Median_age/Range": "49.1–64.4 Median =60.3"}, {"study_type": "patient_studies", "ID": "CANIMM/2282", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "29191843", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": null, "Dose": null, "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": "programmed death-1 (PD1, CD279)", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-1 / PDCD1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "n=20", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2283", "Drug": "Lenalidomide", "Drug_category": "Immunomodulatory Agents (IMiDs)", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Single Drug", "PMID": "31950647", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Relapsed Or Refractory Multiple Myeloma (RRMM)", "System": null, "Dose": null, "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "59", "Male/Female": "30M/29F", "Median_age/Range": "45-89 median=73"}, {"study_type": "patient_studies", "ID": "CANIMM/2180", "Drug": "Trastuzumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "20865050", "Cancer_Type": "Esophageal Cancer", "Cancer_Type_Description": "Esophageal - EAC (Esophageal Adenocarcinoma)", "System": null, "Dose": null, "Technique": "RT-PCR and IHC/ICC,", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunohistochemistry (IHC); Immunocytochemistry (ICC)", "Immune_System-Function_enhanced/numbers_increased": "TAP-2", "Controlled_Terms_Function_enhanced_Number_increased": "TAP2", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03257", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "n=17", "Male/Female": "15M/2F", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2184", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "25972070", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Cancer (HNC)", "System": null, "Dose": "(cetuximab IV 400mg/m2 day 1 then 250 mg/m2 alone days 8, 15, and 22)", "Technique": "IHC and digital image analysis", "Controlled_Technique": "Immunohistochemistry (IHC); Immunostaining/image analysis", "Immune_System-Function_enhanced/numbers_increased": "HLA-B expression, HLA-A -in clinical responders (n=7) STAT-1-in clinical responders (n=7)", "Controlled_Terms_Function_enhanced_Number_increased": "HLA-A; HLA-B; STAT1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "(n=24)- clinical responders (n=7) but not in non-responders (n=17)", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2196", "Drug": "Pembrolizumab (formerly MK-3475 and lambrolizumab)", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB09037", "Target/s_or_mechanism_of_action": "Pembrolizumab binds with high affinity to the cell surface receptor programmed cell death protein 1 (PD-1) and antagonizes its interaction with its known ligands PD-L1 and PD-L2.", "KEGG_Drug__ID": null, "Pubchem_ID": "348000000", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "25428505", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Advanced Melanoma", "System": null, "Dose": "pembrolizumab intravenously in one of three dosing regimens: 2 mg/kg every 3 weeks (2Q3W), 10 mg/kg every 3 weeks (10Q3W), or 10 mg/kg every 2 weeks (10Q2W)", "Technique": "immunohistochemistry, quantitative multiplex immunofluorescence, and next-generation sequencing", "Controlled_Technique": "Immunohistochemistry (IHC); Immunofluorescence assay; Cytokine/multiplex immunoassay; Gene expression/sequencing analysis; Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "intratumoral CD8(+) T cells in treatment responders", "Controlled_Terms_Function_inhibited_Number_decreased": "T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10574", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "46 patients", "Male/Female": "36/10", "Median_age/Range": "responders-65 (45–90) , progression- 64 (36–86)"}, {"study_type": "patient_studies", "ID": "CANIMM/2199", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "26876213", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": null, "Dose": null, "Technique": "immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "autophagy adaptor protein, SQSTM1/p62 in non responders- associated with a worse prognosis", "Controlled_Terms_Negative_Regulation": "SQSTM1 / p62", "KEGG_Drug_ID": "D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "n=23 patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2206", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "26579227", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": null, "Dose": null, "Technique": "Flow cytometry, RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "monoctyic MDSC and granulocytic MDSC in the peripheral circulation-in responders,CD163+ cells and IL-10 transcripts in circulating CD11b+CD14+HLA-DRhi monocytes-in responders IL-10", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells (MDSCs); Granulocytic myeloid-derived suppressor cells (G-MDSCs); Monocytes; IL-10; CD14; CD163; CD11b / ITGAM", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "monocytic MDSC in CD11b+ cells-In non responders", "Controlled_Terms_Negative_Regulation": "Myeloid-derived suppressor cells (MDSCs); Monocytic myeloid-derived suppressor cells (M-MDSCs); CD11b / ITGAM", "KEGG_Drug_ID": "D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Total=29,Responders =10, Non-responders=9", "Male/Female": "2024-09-20 00:00:00", "Median_age/Range": "Responders =60, Non-responders=59"}, {"study_type": "patient_studies", "ID": "CANIMM/2234", "Drug": "Bevacizumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00112", "Target/s_or_mechanism_of_action": "Inhibiting the binding of VEGF to its cell surface receptors.", "KEGG_Drug__ID": null, "Pubchem_ID": "46504473", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "19414323", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon - Advanced Colon Cancer With Multiple Metastases", "System": null, "Dose": "(5 mg/kg) every 2 weeks by intravenous injection", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06409", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "4", "Male/Female": "2024-02-02 00:00:00", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2247", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "25832655", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Cancer (HNC)", "System": null, "Dose": "Cetuximab 250 mg/m2 weekly (after an initial dose of 400 mg/m2)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "circulating and intratumoral NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "CD4+CD25hiFoxp3+ intratumoral Treg TGF-β-on T reg CD39 on T reg CTLA-4 on T reg,CD4+Foxp3+ Treg expressing TIM-3", "Controlled_Terms_Negative_Regulation": "Regulatory T cells (Tregs); TGF-β; CTLA-4; TIM-3; CD39", "KEGG_Drug_ID": "D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "(n=18)", "Male/Female": "2024-06-12 00:00:00", "Median_age/Range": "59.7"}, {"study_type": "patient_studies", "ID": "CANIMM/2252", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "27496866", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Cancer (HNC)", "System": null, "Dose": "(cetuximab IV 400 mg/m2 day 1 then 250 mg/m2 alone days 8, 15, and 22 (UPCI 08-013)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cell expression of CD137  CD137", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; 4-1BB / CD137", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "(n=5 responders, n=12 non responders)", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2255", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "28408386", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Cancer (HNSCC)", "System": null, "Dose": "Cetuximab 250 mg/m^2 was weekly injected and 400 mg/m^2 after an initial dose", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "granzyme B- and perforin-expressing CD8+ TILs", "Controlled_Terms_Function_enhanced_Number_increased": "Tumor-infiltrating lymphocytes (TILs); Perforin / PRF1; Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "CTLA-4+, PD-1+, and TIM-3+CD8+ TILs", "Controlled_Terms_Negative_Regulation": "Tumor-infiltrating lymphocytes (TILs); PD-1 / PDCD1; CTLA-4; TIM-3", "KEGG_Drug_ID": "D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "(n = 18)", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2257", "Drug": "Cetuximab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "29179214", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": "250 mg/m^2 body weight every week after a loading dose of 400 mg/m^2", "Technique": "Flow cytometry,enzyme immunoassay\n system", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD3+ T cells, CD8+ T cells and NK cells IFN-γ CD137 expression on NK cells and CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; CD8+ T cells; T cells; IFN-γ; 4-1BB / CD137", "Immune_System-Function_inhibited/numbers_decreased": "Treg cells IL-6 and IL-10 gradually", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); IL-6; IL-10", "Immune_System_function_unaffected": "CD4+ T cells, NKT-like cells, iNKT cells and DCs", "Controlled_Terms_Unaffected": "Natural killer T cells (NKT cells); CD4+ T cells; T cells; Dendritic cells; iNKT cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "(n =63)", "Male/Female": "39/24", "Median_age/Range": "34–74 years"}, {"study_type": "patient_studies", "ID": "CANIMM/38", "Drug": "Bevacizumab", "Drug_category": "Monoclonal Antbody", "Drugbank_ID": "DB00112", "Target/s_or_mechanism_of_action": "Inhibiting the binding of VEGF to its cell surface receptors.", "KEGG_Drug__ID": null, "Pubchem_ID": "46504473", "STR_LINK_(SMILES)": null, "Single/Combination": null, "PMID": "30889935", "Cancer_Type": "Ovarian Cancer", "Cancer_Type_Description": "Ovarian Cancer", "System": null, "Dose": "bevacizumab 5 mg/kg every 21 days (6 cycles of treatment)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD4 T cells, CD4/CD8 ratio", "Controlled_Terms_Function_enhanced_Number_increased": "CD4+ T cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": "activated Tregs (CD25highCD45RA-FOXP3-: aTregs), resting Treg (CD25+CD45RA+FOXP3+: rTregs)", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); CD25 / IL2RA; CD45RA", "Immune_System_function_unaffected": "CD8 T cells", "Controlled_Terms_Unaffected": "CD8+ T cells; T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06409", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "N=10", "Male/Female": null, "Median_age/Range": "54 years (42y–67y)"}, {"study_type": "patient_studies", "ID": "CANIMM/2238", "Drug": "Everolimus", "Drug_category": "mTOR inhibitor", "Drugbank_ID": "DB01590", "Target/s_or_mechanism_of_action": "Everolimus is a mammalian target of rapamycin (mTOR) kinase inhibitor used to treat various types of malignancies", "KEGG_Drug__ID": null, "Pubchem_ID": "46505248", "STR_LINK_(SMILES)": "[H][C@@]1(C[C@@H](C)[C@]2([H])CC(=O)[C@H](C)\\C=C(C)\\[C@@H](O)[C@@H](OC)C(=O)[C@H](C)C[C@H](C)\\C=C\\C=C\\C=C(C)\\[C@H](C[C@]3([H])CC[C@@H](C)[C@@](O)(O3)C(=O)C(=O)N3CCCC[C@@]3([H])C(=O)O2)OC)CC[C@@H](OCCO)[C@@H](C1)OC", "Single/Combination": "Single Drug", "PMID": "23582881", "Cancer_Type": "Prostate", "Cancer_Type_Description": "Prostate Cancer", "System": null, "Dose": "Everolimus 10 mg daily was taken continuously until disease progression, unacceptable toxicity, symptomatic deterioration, delay of trial treatment >2 wk, patient refusal, or initiation of radiotherapy. In case of relevant toxicities, everolimus was reduced to 5 mg/d and to 5 mg every second day in case of reoccurrence of such toxicity", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "carboxypeptidase M (CPM) and apolipoprotein B (APOB)", "Controlled_Terms_Function_enhanced_Number_increased": "carboxypeptidase M (CPM) and apolipoprotein B (APOB)", "Immune_System-Function_inhibited/numbers_decreased": "CD3, CD4, and CD8 T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "CD8+ T cells; T cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "regulatory T cells (Tregs)", "Controlled_Terms_Negative_Regulation": "Regulatory T cells (Tregs); T cells", "KEGG_Drug_ID": "D02714", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "37", "Male/Female": null, "Median_age/Range": "62 (45–76)"}, {"study_type": "patient_studies", "ID": "CANIMM/92", "Drug": "Platinum-based", "Drug_category": "Platinum compounds", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": null, "PMID": "29642771", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Adenocarcinoma", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD4+ PD-1+ T cells IL-12", "Controlled_Terms_Function_enhanced_Number_increased": "CD4+ T cells; T cells; IL-12; PD-1 / PDCD1", "Immune_System-Function_inhibited/numbers_decreased": "MIP-1β", "Controlled_Terms_Function_inhibited_Number_decreased": "CCL4 / MIP-1β", "Immune_System_function_unaffected": "IL-2", "Controlled_Terms_Unaffected": "IL-2", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "intermediate and classical HLA-DR+ IL-1beta and IL-5", "Controlled_Terms_Negative_Regulation": "IL-5; HLA-DR", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "9 patients", "Male/Female": "2024-07-02 00:00:00", "Median_age/Range": "56.3 (35/74) years"}, {"study_type": "patient_studies", "ID": "CANIMM/2190", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": null, "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "28337274", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Myelodysplastic Syndrome (MDS)", "System": null, "Dose": "(15 mg/M2, I.V.) over a period of 1 h once per day for 5 consecutive days. This course of treatment was repeated every 4 weeks", "Technique": "Flow cytometry,RT-PCR", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR)", "Immune_System-Function_enhanced/numbers_increased": "CD3 and CD8T lymphocyte counts, Th1 polarization in the CD4+ subset and Tc1 polarization in the CD8+ subset MHC Class I and Class II molecules, and ICAM-1 cancer-testis antigens (CTAs)-MAGE-A1, MAGE-A3, and SP17", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; Lymphocytes; MHC class I; ICAM-1 / CD54; Th1 cells; MAGE-A1; MAGE-A3; SP17; MHC class I; MHC class II; Cancer-testis antigens", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03665", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "17", "Male/Female": "2024-09-08 00:00:00", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2191", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase", "KEGG_Drug__ID": null, "Pubchem_ID": "60750", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single Drug", "PMID": "27687804", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Adenocarcinoma", "System": null, "Dose": "(1000 mg/m2) once weekly for 3 weeks (day 1, 8, 15) followed by a resting phase for 2 weeks after the third treatment", "Technique": "Flow cytometry + ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "effector T cells", "Controlled_Terms_Function_enhanced_Number_increased": "T cells", "Immune_System-Function_inhibited/numbers_decreased": "granulocytic MDSCs, Tregs TGFβ-1", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); Myeloid-derived suppressor cells (MDSCs); Granulocytic myeloid-derived suppressor cells (G-MDSCs); TGF-β", "Immune_System_function_unaffected": "IL-6, IL-8, IL-10 and TNFα", "Controlled_Terms_Unaffected": "IL-6; IL-8 / CXCL8; IL-10; TNF-α / TNF", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02368", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "10 patients", "Male/Female": "2024-04-06 00:00:00", "Median_age/Range": "70.3 ± 6 years and 71.3 ± 6.1 years,"}, {"study_type": "patient_studies", "ID": "CANIMM/2193", "Drug": "Decitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB01262", "Target/s_or_mechanism_of_action": "Reactivation of silenced genes and differentiation at low doses, and cytotoxicity at high doses", "KEGG_Drug__ID": null, "Pubchem_ID": "451668", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@H]1C[C@H](O)[C@@H](CO)O1", "Single/Combination": "Single Drug", "PMID": "28337274", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia  - Chronic Lymphocytic Leukaemia (CLL)", "System": null, "Dose": "low-dose lenalidomide (2.5 mg)", "Technique": "immunoblot", "Controlled_Technique": "Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": "5/8 patients showed an increase in IL21R protein", "Controlled_Terms_Function_enhanced_Number_increased": "IL-21", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03665", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "peripheral blood mononuclear cells isolated from CLL patient (n=8)", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2198", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase", "KEGG_Drug__ID": null, "Pubchem_ID": "60750", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single Drug", "PMID": "26449615", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": null, "Dose": "(800 mg/m2 )", "Technique": "immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "MICA expression in tumors was found in 18 of 19 (95 %) samples of the NAC group and CD16", "Controlled_Terms_Function_enhanced_Number_increased": "CD16 / FcγRIIIa; MICA", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02371", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "19 patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2212", "Drug": "Azacytidine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": null, "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "28404876", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Acute Myeloid Leukemia (AML)", "System": null, "Dose": null, "Technique": "sandwich ELISA, Flow cytometry", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "NKG2DL expression in blasts", "Controlled_Terms_Function_enhanced_Number_increased": "NKG2DL expression in blasts", "Immune_System-Function_inhibited/numbers_decreased": "sNKG2DL levels", "Controlled_Terms_Function_inhibited_Number_decreased": "Soluble natural killer group 2D ligands (sNKG2DLs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03021", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "12", "Male/Female": null, "Median_age/Range": "aged 65 ± 12.9 years"}, {"study_type": "patient_studies", "ID": "CANIMM/2222", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase", "KEGG_Drug__ID": null, "Pubchem_ID": "60750", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single Drug", "PMID": "15782312", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreas Cancer", "System": null, "Dose": "1,000 mg/ m2 over 30 min at days 0, 7, 14, and 21", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "BDCA-1+, CD1b myeloid dendritic cell", "Controlled_Terms_Function_inhibited_Number_decreased": "Dendritic cells", "Immune_System_function_unaffected": "T and B-cells ,CD86 and CD80 APCs or CD4+, CD25+ T-cells", "Controlled_Terms_Unaffected": "CD80; CD86; CD25 / IL2RA; Antigen presentation", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02368", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Ten patients", "Male/Female": "2024-05-05 00:00:00", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2236", "Drug": "Fluorouracil", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": null, "Pubchem_ID": "3385", "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O", "Single/Combination": "Single Drug", "PMID": "23202296", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Caspase-1 activation in MDSC", "Controlled_Terms_Negative_Regulation": "Myeloid-derived suppressor cells (MDSCs); Caspase-1", "KEGG_Drug_ID": "D00585", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "24 patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2237", "Drug": "Azacitidine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00928", "Target/s_or_mechanism_of_action": "As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.", "KEGG_Drug__ID": null, "Pubchem_ID": "9444", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=N1)[C@@H]1O[C@H](CO)[C@@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "23242597", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Myelodysplastic Syndrome (MDS)", "System": null, "Dose": "75 mg/m2/day", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Treg", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Th1 and Th2 cells", "Controlled_Terms_Negative_Regulation": "Th1 cells; Th2 cells", "KEGG_Drug_ID": "D03021", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "68", "Male/Female": null, "Median_age/Range": "67 years (range, 35–86 years)"}, {"study_type": "patient_studies", "ID": "CANIMM/2263", "Drug": "Fluorouracil", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": null, "Pubchem_ID": "3385", "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O", "Single/Combination": "Single Drug", "PMID": "31217433", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "caspase-1 activity in HLA-DR- CD33+ CD15+ MDSC", "Controlled_Terms_Negative_Regulation": "Myeloid-derived suppressor cells (MDSCs); HLA-DR; Caspase-1; CD33; CD15", "KEGG_Drug_ID": "D00584", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "26 patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2267", "Drug": "Gemcitabine", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase", "KEGG_Drug__ID": null, "Pubchem_ID": "60750", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Single Drug", "PMID": null, "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": null, "Dose": "1000 mg/m2", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "MDSC", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells (MDSCs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02368", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "5 patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2271", "Drug": "Fluorouracil", "Drug_category": "Nucleoside Analogue", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": null, "Pubchem_ID": "3385", "STR_LINK_(SMILES)": "FC1=CNC(=O)NC1=O", "Single/Combination": "Single Drug", "PMID": "23202296", "Cancer_Type": "Colon Cancer", "Cancer_Type_Description": "Colon Cancer", "System": null, "Dose": null, "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "IL-1β secretion from MDSCs", "Controlled_Terms_Negative_Regulation": "Myeloid-derived suppressor cells (MDSCs); IL-1 family", "KEGG_Drug_ID": "D00585", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "12 patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/138", "Drug": "BRAF inhibitor (vemurafenib)+\n interleukin-2 (aldesleukin)", "Drug_category": "Others/combination", "Drugbank_ID": "DB08881", "Target/s_or_mechanism_of_action": "Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase.", "KEGG_Drug__ID": null, "Pubchem_ID": "42611257", "STR_LINK_(SMILES)": "CCCS(=O(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1", "Single/Combination": "Combination", "PMID": "29721378", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "oral vemurafenib (960 mg twice daily) for\n 2 weeks, and then received HD-IL-2 at 600,000 IU/kg/dose\n intravenously every eight hours to tolerance (maximum\n 14 doses) over five days on days 15–19 of cycle 1 and again on\n days 1–5 of cycle 2.", "Technique": "IHC, Flow cytometry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells, CD4+ FoxP3+ regulatory T cells\n and CD11b+ myeloid cells", "Controlled_Terms_Function_enhanced_Number_increased": "Regulatory T cells (Tregs); CD4+ T cells; CD8+ T cells; T cells; CD11b / ITGAM", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09996", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "N=6", "Male/Female": "3M/3F", "Median_age/Range": "42 (range 23–58)"}, {"study_type": "patient_studies", "ID": "CANIMM/167", "Drug": "Vorinostat and hydroxychloroquine", "Drug_category": "Others/combination", "Drugbank_ID": "DB02546, DB01611", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM).\n Hydroxychloroquine: It has been shown that hydroxychloroquine accumulates in the lysosomes of the malaria parasite, raising the pH of the vacuole.4 This activity interferes with the parasite's ability to proteolyse hemoglobin, preventing the normal growth and replication of the parasite.4 Hydroxychloroquine can also interfere with the action of parasitic heme polymerase, allowing for the accumulation of the toxic product beta-hematin", "KEGG_Drug__ID": null, "Pubchem_ID": "5311, \n 3652", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1,\n CCN(CCO)CCCC(C)NC1=C2C=CC(Cl)=CC2=NC=C1", "Single/Combination": "Combination", "PMID": "27463016", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal - Metastatic Colorectal Cancer", "System": null, "Dose": "VOR 400 mg PO and HCQ 600 mg PO daily, in a 3-week cycle.", "Technique": "immunohistochemistry(n=2),qRT-PCR", "Controlled_Technique": "Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "T cell activation", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; T-cell activation", "Immune_System-Function_inhibited/numbers_decreased": "regulatory T cells (CD25+FoxP3+), myeloid derived suppressor cells (defined as CD11b+HLA-DRlo) and monocytes (CD14+) PD-1 on CD4+and CD8+ T cells autophagy( lysosomal protease cathepsin D and p62 accumulation)", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); Myeloid-derived suppressor cells (MDSCs); CD4+ T cells; CD8+ T cells; T cells; Monocytes; PD-1 / PDCD1; CD14; CD25 / IL2RA; SQSTM1 / p62; CD11b / ITGAM", "Immune_System_function_unaffected": "CD11b+ myeloid cells, dendritic cells (CD11b+CD11c+) or in CD19+ B cells IFN-γ+ and IL-17+", "Controlled_Terms_Unaffected": "B cells; Dendritic cells; IFN-γ; IL-17; CD19; CD11b / ITGAM; CD11c / ITGAX", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06320, \n D08050", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "n=22", "Male/Female": "2024-07-13 00:00:00", "Median_age/Range": "61 years (range 44–74)"}, {"study_type": "patient_studies", "ID": "CANIMM/173", "Drug": "Chidamide (CS055/HBI-8000/Tucidinostat) and Rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB06334, DB00073", "Target/s_or_mechanism_of_action": "Histone deacetylase inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": "12136798, 46505820", "STR_LINK_(SMILES)": "NC1=CC(F)=CC=C1NC(=O)C1=CC=C(CNC(=O)\\C=C\\C2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "31907371", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Lymphoma - Diffuse Large B Cell Lymphoma (DLBCL)", "System": null, "Dose": "Chidamide plus Rituximab for three cycles", "Technique": "PET-CT", "Controlled_Technique": "Positron emission tomography–computed tomography (PET-CT)", "Immune_System-Function_enhanced/numbers_increased": "CR achieved", "Controlled_Terms_Function_enhanced_Number_increased": "Treatment response", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10993, \n D02994", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "1", "Male/Female": "0/1", "Median_age/Range": "74"}, {"study_type": "patient_studies", "ID": "CANIMM/156", "Drug": "FOLFOX regimen (folinic acid, 5-FU and OXP: pre-neoCT biopsies and post-neoCT surgical tissue samples)", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "32079180", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": null, "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ TILs IFNγ tumor programmed cell death 1 ligand 1 (PD-L1) level", "Controlled_Terms_Function_enhanced_Number_increased": "Tumor-infiltrating lymphocytes (TILs); IFN-γ; PD-L1 / CD274", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "19", "Male/Female": "2024-05-14 00:00:00", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/133", "Drug": "Cetuximab (chemotherapy with cetuximab)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "28075526-", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal - Metastatic Colorectal Cancer", "System": null, "Dose": null, "Technique": "HE staining", "Controlled_Technique": "Hematoxylin and eosin (H&E)/histology", "Immune_System-Function_enhanced/numbers_increased": "CD3+ CD8+ and CD56+cells-intratumoral filteration", "Controlled_Terms_Function_enhanced_Number_increased": "CD56 / NCAM1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "n = 13", "Male/Female": "2024-03-10 00:00:00", "Median_age/Range": "64.4 (39–78)"}, {"study_type": "patient_studies", "ID": "CANIMM/116", "Drug": "Cisplatin and oral etoposide (mPE)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00515 (APRD00359), DB00773", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation.\n \n Etoposide inhibits DNA topoisomerase II, thereby inhibiting DNA re-ligation. This causes critical errors in DNA synthesis at the premitotic stage of cell division and can lead to apoptosis of the cancer cell.", "KEGG_Drug__ID": null, "Pubchem_ID": "5702198, \n 36462", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H],\n [H][C@]12COC(=O)[C@]1([H])[C@H](C1=CC(OC)=C(O)C(OC)=C1)C1=CC3=C(OCO3)C=C1[C@H]2O[C@@H]1O[C@]2([H])CO[C@@H](C)O[C@@]2([H])[C@H](O)[C@H]1O", "Single/Combination": "Combination", "PMID": "27752361", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Lung Cancer - Metastatic Non-Small-Cell Lung Cancer", "System": null, "Dose": "cisplatin (30 mg/sqm days 1-3q21) and oral etoposide (50 mg, days 1-15q21) (mPE doublet)", "Technique": "Flow cytometry,Blood cell counts, serum analysis, multiplex cytokine assay", "Controlled_Technique": "Flow cytometry; Cytokine/multiplex immunoassay; Blood/serum analysis", "Immune_System-Function_enhanced/numbers_increased": "Tcms,activated MDICs", "Controlled_Terms_Function_enhanced_Number_increased": "Tcms,activated MDICs", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD3+CD4+, CD3+CD8+ and natural killer cells (CD3-CD16+CD56+;NK) cells", "Controlled_Terms_Unaffected": "NK cells; CD16 / FcγRIIIa; CD56 / NCAM1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00275, \n D00125", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "12", "Male/Female": "2024-02-10 00:00:00", "Median_age/Range": "69 (range 59–83)"}, {"study_type": "patient_studies", "ID": "CANIMM/103", "Drug": "Bevacizumab (mPEBev): cisplatin + oral etoposide (mPE)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00112\n , DB00515 (APRD00359), DB00773", "Target/s_or_mechanism_of_action": "Inhibiting the binding of VEGF to its cell surface receptors.\n Formation of DNA cross-links/alkylation.\n \n Etoposide inhibits DNA topoisomerase II, thereby inhibiting DNA re-ligation. This causes critical errors in DNA synthesis at the premitotic stage of cell division and can lead to apoptosis of the cancer cell.", "KEGG_Drug__ID": null, "Pubchem_ID": "46504473,\n 5702198, \n 36462", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H],\n [H][C@]12COC(=O)[C@]1([H])[C@H](C1=CC(OC)=C(O)C(OC)=C1)C1=CC3=C(OCO3)C=C1[C@H]2O[C@@H]1O[C@]2([H])CO[C@@H](C)O[C@@]2([H])[C@H](O)[C@H]1O", "Single/Combination": "Combination", "PMID": "27752361", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": null, "Dose": "mPEBev", "Technique": "Flow cytometry and bioplex", "Controlled_Technique": "Flow cytometry; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "activated (CD8+CD62L+), central-memory (CD8+C45RA−CCR7+;\n Tcm) and long-term memory (CD8+C45RA−CCR7+CD27+) CTLs; a\n trend to increase regulatory T cells (Treg), activated DCs (CD3−CD19−CD11c+CD14+CD15−),\n expressing either CD83 or CD80, activated MDICs (CD11b+CD14+CD15+) IL10 and G-CSF levels HGF, PECAM-1, Leptin, PDGF-BB, G-CSF and IL8", "Controlled_Terms_Function_enhanced_Number_increased": "Regulatory T cells (Tregs); T cells; Dendritic cells; IL-8 / CXCL8; IL-10; G-CSF / CSF3; CD80; CD14; CD19; Central memory T cells; CCR7; PDGF-BB; HGF; PECAM-1; Leptin; CD62L; CD11b / ITGAM; CD11c / ITGAX; CD15", "Immune_System-Function_inhibited/numbers_decreased": "IFNγ (Th1), IL4 (Th2)\n and IL17 (Th17) levels VEGF, angiopoietin-2 and\n follistatin", "Controlled_Terms_Function_inhibited_Number_decreased": "IFN-γ; IL-4; IL-17; VEGF; Th1 cells; Th2 cells; Th17 cells; Angiopoietin-2; Follistatin", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06409,\n D00275, \n D00125", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "n=47", "Male/Female": "37M/10F", "Median_age/Range": "62 (range 33–82)"}, {"study_type": "patient_studies", "ID": "CANIMM/114", "Drug": "Trichostatin A +tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)", "Drug_category": "Others/combination", "Drugbank_ID": "DB04297", "Target/s_or_mechanism_of_action": "TSA can be used to alter gene expression by interfering with the removal of acetyl groups from histones (histone deacetylases, HDAC) and therefore altering the ability of DNA transcription factors to access the DNA molecules inside chromatin", "KEGG_Drug__ID": null, "Pubchem_ID": "444732", "STR_LINK_(SMILES)": "C[C@H](\\C=C(/C)\\C=C\\C(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C", "Single/Combination": "Combination", "PMID": "16818655", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Lymphocytic Leukaemia (CLL)", "System": null, "Dose": "10 mg lenalidomide (PO) and 1000 mg Ofatumumab IV", "Technique": "Flow cytometry, Multiplex (Luminex)", "Controlled_Technique": "Flow cytometry; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD3+ T cells, CD4+ T cells, CD8+ T cells, Treg, CD16+CD56+NK cells, CD57+CD56+ NK cells CCL2, CCL3, CCL4, IFNa2, IL-12p70 Angiogenic factors bFGF, VEGF", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); NK cells; CD4+ T cells; CD8+ T cells; T cells; IL-12; CCL2 / MCP-1; CCL3 / MIP-1α; CCL4 / MIP-1β; VEGF; CD16 / FcγRIIIa; CD56 / NCAM1; CD57; bFGF", "Immune_System_function_unaffected": "Thrombospondin-1", "Controlled_Terms_Unaffected": "Thrombospondin-1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "34", "Male/Female": "26M/8F", "Median_age/Range": "34–82 (Median 64)"}, {"study_type": "patient_studies", "ID": "CANIMM/40", "Drug": "Bevacizumab ( FOLFIRI,FOLFOX4, XELOX)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00112", "Target/s_or_mechanism_of_action": "Inhibiting the binding of VEGF to its cell surface receptors.", "KEGG_Drug__ID": null, "Pubchem_ID": "46504473", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "21358206", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal - Metastatic Colorectal Cancer", "System": null, "Dose": "5 mg/kg in combination with 2-week regimens and at the dose of 7.5 mg/kg with 3-week regimens.", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "B and T cell", "Controlled_Terms_Function_enhanced_Number_increased": "T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06409", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "51", "Male/Female": "29/22", "Median_age/Range": "60/31–82"}, {"study_type": "patient_studies", "ID": "CANIMM/62", "Drug": "DC-KRN7000+lenolidamide", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "23100308", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Asymptomatic Multiple Myeloma (AMM)", "System": null, "Dose": "LEN:10 mg/d for 1-21 days, DC 10 million on day 8 of ach cycle", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD1d−GalCer+Vα24−Vβ11+ subset of iNKT cells, CD16 expression on CD14+ cells(monocytes) soluble IL2 receptor NKG2D ON NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; Monocytes; IL-2; CD14; CD16 / FcγRIIIa; NKG2D / KLRK1; iNKT cells; CD1d", "Immune_System-Function_inhibited/numbers_decreased": "Vα24+Vβ11+ classic iNKT cells", "Controlled_Terms_Function_inhibited_Number_decreased": "iNKT cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "N=6", "Male/Female": "4M/2F", "Median_age/Range": "60-73"}, {"study_type": "patient_studies", "ID": "CANIMM/96", "Drug": "Sorafenib and temozolomide", "Drug_category": "Others/combination", "Drugbank_ID": "DB00398, DB00853", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis. MZ is a DNA alkylating agent known to induce cell cycle arrest at G2/M and to eventually lead to apoptosis. At physiologic pH it is converted to the short-lived active compound, MTIC. MTIC is further hydrolyzed to 5-amino-imidazole-4-carboxamide (AIC) and to methylhydrazine.", "KEGG_Drug__ID": null, "Pubchem_ID": "216239, \n 5394", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1,\n CN1N=NC2=C(N=CN2C1=O)C(N)=O", "Single/Combination": "Combination", "PMID": "24197135", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Metastatic Melanoma", "System": null, "Dose": "temozolomide (Schering Plough; 100–150 mg/m2 daily for 7 days every 2 weeks) and sorafenib (Bayer; 400–800 mg twice daily without interruption)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD4(+)NKG2D(+) T cells (IL)-15Rα", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; NKG2D / KLRK1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524, \n D06067", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "63", "Male/Female": "35/28", "Median_age/Range": "48.5 13.8 [22–75]"}, {"study_type": "patient_studies", "ID": "CANIMM/87", "Drug": "Lenalidomide+Cetuximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB00002", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326, 46507042", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "24244687", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer - Kras-Mutant Metastatic Colorectal Cancer", "System": null, "Dose": "lenalidomide+Cetuximab", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cells, Absolute lymphocytes,Central memory T cytotoxic cells, total memory T helper cells, central memory T helper cells, Naive T cytotoxic cells, naive T helper cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; Lymphocytes; Central memory T cells", "Immune_System-Function_inhibited/numbers_decreased": "B cells", "Controlled_Terms_Function_inhibited_Number_decreased": "B cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687, D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "N=29", "Male/Female": "16M, 13F", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/75", "Drug": "Gemcitabine plus cisplatin", "Drug_category": "Others/combination", "Drugbank_ID": "DB00515 (APRD00359), DB00441", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation, Inhibition of DNA polymerase", "KEGG_Drug__ID": null, "Pubchem_ID": "5702198, 60750", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H], NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Combination", "PMID": "25659373", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Nonsmall-Cell Lung Cancer (NSCLC)", "System": null, "Dose": "gemcitabine 1250 mg/m2 on days 1 and 8, and cisplatin 75 mg/m2 on day 1", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD4(+)CD25(+)FOXP3(+)", "Controlled_Terms_Function_inhibited_Number_decreased": "CD25 / IL2RA", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00275,D02368", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "40 patients", "Male/Female": "2024-10-30 00:00:00", "Median_age/Range": "20-75"}, {"study_type": "patient_studies", "ID": "CANIMM/47", "Drug": "Cetuximab-based therapy", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "25832655", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Cancer (HNC)", "System": null, "Dose": "Cetuximab 250 mg/m2 days weekly (after an initial dose of 400 mg/m2), docetaxel 75 mg/m2 day 1, cisplatin 75 mg/m2 day 1, repeated every 21 days-3 cycles, then radiotherapy to 70 Gy (2 Gy/d) with concurrent cetuximab 250 mg/m2 weekly cisplatin 30 mg/m2, then maintenance cetuximab for 6 months", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "CD4+CD25hi Treg", "Controlled_Terms_Negative_Regulation": "Regulatory T cells (Tregs)", "KEGG_Drug_ID": "D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "n=22", "Male/Female": "2024-09-13 00:00:00", "Median_age/Range": "60"}, {"study_type": "patient_studies", "ID": "CANIMM/147", "Drug": "Cisplatin-based NAC", "Drug_category": "Platinum compounds", "Drugbank_ID": "DB00515 (APRD00359)", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation", "KEGG_Drug__ID": null, "Pubchem_ID": "5702198", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H]", "Single/Combination": null, "PMID": "31404614", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "NSCLC", "System": null, "Dose": null, "Technique": "immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-L1 expression on tumor as well as immune cells", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": "D00275", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "39 patients with available pre- and post-chemotherapy matched tumor tissues were identified.", "Male/Female": "2024-10-29 00:00:00", "Median_age/Range": "56.5"}, {"study_type": "patient_studies", "ID": "CANIMM/86", "Drug": "Lenalidomide-rituximab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB00002", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326, 46507042", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O", "Single/Combination": "Combination", "PMID": "27458141", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal, Head And Neck Squamous Cell Cancers (Hnscc)", "System": null, "Dose": "Cetuximab 500 mg/m2 every 2\n weeks (days 1 and 15), Lenalidomide (three dose levels 15, 20, and 25 mg daily for 21 days in 28 day cycle.", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "T regulatory cells, T cells, NK cells, and monocytes IL2, IL12, IFNg,\n TNFa, VEGF, and FGF-basic were", "Controlled_Terms_Unaffected": "NK cells; T cells; Monocytes; IFN-γ; IL-2; IL-12; VEGF", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687, D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "N=22", "Male/Female": "16M/6F", "Median_age/Range": "Median=61, range 44–71"}, {"study_type": "patient_studies", "ID": "CANIMM/67", "Drug": "Exemestane plus Entinostat (EE)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00990, DB11841", "Target/s_or_mechanism_of_action": "Exemestane selectively inhibits aromatase activity in vitro, in a time-dependent and irreversible manner, suggesting the mechanism of action that exemestane covalently binds to aromatase as a pseudo-substrate and inactivates the enzyme. Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": "4261, 60198", "STR_LINK_(SMILES)": "[H][C@@]12CCC(=O)[C@@]1(C)CC[C@@]1([H])[C@@]2([H])CC(=C)C2=CC(=O)C=C[C@]12C,\n NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "27999738", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "exemestane 25 mg by mouth once daily plus entinostat 5 mg by mouth once weekly continued until progressive disease or unacceptable toxicity", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD14+HLA-DRhi monocytes as a percentage of CD45+ cells HLA-DR expression on the total CD14+ monocyte", "Controlled_Terms_Function_enhanced_Number_increased": "Monocytes; CD14; HLA-DR", "Immune_System-Function_inhibited/numbers_decreased": "monocytic MDSCs, granulocytic MDSCs CD40 on MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells (MDSCs); Monocytic myeloid-derived suppressor cells (M-MDSCs); Granulocytic myeloid-derived suppressor cells (G-MDSCs)", "Immune_System_function_unaffected": "immune checkpoint receptors PD-1, CTLA-4, and T-cell immunoglobulin and mucin-domain containing-3 (TIM-3), on T-cell subsets", "Controlled_Terms_Unaffected": "PD-1 / PDCD1; CTLA-4; TIM-3", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338, D00963", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "blood samples from 34 patients", "Male/Female": "0/34", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/34", "Drug": "Gemcitabine and capecitabine", "Drug_category": "Others/combination", "Drugbank_ID": "DB00441,DB01101", "Target/s_or_mechanism_of_action": "Gemicitabine: Inhibition of DNA polymerase, Capecitabine: FdUMP inhibits DNA synthesis by reducing normal thymidine production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate.", "KEGG_Drug__ID": null, "Pubchem_ID": "########", "STR_LINK_(SMILES)": "NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F, CCCCCOC(=O)NC1=NC(=O)N(C=C1F)[C@@H]1O[C@H](C)[C@@H](O)[C@H]1O", "Single/Combination": "Combination", "PMID": "26931369", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic -Advanced Pancreatic Ductal Adenocarcinoma", "System": null, "Dose": "Gemcitabine was given intravenously at 1000 mg m−2 weekly × 3 every 4 weeks with orally administered capecitabine at 1660 mg m−2 per day (830 mg m−2 twice daily) for 3 weeks followed by 1 week's rest", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "GM-CSF, IL-6 and CRP.", "Controlled_Terms_Unaffected": "IL-6; GM-CSF / CSF2; CRP", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02368,D01223", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "38 patients", "Male/Female": "24 /14", "Median_age/Range": "64.0 (44–79)"}, {"study_type": "patient_studies", "ID": "CANIMM/1665", "Drug": "Cisplatin and gemcitabine", "Drug_category": "Others/combination", "Drugbank_ID": "DB00515 (APRD00359), DB00441", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation, Inhibition of DNA polymerase", "KEGG_Drug__ID": null, "Pubchem_ID": "5702198, 60750", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H], NC1=NC(=O)N(C=C1)[C@@H]1O[C@H](CO)[C@@H](O)C1(F)F", "Single/Combination": "Combination", "PMID": "23451142", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": null, "Dose": "first line chemotherapy with CDDP (mean dose 70 mg/m2) on day 1 plus GEM (GEMZAR®; Eli Lilly and Company, Indianapolis, IN; mean dose 1000 mg/m2) on day 1, 8, and 15 of a 28-day cycle. Treatment was planned for a maximum of six cycles (median 4, range 1–6) unless it was discontinued because of progressive disease, stable disease, unacceptable toxicity, or death.", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00275,D02368", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "30 patients", "Male/Female": "2024-09-21 00:00:00", "Median_age/Range": "62±11.9"}, {"study_type": "patient_studies", "ID": "CANIMM/119", "Drug": "Entinostat and high dose IL-2", "Drug_category": "Others/combination", "Drugbank_ID": "DB11841", "Target/s_or_mechanism_of_action": "Entinostat, also known as SNDX-275 and MS-275, is a benzamide histone deacetylase inhibitor undergoing clinical trials for treatment of various cancers", "KEGG_Drug__ID": null, "Pubchem_ID": "4261", "STR_LINK_(SMILES)": "NC1=CC=CC=C1NC(=O)C1=CC=C(CNC(=O)OCC2=CN=CC=C2)C=C1", "Single/Combination": "Combination", "PMID": "28939740", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma", "System": null, "Dose": "One cycle of treatment (85 days) consisted of 2 courses of high dose IL-2 600,000 units/kg administered intravenously every 8 hrs. on day 1–5 and day 15–19 (± 7 days) (maximum 28 doses) 4, and entinostat orally (1–2 hrs. prior to IL-2 infusion) given once every 2 weeks starting on day-14, administered before IL-2 infusion on day 1, 15, and then continuously", "Technique": "Flow cytometry,Immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "tumor infiltrating CD8 cells in patients with either prolonged stable disease (SD)or PR ,activated antigen presenting cells (APC)", "Controlled_Terms_Function_enhanced_Number_increased": "Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "Treg infiltration, peripheral Treg( in 5 patients who achieved an objective response as compared to 7 patients who had progressive disease)", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09338", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "47 patients", "Male/Female": null, "Median_age/Range": "58 (31–68)"}, {"study_type": "patient_studies", "ID": "CANIMM/149", "Drug": "Docetaxel, cisplatin and 5-FU (TPF)", "Drug_category": "Others/combination", "Drugbank_ID": "1. DB01248 (APRD00932), 2. DB00515 (APRD00359), 3. DB00544", "Target/s_or_mechanism_of_action": "1. Inhibition of tubulin depolymerization, 2. Formation of DNA cross-links/alkylation, 3. Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": null, "Pubchem_ID": "96024562, 5702198, 3385", "STR_LINK_(SMILES)": "Docetaxel-[H][C@@]12C[C@H](O)[C@@]3(C)C(=O)[C@H](O)C4=C(C)[C@H](C[C@@](O)([C@@H](OC(=O)C5=CC=CC=C5)[C@]3([H])[C@@]1(CO2)OC(C)=O)C4(C)C)OC(=O)[C@H](O)[C@@H](NC(=O)OC(C)(C)C)C1=CC=CC=C0, Cisplatin-[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H], 5-FU-FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "28637493", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Oral Squamous Cell Carcinoma (OSCC).", "System": null, "Dose": "docetaxel 75 mg/m2 intravenously on day 1, followed by cisplatin 75 mg/m2 intravenously on day 1, followed by 5-FU 750 mg/m2/day as a 120-h continuous intravenous infusion on days 1 through 5, every 3 weeks for 2 cycles.", "Technique": "immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Ki-67 and NLRP3 in OSCC tissues", "Controlled_Terms_Negative_Regulation": "Ki-67; NLRP3", "KEGG_Drug_ID": "1. D07866, 2. D00275, 3. D00584", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "103", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/152", "Drug": "FEC + docetaxel", "Drug_category": "Others/combination", "Drugbank_ID": "DB01248 (APRD00932)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": null, "Pubchem_ID": "96024562", "STR_LINK_(SMILES)": "[H][C@@]12C[C@H](O)[C@@]3(C)C(=O)[C@H](O)C4=C(C)[C@H](C[C@@](O)([C@@H](OC(=O)C5=CC=CC=C5)[C@]3([H])[C@@]1(CO2)OC(C)=O)C4(C)C)OC(=O)[C@H](O)[C@@H](NC(=O)OC(C)(C)C)C1=CC=CC=C1", "Single/Combination": "Combination", "PMID": "29138861", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "5-fluorouracil (500 mg/m2 , intravenous injection on day 1) -epirubicin (60-100 mg/m2 , intravenous injection on day 1) -cyclophosphamide (500 mg/m2 , intravenous injection on day 1) / every 3 weeks", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "HMGB1 and calreticulin in tumor microenvironment", "Controlled_Terms_Function_enhanced_Number_increased": "HMGB1; Calreticulin / CRT", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07867", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "14", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/168", "Drug": "5-fluorouracil (5-FU)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00544", "Target/s_or_mechanism_of_action": "Fluorouracil is an antineoplastic anti-metabolite. 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Calreticulin / CRT", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "5", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/151", "Drug": "FEC + docetaxel", "Drug_category": "Others/combination", "Drugbank_ID": "DB01248 (APRD00932)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": null, "Pubchem_ID": "96024562", "STR_LINK_(SMILES)": "[H][C@@]12C[C@H](O)[C@@]3(C)C(=O)[C@H](O)C4=C(C)[C@H](C[C@@](O)([C@@H](OC(=O)C5=CC=CC=C5)[C@]3([H])[C@@]1(CO2)OC(C)=O)C4(C)C)OC(=O)[C@H](O)[C@@H](NC(=O)OC(C)(C)C)C1=CC=CC=C0", "Single/Combination": "Combination", "PMID": "29138861", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "5-fluorouracil (500 mg/m2 , intravenous injection on day 1) -epirubicin (60-100 mg/m2 , intravenous injection on day 1) -cyclophosphamide (500 mg/m2 , intravenous injection on day 1) / every 3 weeks", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "HMGB1 and calreticulin in tumor microenvironment", "Controlled_Terms_Function_enhanced_Number_increased": "HMGB1; Calreticulin / CRT", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07866", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "14", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/153", "Drug": "FEC + docetaxel + trastuzumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB01248 (APRD00932)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": null, "Pubchem_ID": "96024562", "STR_LINK_(SMILES)": "[H][C@@]12C[C@H](O)[C@@]3(C)C(=O)[C@H](O)C4=C(C)[C@H](C[C@@](O)([C@@H](OC(=O)C5=CC=CC=C5)[C@]3([H])[C@@]1(CO2)OC(C)=O)C4(C)C)OC(=O)[C@H](O)[C@@H](NC(=O)OC(C)(C)C)C1=CC=CC=C2", "Single/Combination": "Combination", "PMID": "29138861", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "5-fluorouracil (500 mg/m2 , intravenous injection on day 1) -epirubicin (60-100 mg/m2 , intravenous injection on day 1) -cyclophosphamide (500 mg/m2 , intravenous injection on day 1) / every 3 weeks", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "HMGB1 and calreticulin in tumor microenvironment", "Controlled_Terms_Function_enhanced_Number_increased": "HMGB1; Calreticulin / CRT", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07868", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "14", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/143", "Drug": "5-fluorouracil + cisplatin", "Drug_category": "Others/combination", "Drugbank_ID": "DB00515 (APRD00359),DB00544", "Target/s_or_mechanism_of_action": "Formation of DNA cross-links/alkylation, Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA", "KEGG_Drug__ID": null, "Pubchem_ID": "5702198, 3385", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt](Cl)(Cl)[N]([H])([H])[H], FC1=CNC(=O)NC1=O", "Single/Combination": "Combination", "PMID": "29138861", "Cancer_Type": "Esophageal Cancer", "Cancer_Type_Description": "Esophageal Squamous Cell Carcinoma (ESCC)", "System": null, "Dose": null, "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "HMGB1 and calreticulin in tumor microenvironment", "Controlled_Terms_Function_enhanced_Number_increased": "HMGB1; Calreticulin / CRT", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00275, D00584", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "8", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/108", "Drug": "Dabrafenib + trametinib", "Drug_category": "Others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "44462760, 11707110", "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "28123875", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": "2 mg orally daily", "Technique": "Flow cytometry, immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cell infiltrates", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064, D10175", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Melanoma biopsies from patients treated at the Melanoma Institute Australia Sydney and the Netherlands Cancer Institute", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/175", "Drug": "Dabrafenib + trametinib", "Drug_category": "Others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. \n trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of_ MEK1_ and MEK2 kinase activity.", "KEGG_Drug__ID": null, "Pubchem_ID": "44462760, 11707110", "STR_LINK_(SMILES)": "CC(C(C)C1=NC(=C(S1)C1=NC(N)=NC=C1)C1=C(F)C(NS(=O(=O)C2=C(F)C=CC=C2F)=CC=C1,\n CN1C(=O)C(C)=C2N(C(=O)N(C3CC3)C(=O)C2=C1NC1=CC=C(I)C=C1F)C1=CC(NC(C)=O)=CC=C1", "Single/Combination": "Combination", "PMID": "25256614", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Skin - Melanoma", "System": null, "Dose": null, "Technique": "qPCR analysis,histology", "Controlled_Technique": "Polymerase chain reaction (PCR/qPCR); Hematoxylin and eosin (H&E)/histology", "Immune_System-Function_enhanced/numbers_increased": "CD68, M1 marker CD86 and the M2 marker CD163-indicating an accumulation of M1 and M2 polarized macrophages", "Controlled_Terms_Function_enhanced_Number_increased": "Macrophages; CD86; CD68; CD163", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "TNFα expression  MITF expression", "Controlled_Terms_Negative_Regulation": "TNF-α / TNF; MITF", "KEGG_Drug_ID": "D10064, D10175", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "paired BRAFV600E positive tumor biopsies from patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/39", "Drug": "Bevacizumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB00112", "Target/s_or_mechanism_of_action": "Inhibiting the binding of VEGF to its cell surface receptors.", "KEGG_Drug__ID": null, "Pubchem_ID": "46504473", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "18193223", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "DC", "Controlled_Terms_Function_enhanced_Number_increased": "Dendritic cells", "Immune_System-Function_inhibited/numbers_decreased": "immature myeloid cells (Lin− HLA-DR−, B)", "Controlled_Terms_Function_inhibited_Number_decreased": "HLA-DR", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06409", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "19", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/41", "Drug": "Bevacizumab plus chemotherapy", "Drug_category": "Others/combination", "Drugbank_ID": "DB00112", "Target/s_or_mechanism_of_action": "Inhibiting the binding of VEGF to its cell surface receptors.", "KEGG_Drug__ID": null, "Pubchem_ID": "46504473", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "23108136", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal - Metastatic Colorectal Cancer", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Treg", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06409", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "9", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/46", "Drug": "Cetuximab-based therapy", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "23444227", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "EGFR-specific T cells", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; EGFR", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "(n=17)", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/74", "Drug": "Gemcitabine based regimen", "Drug_category": "Others/combination", "Drugbank_ID": "DB00441", "Target/s_or_mechanism_of_action": "Inhibition of DNA polymerase", "KEGG_Drug__ID": null, "Pubchem_ID": "60750", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "23860726", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Pancreatic Cancer", "System": null, "Dose": "Eight patients received GEM regimens, 10 received GEM ? S1 regimens, and 14 received GEM ? S1 regimens following radiation therapy (30 Gy). S1 is an orally administered drug consisting of a combination of tegafur, 5-chloro-1,4-dihydroxypyridine, and oteracil potassium. The GEM regimen consisted of an intravenous dose of 1,000 mg/m2 GEM on days 1, 8, and 15, repeated every 4 weeks. The GEM ? S1 regimen consisted of an intravenous dose of 1,000 mg/m2 GEM on days 8 and 15, combined with 60 mg/m2 oral S-1 on days 1–14. All patients received two to six courses of chemotherapy", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": "CD4 T cells, CD8 T cells and NK cells (CD3-CD56 cells)", "Controlled_Terms_Unaffected": "NK cells; CD4+ T cells; CD8+ T cells; T cells; CD56 / NCAM1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D02373", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "32 patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/65", "Drug": "Docetaxel+cisplatin", "Drug_category": "Others/combination", "Drugbank_ID": "DB01248 (APRD00932)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": null, "Pubchem_ID": "96024562", "STR_LINK_(SMILES)": "[H][C@@]12C[C@H](O)[C@@]3(C)C(=O)[C@H](O)C4=C(C)[C@H](C[C@@](O)([C@@H](OC(=O)C5=CC=CC=C5)[C@]3([H])[C@@]1(CO2)OC(C)=O)C4(C)C)OC(=O)[C@H](O)[C@@H](NC(=O)OC(C)(C)C)C1=CC=CC=C3", "Single/Combination": "Combination", "PMID": "24868562", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Nonsmall-Cell Lung Cancer (NSCLC)", "System": null, "Dose": "cisplatin (75 mg/m2) plus docetaxel (30 mg/m2", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "T reg", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "1. D07866, 2. D00275", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "17 NSCLC patients- treated for 4 cycles.", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/70", "Drug": "Folinic acid, 5-fluorouracil (5FU), and CPT11", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "25209187", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "MDSCs", "Controlled_Terms_Negative_Regulation": "Myeloid-derived suppressor cells (MDSCs)", "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "4", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/71", "Drug": "Folinic acid, 5FU, and oxaliplatin", "Drug_category": "Others/combination", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "25209187", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal Cancer (CRC)", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells (MDSCs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "6", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2189", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "28808483", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": "400 mg/day", "Technique": "Flow cytometry.ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD4+CD25+ T cells IL-10, IL-4 and TGF-β FOXP3, GITR and CTLA-4", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4+ T cells; T cells; IL-4; IL-10; TGF-β; CTLA-4; CD25 / IL2RA; GITR", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "12", "Male/Female": "2024-05-07 00:00:00", "Median_age/Range": "38 years, range, 25–54 years"}, {"study_type": "patient_studies", "ID": "CANIMM/7", "Drug": "SAHA and cladribine", "Drug_category": "Others/combination", "Drugbank_ID": "DB02546, DB00242", "Target/s_or_mechanism_of_action": "Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC50< 86 nM). \n cladribine is phosphorylated by deoxycytidine kinase to the nucleotidecladribine triphosphate (CdATP; 2-chloro-2′-deoxyadenosine 5′-triphosphate), which accumulates and is incorporated into DNA in cells such as lymphocytes that contain high levels of deoxycytidine kinase and low levels of deoxynucleotidase, resulting in DNA strand breakage and inhibition of DNA synthesis and repair.", "KEGG_Drug__ID": null, "Pubchem_ID": "5311, 20279", "STR_LINK_(SMILES)": "ONC(=O)CCCCCCC(=O)NC1=CC=CC=C1\n NC1=C2N=CN([C@H]3C[C@H](O)[C@@H](CO)O3)C2=NC(Cl)=N1", "Single/Combination": "Combination", "PMID": "25284154", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia  - Chronic Lymphocytic Leukaemia (CLL)", "System": null, "Dose": "Acalabrutinib treatment: Each cycle is 4 weeks. Cycle 3 indicates samples obtained after 2 cycles (8 weeks into treatment), and cycle 6 indicates samples obtained after 5 cycles (20 weeks into treatment)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "IFN-γ+, IL-4+, and TNF+ cells CD200 and BTLA as well as IL-10 production by CLL cells, CTLA-4 expression on T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "T cells; IFN-γ; IL-4; IL-10; TNF-α / TNF; CTLA-4; BTLA", "Immune_System_function_unaffected": "IL-17–producing cells", "Controlled_Terms_Unaffected": "IL-17", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06320, \n D01370", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "N=13", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/45", "Drug": "Cetuximab + motolimod", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002, DB12303", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR. Motolimod has been used in trials studying the treatment of Lymphoma, Tongue Cancer, Ovarian Cancer, Adult Solid Neoplasm, and Fallopian Tube Cancer, among others.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507042, 16049404", "STR_LINK_(SMILES)": "CCCN(CCC)C(=O)C1=CC2=CC=C(C=C2N=C(N)C1)C1=CC=C(C=C1)C(=O)N1CCCC1", "Single/Combination": "Combination", "PMID": "29061643", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck Squamous Cell Carcinoma (HNSCC)", "System": null, "Dose": "subcutaneous motolimod injection (2.5 mg/m2) and intravenous cetuximab (initial dose of 400 mg/m2 followed by weekly infusions at 250 mg/m2) administered once weekly starting on Day 1 for a minimum of 3 weeks and a maximum of 4 weeks (i.e., Days 1, 8, 15, and 22) prior to scheduled surgery, which was to be performed within 2 days of the last dose of motolimod received", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "EGFR tetramer+ CD8 T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells; EGFR", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "(n=5)", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/48", "Drug": "Cetuximab-based therapy", "Drug_category": "Others/combination", "Drugbank_ID": "DB00002", "Target/s_or_mechanism_of_action": "Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507042", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "29354119", "Cancer_Type": "Colorectal Cancer", "Cancer_Type_Description": "Colorectal - Metastatic Colorectal Cancer", "System": null, "Dose": "Cetuximab was administered in the dose of 500 mg/m2 in combination with irinotecan in the dose of 180 mg/m^2 in 2-week intervals, or as monotherapy in the same regimen", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "CD16+, CD56+, and CD16+CD56+ lymphocytes", "Controlled_Terms_Negative_Regulation": "Lymphocytes; CD16 / FcγRIIIa; CD56 / NCAM1", "KEGG_Drug_ID": "D03455", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "50 patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/4", "Drug": "Cyclophosphamide + mTOR inhibitor everolimus", "Drug_category": "Others/combination", "Drugbank_ID": "DB00531", "Target/s_or_mechanism_of_action": "Inhibition of protein synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": "2907", "STR_LINK_(SMILES)": "ClCCN(CCCl)P1(=O)NCCCO1", "Single/Combination": "Combination", "PMID": "30652208", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal - Metastatic Renal Cell Cancer", "System": null, "Dose": "50 mg of CTX once daily and continuously administered, in combination with the standard dose of 10 mg everolimus", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": "Treg ,mMDSC", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07760", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Forty patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/13", "Drug": "Carboplatin and a taxane", "Drug_category": "Others/combination", "Drugbank_ID": "DB00958", "Target/s_or_mechanism_of_action": "Carboplatin undergoes activation inside cells and forms reactive platinum complexes that cause the intra- and inter-strand cross-linkage of DNA molecules within the cell.", "KEGG_Drug__ID": null, "Pubchem_ID": "38904", "STR_LINK_(SMILES)": "[H][N]([H])([H])[Pt]1(OC(=O)C2(CCC2)C(=O)O1)[N]([H])([H])[H]", "Single/Combination": "Combination", "PMID": "29500278", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": null, "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "CCL2 (MCP-1), CCL7 (MCP-3), and CCL8 (MCP-2)-cancer stem-like cell (CSC) phenotype and contributing to tumor relapse", "Controlled_Terms_Negative_Regulation": "CCL2 / MCP-1; CCL7; CCL8", "KEGG_Drug_ID": "D01363", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "21 samples", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/1834", "Drug": "Lenalidomide+melphalan and autologous stem cell transplantation (ASCT)", "Drug_category": "Others/combination", "Drugbank_ID": "DB00480, DB01042", "Target/s_or_mechanism_of_action": "In vivo, lenalidomide induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity. \n Melphalan attaches alkyl groups to the N-7 position of guanine and N-3 position of adenine, leading to the formation of monoadducts, and DNA fragmenting when repair enzymes attempt to correct the error. It can also cause DNA cross-linking from the N-7 position of one guanine to the N-7 position of another, preventing DNA strands from separating for synthesis or transcription. Finally, melphalan can induce a number of different mutations.", "KEGG_Drug__ID": null, "Pubchem_ID": "216326, \n 460612", "STR_LINK_(SMILES)": "NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O,\n N[C@@H](CC1=CC=C(C=C1)N(CCCl)CCCl)C(O)=O", "Single/Combination": "Combination", "PMID": "24032527", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": null, "Dose": null, "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "NKT cell frequency", "Controlled_Terms_Function_inhibited_Number_decreased": "Natural killer T cells (NKT cells)", "Immune_System_function_unaffected": "CD25", "Controlled_Terms_Unaffected": "CD25 / IL2RA", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04687, \n D00369", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "N=11", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/1993", "Drug": "Thalidomide+dexamethasone", "Drug_category": "Others/combination", "Drugbank_ID": "DB01041", "Target/s_or_mechanism_of_action": "Previous research indicate that thalidomide binds to cerebron, a component of the E3 ubiquitin ligase complex, to selectively degrade the transcription factor IKZF3 and IKZF1. These 2 transcription factors are vital for the proliferation and survival of malignant myeloma cells", "KEGG_Drug__ID": null, "Pubchem_ID": "5426", "STR_LINK_(SMILES)": "O=C1N(C2CCC(=O)NC2=O)C(=O)C2=CC=CC=C12", "Single/Combination": "Combination", "PMID": "31168767", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": null, "Dose": "dexamethasone (40 mg/week in\n fit patients and 20 mg/week in unfit patients) median of 10 months", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00754", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "23(Not acheving CR or PR)", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/1994", "Drug": "Thalidomide+melphalan+prednisone", "Drug_category": "Others/combination", "Drugbank_ID": "DB01041, DB01042, DB00635", "Target/s_or_mechanism_of_action": "Previous research indicate that thalidomide binds to cerebron, a component of the E3 ubiquitin ligase complex, to selectively degrade the transcription factor IKZF3 and IKZF1. These 2 transcription factors are vital for the proliferation and survival of malignant myeloma cells.\n Melphalan attaches alkyl groups to the N-7 position of guanine and N-3 position of adenine, leading to the formation of monoadducts, and DNA fragmenting when repair enzymes attempt to correct the error. It can also cause DNA cross-linking from the N-7 position of one guanine to the N-7 position of another, preventing DNA strands from separating for synthesis or transcription. Finally, melphalan can induce a number of different mutations.\n Prednisone is first metabolized in the liver to its active form, prednisolone, a glucocorticoid agonist corticosteroid", "KEGG_Drug__ID": null, "Pubchem_ID": "5426, 460612, 5865", "STR_LINK_(SMILES)": "O=C1N(C2CCC(=O)NC2=O)C(=O)C2=CC=CC=C12,\n N[C@@H](CC1=CC=C(C=C1)N(CCCl)CCCl)C(O)=O,\n [H][C@@]12CC[C@](O)(C(=O)CO)[C@@]1(C)CC(=O)[C@@]1([H])[C@@]2([H])CCC2=CC(=O)C=C[C@]12C", "Single/Combination": "Combination", "PMID": "31168767", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple Myeloma (MM)", "System": null, "Dose": "MPT regimen (melphalan 16 mg/m2/day for 4 days, prednisone 100 mg/day, 4 days, and thalidomide 100 mg/day continuously) was given every 4 weeks for a median of\n 10 months", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": "CD4+ T cells, CD8+ T cells, NK cells, NKT cells, CD19+ B cells,", "Controlled_Terms_Function_enhanced_Number_increased": "Natural killer T cells (NKT cells); NK cells; CD4+ T cells; CD8+ T cells; T cells; B cells; CD19", "Immune_System-Function_inhibited/numbers_decreased": "iNKT cells,CD4+ CD25+ FoxP3+ Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); CD25 / IL2RA; iNKT cells", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00754, D00369, D00473", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "45 (complete remission)", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2216", "Drug": "Oral etoposide (mPE)", "Drug_category": "Podophyllotoxins", "Drugbank_ID": "DB00773", "Target/s_or_mechanism_of_action": "Etoposide inhibits DNA topoisomerase II, thereby inhibiting DNA re-ligation. This causes critical errors in DNA synthesis at the premitotic stage of cell division and can lead to apoptosis of the cancer cell.", "KEGG_Drug__ID": null, "Pubchem_ID": "36462", "STR_LINK_(SMILES)": "[H][C@]12COC(=O)[C@]1([H])[C@H](C1=CC(OC)=C(O)C(OC)=C1)C1=CC3=C(OCO3)C=C1[C@H]2O[C@@H]1O[C@]2([H])CO[C@@H](C)O[C@@]2([H])[C@H](O)[C@H]1O", "Single/Combination": "Single Drug", "PMID": "27752361", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": null, "Dose": "mPE", "Technique": "Flow cytometry and bioplex", "Controlled_Technique": "Flow cytometry; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "activated MDICs (CD11b+CD14+CD15+) IL10 and G-CSF levels, IL8 and IFNγ HGF, PECAM-1, Leptin, PDGF-BB, G-CSF and IL8", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-8 / CXCL8; IL-10; G-CSF / CSF3; CD14; PDGF-BB; HGF; PECAM-1; Leptin; CD11b / ITGAM; CD15", "Immune_System-Function_inhibited/numbers_decreased": "IL8 and IFNγ VEGF, angiopoietin-2 and\n follistatin", "Controlled_Terms_Function_inhibited_Number_decreased": "IFN-γ; IL-8 / CXCL8; VEGF; Angiopoietin-2; Follistatin", "Immune_System_function_unaffected": "CD3+CD4+, CD3+CD8+ and natural killer cells (CD3-CD16+\n CD56+;NK) cells, central-memory (CD8+C45RA−CCR7+;\n Tcm)", "Controlled_Terms_Unaffected": "NK cells; CD16 / FcγRIIIa; CD56 / NCAM1; Central memory T cells; CCR7", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00125", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "n=12", "Male/Female": "10M/2F", "Median_age/Range": "69 (range 59–83)"}, {"study_type": "patient_studies", "ID": "CANIMM/2197", "Drug": "Paclitaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01229 (APRD00259, DB05261, DB05927, DB05526, DB05281)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": null, "Pubchem_ID": "36314", "STR_LINK_(SMILES)": "[H][C@]12[C@H](OC(=O)C3=CC=CC=C3)[C@]3(O)C[C@H](OC(=O)[C@H](O)[C@@H](NC(=O)C4=CC=CC=C4)C4=CC=CC=C4)C(C)=C([C@@H](OC(C)=O)C(=O)[C@]1(C)[C@@H](O)C[C@H]1OC[C@@]21OC(C)=O)C3(C)C", "Single/Combination": "Single Drug", "PMID": "11595690", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "200 mg/m2 q2w, 4 treatments)", "Technique": "Immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "tumor infiltrating lymphocytes (TILs)", "Controlled_Terms_Function_enhanced_Number_increased": "Tumor-infiltrating lymphocytes (TILs); 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CD4+ T cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": "CD4+CD25highCD127-FoxP3+ Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07866", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "15 patients with hormone refractory metastatic prostate cancer", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2269", "Drug": "Docetaxel", "Drug_category": "Taxanes", "Drugbank_ID": "DB01248 (APRD00932)", "Target/s_or_mechanism_of_action": "Inhibition of tubulin depolymerization", "KEGG_Drug__ID": null, "Pubchem_ID": "96024562", "STR_LINK_(SMILES)": "[H][C@@]12C[C@H](O)[C@@]3(C)C(=O)[C@H](O)C4=C(C)[C@H](C[C@@](O)([C@@H](OC(=O)C5=CC=CC=C5)[C@]3([H])[C@@]1(CO2)OC(C)=O)C4(C)C)OC(=O)[C@H](O)[C@@H](NC(=O)OC(C)(C)C)C1=CC=CC=C4", "Single/Combination": "Single Drug", "PMID": "12085250", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "100 mg m^2", "Technique": "ELISA", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IL-6, GM-CSF, IFN-γ levels,", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; IL-6; GM-CSF / CSF2", "Immune_System-Function_inhibited/numbers_decreased": "IL-1, TNF, and PGE2", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-1 family; TNF-α / TNF; PGE2", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D07866", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Fifteen patients received Docetaxel", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2202", "Drug": "Neoadjuvant trastuzumab", "Drug_category": "topoisomerase I inhibitor", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene.", "KEGG_Drug__ID": null, "Pubchem_ID": "46507516", "STR_LINK_(SMILES)": null, "Single/Combination": "Single Drug", "PMID": "31618954", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast Cancer", "System": null, "Dose": "neoadjuvant trastuzumab", "Technique": "IHC", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "All seven tumors were also positive for CD8+ T cells, and six out of seven were positive for CD4+ T cells  only four out of eight tumors were positive for the PD-1 immune checkpoint molecule, which is indicative of an exhausted immune environmen high levels of nuclear NF-κB/p65RelA", "Controlled_Terms_Function_enhanced_Number_increased": "CD4+ T cells; CD8+ T cells; T cells; PD-1 / PDCD1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03257", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Eight FFPE tumor samples (N=8)", "Male/Female": null, "Median_age/Range": "Patients were between 36 and 61 years of age"}, {"study_type": "patient_studies", "ID": "CANIMM/2186", "Drug": "Gefitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00317", "Target/s_or_mechanism_of_action": "Gefitinib is an inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase that binds to the adenosine triphosphate (ATP)-binding site of the enzyme.", "KEGG_Drug__ID": null, "Pubchem_ID": "123631", "STR_LINK_(SMILES)": "COC1=C(OCCCN2CCOCC2)C=C2C(NC3=CC(Cl)=C(F)C=C3)=NC=NC2=C1", "Single/Combination": "Single Drug", "PMID": "28260924", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Non-Small Cell Lung Cancer (NSCLC))", "System": null, "Dose": "(orally, 250 mg/day)", "Technique": "Flow cytometry, immunohistochemistry (IHC), cytokine detection kit", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC); Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "natural killer cells interferon-gamma (INF-γ)", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": "interleukin (IL)-6", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-6", "Immune_System_function_unaffected": "IL-2, IL-4, and IL-10", "Controlled_Terms_Unaffected": "IL-2; IL-4; IL-10", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "expression of PD-L1", "Controlled_Terms_Negative_Regulation": "PD-L1 / CD274", "KEGG_Drug_ID": "D01977", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "54", "Male/Female": "26/28", "Median_age/Range": "(18 - 75 )years"}, {"study_type": "patient_studies", "ID": "CANIMM/2187", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": "3062316", "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "30705677", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Chronic Myeloid Leukemia", "System": null, "Dose": "upto 100 mg dasatinib daily", "Technique": "Flow cytometry,killing assay", "Controlled_Technique": "Flow cytometry; Cytotoxicity/release assay; Cellular cytotoxicity/function assay", "Immune_System-Function_enhanced/numbers_increased": "CD3−CD16brCD56dim NK cells, NKG2D and NKp30 of NK cells(activating receptors), NK cytotoxicity", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; NKG2D / KLRK1; NKp30 / NCR3; Cytotoxicity / cytolysis", "Immune_System-Function_inhibited/numbers_decreased": "NKG2A-a inhibitory receptor of NK cell", "Controlled_Terms_Function_inhibited_Number_decreased": "NK cells; NKG2A", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "30", "Male/Female": null, "Median_age/Range": "50 (23–80)"}, {"study_type": "patient_studies", "ID": "CANIMM/2188", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": "3062316", "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "22211798", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": null, "Technique": "Flow cytometry,NK-cell reactivity assay, Th e Bio-Plex ™ Suspension Array system", "Controlled_Technique": "Flow cytometry; Cellular cytotoxicity/function assay; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "CD3 + CD57 + cells, natural killer (NK)-cell interleukin-8 (IL-8), interferon-γ inducible protein-10 (IP-10) and monocyte chemoattractant protein-1 (MCP-1),(GM-CSF) CD56 + CD57 +", "Controlled_Terms_Function_enhanced_Number_increased": "Monocytes; IFN-γ; IL-8 / CXCL8; GM-CSF / CSF2; CCL2 / MCP-1; CXCL10 / IP-10; CD56 / NCAM1; CD57", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "18", "Male/Female": null, "Median_age/Range": "63 years (range, 21 – 79)"}, {"study_type": "patient_studies", "ID": "CANIMM/2200", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "27698808", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": null, "Technique": "immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": "interstitial lymphocytic aggregates and infiltrates-T and B cells CD3 and CD20 infiltrates", "Controlled_Terms_Function_enhanced_Number_increased": "B cells; 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PD-L1 / CD274", "KEGG_Drug_ID": "D08524", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "23", "Male/Female": "2024-03-20 00:00:00", "Median_age/Range": "median age of 64.7 years"}, {"study_type": "patient_studies", "ID": "CANIMM/2204", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "22833259", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "sorafenib (400 mg/day, 8–14 weeks)", "Technique": "Flow cytometry, immunoblotting", "Controlled_Technique": "Flow cytometry; Western blot/immunoblot analysis", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Tregs   phosphorylation of SMAD2 and SMAD3, pJNK and pERK", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); SMAD2; SMAD3; ERK / MAPK; p-JNK", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "22 HCC patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2208", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "24323358", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastrointestinal Stromal Tumor (GIST)", "System": null, "Dose": null, "Technique": "Flow cytometry, immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "TAMs and TAMs to become M2-like TAMs and TAMs to become M2-like", "Controlled_Terms_Function_inhibited_Number_decreased": "Tumor-associated macrophages (TAMs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "18", "Male/Female": "2024-04-14 00:00:00", "Median_age/Range": "58 (43-81)"}, {"study_type": "patient_studies", "ID": "CANIMM/2211", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "21533122", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastrointestinal Stromal Tumor (GIST)", "System": null, "Dose": "400 mg/daily", "Technique": "Flow cytometry.ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "CD20+CD5+sIgM+ cells IgM,stromal-derived factor-1 and the B-lymphocyte-activating factor of the tumor necrosis factor family,bone morphogenetic proteins-2 and −7", "Controlled_Terms_Function_enhanced_Number_increased": "B cells; Lymphocytes; TNF-α / TNF; CD20 / MS4A1", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "40", "Male/Female": "25/15", "Median_age/Range": "53 (22–73)"}, {"study_type": "patient_studies", "ID": "CANIMM/2213", "Drug": "Nilotinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB04868", "Target/s_or_mechanism_of_action": "Nilotinib binds to and stabilizes the inactive conformation of the kinase domain of Abl protein.", "KEGG_Drug__ID": null, "Pubchem_ID": "644241", "STR_LINK_(SMILES)": "CC1=CN(C=N1)C1=CC(NC(=O)C2=CC=C(C)C(NC3=NC=CC(=N3)C3=CN=CC=C3)=C2)=CC(=C1)C(F)(F)F", "Single/Combination": "Single Drug", "PMID": "28808483", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": "300 mg twice daily", "Technique": "Flow cytometry.ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "IL-10 and IL-4 GITR and CTLA-4", "Controlled_Terms_Function_inhibited_Number_decreased": "IL-4; IL-10; CTLA-4; GITR", "Immune_System_function_unaffected": "TGF-β", "Controlled_Terms_Unaffected": "TGF-β", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08953", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "8", "Male/Female": "2024-05-03 00:00:00", "Median_age/Range": "mean age, 43 years, range, 28–56 years"}, {"study_type": "patient_studies", "ID": "CANIMM/2214", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": "3062316", "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "28808483", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": "100 mg/day", "Technique": "Flow cytometry.ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD4+CD25+ T cells IL-10, IL-4 and TGF-β FOXP3, GITR and CTLA-4", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4+ T cells; T cells; IL-4; IL-10; TGF-β; CTLA-4; CD25 / IL2RA; GITR", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "11", "Male/Female": "2024-06-05 00:00:00", "Median_age/Range": "mean age, 43 years, range, 28–56"}, {"study_type": "patient_studies", "ID": "CANIMM/2218", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "31428530", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": null, "Technique": "Multiplex Inflammation immunoassay, Flow cytometry", "Controlled_Technique": "Flow cytometry; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "CD56+ CD16+ NK cells MCP-1, CX3CL1. TWEAK and TRAIL", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; CCL2 / MCP-1; CD16 / FcγRIIIa; CD56 / NCAM1; CX3CL1; TRAIL; TWEAK", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "20", "Male/Female": "2024-09-11 00:00:00", "Median_age/Range": "58[30–81]"}, {"study_type": "patient_studies", "ID": "CANIMM/2219", "Drug": "Nilotinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB04868", "Target/s_or_mechanism_of_action": "Nilotinib binds to and stabilizes the inactive conformation of the kinase domain of Abl protein.", "KEGG_Drug__ID": null, "Pubchem_ID": "644241", "STR_LINK_(SMILES)": "CC1=CN(C=N1)C1=CC(NC(=O)C2=CC=C(C)C(NC3=NC=CC(=N3)C3=CN=CC=C3)=C2)=CC(=C1)C(F)(F)F", "Single/Combination": "Single Drug", "PMID": "22211798", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Chronic Myeloid Leukemia", "System": null, "Dose": null, "Technique": "Flow cytometry,NK-cell reactivity assay, Th e Bio-Plex ™ Suspension Array system", "Controlled_Technique": "Flow cytometry; Cellular cytotoxicity/function assay; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "interleukin-8 (IL-8), interferon-γ inducible protein-10 (IP-10) and monocyte chemoattractant protein-1 (MCP-1)", "Controlled_Terms_Function_enhanced_Number_increased": "Monocytes; IFN-γ; IL-8 / CXCL8; CCL2 / MCP-1; CXCL10 / IP-10", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "NK-cell", "Controlled_Terms_Negative_Regulation": "NK cells", "KEGG_Drug_ID": "D08953", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "9", "Male/Female": null, "Median_age/Range": "45 years (range, 21 – 73)"}, {"study_type": "patient_studies", "ID": "CANIMM/2220", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "22211798", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Chronic Myeloid Leukemia", "System": null, "Dose": null, "Technique": "Flow cytometry,NK-cell reactivity assay, Th e Bio-Plex ™ Suspension Array system", "Controlled_Technique": "Flow cytometry; Cellular cytotoxicity/function assay; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "interleukin-8 (IL-8), interferon-γ inducible protein-10 (IP-10) and monocyte chemoattractant protein-1 (MCP-1),(GM-CSF)", "Controlled_Terms_Function_enhanced_Number_increased": "Monocytes; IFN-γ; IL-8 / CXCL8; GM-CSF / CSF2; CCL2 / MCP-1; CXCL10 / IP-10", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "36", "Male/Female": null, "Median_age/Range": "58 years (range, 21 – 85)"}, {"study_type": "patient_studies", "ID": "CANIMM/2221", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "2406856", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": "400 mg.", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Treg", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "40", "Male/Female": "18/22", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2228", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "20839259", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma (RCC)", "System": null, "Dose": "sorafenib 400 mg twice daily", "Technique": "Flow cytometry and immunohistochemistry", "Controlled_Technique": "Flow cytometry; Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "tumour-infiltrating Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "11 patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2229", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": "5329102", "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "19276286", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal Cell Carcinoma (RCC)", "System": null, "Dose": "(50 mg by mouth daily)", "Technique": "Flow cytometry.ELISA", "Controlled_Technique": "Flow cytometry; Enzyme-linked immunosorbent assay (ELISA)", "Immune_System-Function_enhanced/numbers_increased": "IFN-g –producing T cells IFNgamma", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; IFN-γ", "Immune_System-Function_inhibited/numbers_decreased": "MDSC, CD3(+)CD4(+)CD25(hi)Foxp3(+) Treg", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); Myeloid-derived suppressor cells (MDSCs); CD25 / IL2RA", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "23", "Male/Female": null, "Median_age/Range": "57 years (range, 41-80),"}, {"study_type": "patient_studies", "ID": "CANIMM/2233", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "19351841", "Cancer_Type": "Stomach Cancer", "Cancer_Type_Description": "Gastrointestinal Stromal Tumor (GIST)", "System": null, "Dose": "400 mg- 800 mg", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cell IFN-gamma production IFN-gamma production", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "56", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2239", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "23758044", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": "≥400 mg ⁄ <400 mg", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "natural killer (NK) cells- interferon (IFN)-γ(+) CD3(-) CD56(+) cells,effector memory CD8(+) T cells, - IFN-γ(+) CCR7(-) CD45RO(+) CD8(+) cells", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; IFN-γ; CD56 / NCAM1; Effector memory T cells; CCR7; CD45RO", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "42", "Male/Female": "28/14", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2241", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": "3062316", "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "24297450", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": "100 mg", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "T, NK, CD8+ T, and CD57+CD14- cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD14; CD57", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "50", "Male/Female": "37/13", "Median_age/Range": "53.7 (range 16–87)"}, {"study_type": "patient_studies", "ID": "CANIMM/2244", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": "5329102", "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "24353914", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal - Metastatic Renal Cell Cancer", "System": null, "Dose": "50 mg sunitinib monotherapy daily", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "Treg", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "10", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2245", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "25014230", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "(MDSCs),Treg", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); Myeloid-derived suppressor cells (MDSCs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "19", "Male/Female": "2024-08-11 00:00:00", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2248", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": "3062316", "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "26103598", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": "(100 mg day(-1) )", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "natural killer (NK) cell or cytotoxic T lymphocyte", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; Lymphocytes", "Immune_System-Function_inhibited/numbers_decreased": "Treg", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "52", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2249", "Drug": "Nilotinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB04868", "Target/s_or_mechanism_of_action": "Nilotinib binds to and stabilizes the inactive conformation of the kinase domain of Abl protein.", "KEGG_Drug__ID": null, "Pubchem_ID": "644241", "STR_LINK_(SMILES)": "CC1=CN(C=N1)C1=CC(NC(=O)C2=CC=C(C)C(NC3=NC=CC(=N3)C3=CN=CC=C3)=C2)=CC(=C1)C(F)(F)F", "Single/Combination": "Single Drug", "PMID": "26746653", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Chronic Myeloid Leukemia", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "expansion of BM lymphocytes-CD19+ B cells and CD3negCD16/56+ NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; B cells; Lymphocytes; CD19", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08953", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "9", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2250", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": "3062316", "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "26746653", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Chronic Myeloid Leukemia", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "expansion of BM lymphocytes-expansion of BM lymphocytes-CD19+ B cells and CD3negCD16/56+ NK cells + Increased PB lymphocyte,increased CD8+CD57+ and CD8+HLA-DR+ cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; B cells; Lymphocytes; CD19; CD57; HLA-DR", "Immune_System-Function_inhibited/numbers_decreased": "T regulatory cells", "Controlled_Terms_Function_inhibited_Number_decreased": "T reg", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "25", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2251", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "26746653", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Chronic Myeloid Leukemia", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "expansion of BM lymphocytes-CD19+ B cells and CD3negCD16/56+ NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; B cells; Lymphocytes; CD19", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "71", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2253", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "27540594", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD4+CD127+ T effector cells IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; CD127", "Immune_System-Function_inhibited/numbers_decreased": "CD4+PD-1+ T cells and CD8+PD-1+ T cells, Foxp3+ Tregs IL-10 and TGF-β1", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); CD4+ T cells; CD8+ T cells; T cells; IL-10; TGF-β; PD-1 / PDCD1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "19 patients", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2254", "Drug": "Cabozantinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB08875", "Target/s_or_mechanism_of_action": "Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.", "KEGG_Drug__ID": null, "Pubchem_ID": "25102847", "STR_LINK_(SMILES)": "COC1=CC2=C(C=C1OC)C(OC1=CC=C(NC(=O)C3(CC3)C(=O)NC3=CC=C(F)C=C3)C=C1)=CC=N2", "Single/Combination": "Single Drug", "PMID": "27789775", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Breast - Metastatic Triplenegative Breast Cancer  (mTNBC)", "System": null, "Dose": "Treatment consisted of oral dosing of cabozantinib at 60 mg daily over a 21‐day cycle. Patients underwent radiographic restaging at 6 weeks and every 9 weeks thereafter. Patients with complete or partial RECIST responses continued to receive study treatment, whereas those with progressive disease were taken off study. Dose reductions for toxicity occurred if patients experienced grade 3 or 4 neutropenia or thrombocytopenia, or nonhematologic adverse events. From the starting dose of 60 mg daily, doses were reduced as needed to 40 and 20 mg daily", "Technique": "Flow cytometry,enzyme‐linked immunosorbent assay", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "circulating CD3 + cells and CD3 + CD4‐CD8 + T lymphocytes at days 22 and 64 PlGF, VEGF, and VEGF‐D, Plasma CAIX", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; Lymphocytes; VEGF", "Immune_System-Function_inhibited/numbers_decreased": "CD14+ monocytes at days 22 and 64", "Controlled_Terms_Function_inhibited_Number_decreased": "Monocytes; CD14", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Plasma sVEGFRl, sMET, sTIE‐2, or bFGF", "Controlled_Terms_Negative_Regulation": "bFGF", "KEGG_Drug_ID": "D10062", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Thirty‐five mTNBC patients", "Male/Female": null, "Median_age/Range": "50 years (range 31–78)"}, {"study_type": "patient_studies", "ID": "CANIMM/2258", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": "3062316", "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "29218828", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Chronic Myeloid Leukemia", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "monocytic subset (M-MDSC)", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells (MDSCs); Monocytic myeloid-derived suppressor cells (M-MDSCs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "42", "Male/Female": "26/16", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2259", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": "3062316", "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "29407585", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Chronic Myeloid Leukemia", "System": null, "Dose": "100 mg of dasatinib once daily", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NK cell differentiation (CD3-CD57+/CD3-CD56+)", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; CD56 / NCAM1; CD57", "Immune_System-Function_inhibited/numbers_decreased": "CD4+CD25+CD127 low Tregs", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); CD25 / IL2RA; CD127", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "52", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2260", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": "3062316", "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "30151740", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": "(dose range 70–100 mg/day)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "large granular lymphocytes (LGLs)-CD57+ cytotoxic CD4+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4+ T cells; T cells; Lymphocytes; CD57", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "22", "Male/Female": "2024-08-14 00:00:00", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2261", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "30705677", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Chronic Myeloid Leukemia", "System": null, "Dose": "upto 400 mg daily", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NKG2D and NKp30 of NK cells(activating receptors)", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; NKG2D / KLRK1; NKp30 / NCR3", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "21", "Male/Female": null, "Median_age/Range": "51 (28–84)"}, {"study_type": "patient_studies", "ID": "CANIMM/2262", "Drug": "Nilotinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB04868", "Target/s_or_mechanism_of_action": "Nilotinib binds to and stabilizes the inactive conformation of the kinase domain of Abl protein.", "KEGG_Drug__ID": null, "Pubchem_ID": "644241", "STR_LINK_(SMILES)": "CC1=CN(C=N1)C1=CC(NC(=O)C2=CC=C(C)C(NC3=NC=CC(=N3)C3=CN=CC=C3)=C2)=CC(=C1)C(F)(F)F", "Single/Combination": "Single Drug", "PMID": "30705677", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Chronic Myeloid Leukemia", "System": null, "Dose": "upto 600 mg nilotinib daily", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "NKG2D and NKp30 of NK cells(activating receptors)", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; NKG2D / KLRK1; NKp30 / NCR3", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08953", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "37", "Male/Female": null, "Median_age/Range": "50 (29–80)"}, {"study_type": "patient_studies", "ID": "CANIMM/2264", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "31391334", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": null, "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "CD8+Ki67+ T cells producing IFN-γ IFN-γ", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells; IFN-γ; Ki-67", "Immune_System-Function_inhibited/numbers_decreased": "ERK+flt-3+ Tregs and MDSCs p-ERK", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); Myeloid-derived suppressor cells (MDSCs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08524", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "30 patients", "Male/Female": "2024-04-26 00:00:00", "Median_age/Range": "65(56-84)"}, {"study_type": "patient_studies", "ID": "CANIMM/2265", "Drug": "Imatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00619", "Target/s_or_mechanism_of_action": "It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia.", "KEGG_Drug__ID": null, "Pubchem_ID": "5291", "STR_LINK_(SMILES)": "CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1", "Single/Combination": "Single Drug", "PMID": "31704808", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": "h ≤400 mg/d imatinib", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "effector/memory CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells", "Immune_System-Function_inhibited/numbers_decreased": "eT reg cells", "Controlled_Terms_Function_inhibited_Number_decreased": "Effector regulatory T cells (eTregs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D01441", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "93", "Male/Female": "58/35", "Median_age/Range": "60.1 (23–85)"}, {"study_type": "patient_studies", "ID": "CANIMM/2266", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": "3062316", "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "31824308", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": "first line or second line dasatinib (100 mg QD)", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "lymphocytosis - redistribution of naïve and memory populations of all lymphocyte subsets including CD4+ and CD8+ T-cells and B-cells.", "Controlled_Terms_Function_enhanced_Number_increased": "Lymphocytes", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "17", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2268", "Drug": "Dasatinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01254", "Target/s_or_mechanism_of_action": "Dasatinib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply.", "KEGG_Drug__ID": null, "Pubchem_ID": "3062316", "STR_LINK_(SMILES)": "CC1=NC(NC2=NC=C(S2)C(=O)NC2=C(C)C=CC=C2Cl)=CC(=N1)N1CCN(CCO)CC1", "Single/Combination": "Single Drug", "PMID": "30588140", "Cancer_Type": "Leukemia", "Cancer_Type_Description": "Leukemia - Chronic Myeloid Leukemia", "System": null, "Dose": null, "Technique": "ELISA +microscopic examination.", "Controlled_Technique": "Enzyme-linked immunosorbent assay (ELISA); Microscopy", "Immune_System-Function_enhanced/numbers_increased": "lymphocytosis", "Controlled_Terms_Function_enhanced_Number_increased": "Lymphocytes", "Immune_System-Function_inhibited/numbers_decreased": "PDMPs, sVCAM-1, and TGFβ1", "Controlled_Terms_Function_inhibited_Number_decreased": "TGF-β", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03658", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "24", "Male/Female": "2024-04-20 00:00:00", "Median_age/Range": "54.5"}, {"study_type": "patient_studies", "ID": "CANIMM/2272", "Drug": "Sorafenib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB00398", "Target/s_or_mechanism_of_action": "Sorafenib exerts its action through inhibition of several kinases involved in both tumour cell proliferation and angiogenesis.", "KEGG_Drug__ID": null, "Pubchem_ID": "216239", "STR_LINK_(SMILES)": "CNC(=O)C1=NC=CC(OC2=CC=C(NC(=O)NC3=CC(=C(Cl)C=C3)C(F)(F)F)C=C2)=C1", "Single/Combination": "Single Drug", "PMID": "32099055", "Cancer_Type": "Hepatocellular Cancer", "Cancer_Type_Description": "Hepatocellular Carcinoma (HCC)", "System": null, "Dose": "400 mg, twice daily", "Technique": "multiplexed fluorescent bead-based immunoassays with the Milliplex Map Kit", "Controlled_Technique": "Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "sBTLA, sLAG-3, sCTLA-4, sPD-1, sCD80, sCD86 and sPD-L1", "Controlled_Terms_Negative_Regulation": "Soluble B- and T-lymphocyte attenuator (sBTLA); Soluble lymphocyte activation gene 3 (sLAG-3); Soluble cytotoxic T-lymphocyte-associated protein 4 (sCTLA-4); Soluble programmed cell death protein 1 (sPD-1); Soluble CD80 (sCD80); Soluble CD86 (sCD86); Soluble programmed death-ligand 1 (sPD-L1)", "KEGG_Drug_ID": "D08524", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "53 patients", "Male/Female": "36 males and 17 females", "Median_age/Range": "71 (range, 21–89) years]"}, {"study_type": "patient_studies", "ID": "CANIMM/2275", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": "5329102", "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "20948437", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Primary Renal Cell Carcinoma", "System": null, "Dose": "50 mg daily", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "intratumoral Treg", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "7", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2276", "Drug": "Sunitinib", "Drug_category": "Tyrosine kinase inhibitor", "Drugbank_ID": "DB01268", "Target/s_or_mechanism_of_action": "Inhibits cellular signalling by targeting multiple receptor tyrosine kinases (RTKs).", "KEGG_Drug__ID": null, "Pubchem_ID": "5329102", "STR_LINK_(SMILES)": "CCN(CC)CCNC(=O)C1=C(C)NC(\\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C", "Single/Combination": "Single Drug", "PMID": "20948437", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Renal - Metastatic Renal Cell Cancer", "System": null, "Dose": "50 mg daily", "Technique": null, "Controlled_Technique": null, "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "CD3+CD4+CD25(hi) Foxp3+ regulatory T cells", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); CD4+ T cells; T cells; CD25 / IL2RA", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D06402", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "28", "Male/Female": "2024-04-24 00:00:00", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/19", "Drug": "Cisplatin + acclerated radiotherapy", "Drug_category": "Platinum compounds", "Drugbank_ID": null, "Target/s_or_mechanism_of_action": null, "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": null, "PMID": "21765211", "Cancer_Type": "Head and Neck Cancer", "Cancer_Type_Description": "Head And Neck - Advanced Squamous Cell Carcinoma Of The Head And Neck", "System": null, "Dose": "weekly 40 mg/m2)", "Technique": "immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC)", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "STAT 6 MODULATION-STAT6-expressing head and neck cancer displayed enhanced recurrence-free survival upon treatment with cisplatin-based chemoradiation compared with patients with STAT6-negative tumors,", "Controlled_Terms_Function_inhibited_Number_decreased": "STAT6", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D00275", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "58 samples with advanced squamous cell carcinoma of the head and neck", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2284", "Drug": "Cobimetinib + Atezolizumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB05239 + DB11595", "Target/s_or_mechanism_of_action": "Cobimetinib inhibits MEK1/MAP2K1 and MEK2/MAP2K2; atezolizumab blocks PD-L1/CD274", "KEGG_Drug__ID": null, "Pubchem_ID": "16222096", "STR_LINK_(SMILES)": "C1CCN[C@@H](C1)C2(CN(C2)C(=O)C3=C(C(=C(C=C3)F)F)NC4=C(C=C(C=C4)I)F)O", "Single/Combination": "Combination", "PMID": "35833954", "Cancer_Type": "Bile Duct Carcinoma", "Cancer_Type_Description": "Advanced/metastatic biliary tract cancer", "System": null, "Dose": "Cobimetinib 60 mg orally daily, 21 days on/7 days off + atezolizumab 840 mg IV every 2 weeks", "Technique": "Flow cytometry, Luminex assay", "Controlled_Technique": "Flow cytometry; Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": "Combination treatment increased CD4⁺TIM3⁺ T cells;BTLA+CD8+ cells, IL-23, IL-8 and RANTES , tumor analysis also showed enhanced antigen-processing/presentation gene expression and increased CD8/FoxP3 ratio", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; IL-8 / CXCL8; IL-23; TIM-3; BTLA; CD4; CD8; FOXP3; Antigen presentation", "Immune_System-Function_inhibited/numbers_decreased": "Decreased CD8⁺VISTA⁺ T cells; decreased plasma PDGF-BB, BDNF and PlGF-1", "Controlled_Terms_Function_inhibited_Number_decreased": "T cells; VISTA; CD8", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "T cells; TIM-3; CD4", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10405 + D10773", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "77 randomized/treated; 38 combination arm; immune analyses: 70 PBMC, 51 plasma overall", "Male/Female": "48 Female / 29 Male", "Median_age/Range": "63 years (44–86)"}, {"study_type": "patient_studies", "ID": "CANIMM/2285", "Drug": "Cobimetinib + Atezolizumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB05239 + DB11595", "Target/s_or_mechanism_of_action": "Cobimetinib inhibits MEK1/2/MAPK signaling; atezolizumab blocks PD-L1-mediated immune suppression", "KEGG_Drug__ID": null, "Pubchem_ID": "16222096 + 138611", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "34389557", "Cancer_Type": "Bile Duct Carcinoma", "Cancer_Type_Description": "Metastatic biliary tract cancers: intrahepatic cholangiocarcinoma, extrahepatic cholangiocarcinoma, gallbladder cancer", "System": null, "Dose": "Atezolizumab 840 mg IV days 1 & 15 + cobimetinib 60 mg orally daily, days 1–21 of each 28-day cycle", "Technique": "Flow cytometry; CD8+ T-cell activation analysis", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "CD38+ CD8+ and PD-1+TIM3− CD8+ populations remained approximately unchanged", "Controlled_Terms_Unaffected": "PD-1 / PDCD1; TIM-3; CD8; CD38", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10405 + D10732", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "34", "Male/Female": null, "Median_age/Range": "63 years (44–86)"}, {"study_type": "patient_studies", "ID": "CANIMM/2286", "Drug": "Carboplatin + Atezolizumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB11595", "Target/s_or_mechanism_of_action": "Carboplatin: causes DNA damage. Atezolizumab: blocks PD-L1-mediated immune inhibition, potentially restoring T-cell activity", "KEGG_Drug__ID": null, "Pubchem_ID": "426756", "STR_LINK_(SMILES)": "C1CC(C1)(C(=O)O)C(=O)O.[NH2-].[NH2-].[Pt+2]", "Single/Combination": "Combination", "PMID": "37038006", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Metastatic breast cancer, including ER-positive/HER2-negative and triple-negative disease", "System": null, "Dose": "Carboplatin: AUC 1.5 mg·mL⁻¹·min⁻¹ weekly for up to 12 weeks; atezolizumab: 1200 mg IV every 3 weeks, beginning in week 3", "Technique": "Flow cytometry; immunohistochemistry; immune-related gene-expression analysis", "Controlled_Technique": "Immunohistochemistry (IHC); Flow cytometry; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "Increased tumor-infiltrating CD8+ T cells; increased circulating PD-1+CTLA-4+CD8+ T cells; increased immune-related gene signatures", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells; PD-1 / PDCD1; CTLA-4; CD8", "Immune_System-Function_inhibited/numbers_decreased": "Decreased circulating neutrophils, basophils and eosinophils; decreased neutrophil-to-lymphocyte ratio", "Controlled_Terms_Function_inhibited_Number_decreased": "Lymphocytes; Neutrophils; Basophils; Eosinophils", "Immune_System_function_unaffected": "Total circulating T cells, CD4+ T cells and CD8+ T-cell levels were largely unchanged; stromal tumor-infiltrating lymphocytes were largely unaffected", "Controlled_Terms_Unaffected": "CD4+ T cells; CD8+ T cells; T cells; Tumor-infiltrating lymphocytes (TILs); Lymphocytes; CD4; CD8", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "T cells", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "26", "Male/Female": "Female", "Median_age/Range": "Median 60 years; range 45–69 years (study population)"}, {"study_type": "patient_studies", "ID": "CANIMM/2287", "Drug": "Pembrolizumab + mRNA-2752", "Drug_category": "Others/combination", "Drugbank_ID": "DB09037", "Target/s_or_mechanism_of_action": "Blocks PD-1 signaling, releasing inhibitory signals on antitumor T cells", "KEGG_Drug__ID": null, "Pubchem_ID": "481101797", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "39821301", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "High-risk ductal carcinoma in situ", "System": null, "Dose": "2–8 mg intratumorally; 2–4 doses every 2–3 weeks. Recommended combination dose: 4 mg", "Technique": "multiplex immunofluorescence", "Controlled_Technique": "Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "higher baseline tumor-infiltrating lymphocytes (TILs) ; programmed cell death ligand 1–positive (PD-L1+) cells", "Controlled_Terms_Function_enhanced_Number_increased": "Tumor-infiltrating lymphocytes (TILs); Lymphocytes; PD-L1 / CD274", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10574", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "10 patients", "Male/Female": "Female", "Median_age/Range": "Median: 46 years; range: 35–80 years"}, {"study_type": "patient_studies", "ID": "CANIMM/2288", "Drug": "Pembrolizumab + capecitabine", "Drug_category": "Others/combination", "Drugbank_ID": "DB09037; DB01101", "Target/s_or_mechanism_of_action": "Pembrolizumab blocks PD-1 signaling; capecitabine is converted to 5-fluorouracil and inhibits thymidylate synthase and DNA/RNA synthesis", "KEGG_Drug__ID": null, "Pubchem_ID": "481101797", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "35086949", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Metastatic TNBC; first- or second-line treatment", "System": null, "Dose": "Pembrolizumab 200 mg IV day 1 every 3 weeks; capecitabine 2000 mg orally twice daily days 1–7 every 2 weeks", "Technique": "Flow cytometry; T-cell receptor (TCR) immunosequencing", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Tumor-associated T-cell clones expanded in some patients", "Controlled_Terms_Function_enhanced_Number_increased": "T cells", "Immune_System-Function_inhibited/numbers_decreased": "Peripheral CD3+ T cells decreased over time (average fold change −0.42", "Controlled_Terms_Function_inhibited_Number_decreased": "T cells; CD3", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10574; D01209", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "29 patients, 14 patients in capecitabine arm", "Male/Female": "28 female /1 male", "Median_age/Range": "Mean 63 years"}, {"study_type": "patient_studies", "ID": "CANIMM/2289", "Drug": "Pembrolizumab + paclitaxel", "Drug_category": "Others/combination", "Drugbank_ID": "DB09037; DB01229", "Target/s_or_mechanism_of_action": "Pembrolizumab blocks PD-1 signaling; paclitaxel stabilizes microtubules and inhibits cell division", "KEGG_Drug__ID": null, "Pubchem_ID": "481101797", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "35086949", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "Metastatic TNBC; first- or second-line treatment", "System": null, "Dose": "Pembrolizumab 200 mg IV day 1 every 3 weeks; paclitaxel 80 mg/m² IV on days 1, 8 and 15 every 3 weeks; dexamethasone premedication also used", "Technique": "Flow cytometry; T-cell receptor (TCR) immunosequencing", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Tumor-associated T-cell clones expanded in some patients", "Controlled_Terms_Function_enhanced_Number_increased": "T cells", "Immune_System-Function_inhibited/numbers_decreased": "Peripheral CD3+ T cells decreased over time (average fold change −0.56)", "Controlled_Terms_Function_inhibited_Number_decreased": "T cells; CD3", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10574; D01705", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "29 patients, 15 patients in paclitaxel arm", "Male/Female": "28 female /1 male", "Median_age/Range": "Mean 56 years"}, {"study_type": "patient_studies", "ID": "CANIMM/2290", "Drug": "Trastuzumab+ nelipepimut-S (NPS/E75) + GM-CSF", "Drug_category": "Others/combination", "Drugbank_ID": "DB00072", "Target/s_or_mechanism_of_action": "Binds HER2/ERBB2 extracellular domain; inhibits HER2 signaling and promotes antibody-dependent cell-mediated cytotoxicity (ADCC); facilitates dendritic-cell uptake/cross-presentation of HER2 antigen and CD8⁺ T-cell priming", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "32071118", "Cancer_Type": "Breast cancer", "Cancer_Type_Description": "High-risk, HER2-low expressing breast cancer", "System": null, "Dose": "Trastuzumab: 8 mg/kg loading, then 6 mg/kg IV every 3 weeks for 1 year. NPS: 1,000 μg + GM-CSF 250 μg, intradermally", "Technique": "dextramer assay", "Controlled_Technique": "Dextramer assay", "Immune_System-Function_enhanced/numbers_increased": "HER2/E75-specific CD8⁺ CTLs", "Controlled_Terms_Function_enhanced_Number_increased": "CD8", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D03257", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "275 disease-free patients after standard therapy,136 NPS+GM-CSF and 139 control", "Male/Female": "Female", "Median_age/Range": "Vaccine arm median 52.2 years; control 50.5 years"}, {"study_type": "patient_studies", "ID": "CANIMM/2291", "Drug": "pembrolizumab + radiotherapy", "Drug_category": "Others/combination", "Drugbank_ID": "DB09037", "Target/s_or_mechanism_of_action": "Binds PD-1 (PDCD1/CD279) and blocks its interaction with PD-L1 and PD-L2, releasing inhibitory checkpoint signaling and restoring T-cell effector activity", "KEGG_Drug__ID": null, "Pubchem_ID": "481101797", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "42420295", "Cancer_Type": "Kidney", "Cancer_Type_Description": "Stage IV oligometastatic ccRCC; RAPPORT phase I/II trial", "System": null, "Dose": "SABR to all metastatic sites followed by 8 cycles of pembrolizumab (200 mg every 3 weeks)", "Technique": "Cytometry by time-of-flight (CyTOF); NanoString gene-expression profiling; multiplex immunohistochemistry (mIHC), flow cytometry", "Controlled_Technique": "Immunohistochemistry (IHC); Flow cytometry; Mass cytometry (CyTOF); NanoString gene-expression profiling", "Immune_System-Function_enhanced/numbers_increased": "Ki-67+ CD8+ and CD4+ T cells; sustained activated, cytotoxic and memory-like T-cell populations; maintenance and sharing of pre-existing tumour-enriched TCR clones; greater baseline intratumoural cytotoxic T-cell infiltration (PD-1+ CD8+ and PD-1+ CD4+ T cells, and to GzmK+ CD8+ T cells) and closer proximity of CD8+ T cells to tumour cells; NK-cell activation, T cell infiltration (CD8B, CD8A, CD3D, CD3E), pro-inflammatory cytotoxicity (GzmM, GzmA, GzmH, GzmK, IFN-γ, NCR1), adaptive immunity (IL-2RB, IL-4, IRF7, PRAME), T cell co-stimulation and activation (TNFRSF9, TNFRSF14, TNFRSF12A, CD80, FOXP3, KLRK, LCK, SAA1), and inhibitory markers (PDCD1, PD-L1, LAG-3, CD274, TIGIT)", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells; CD4+ T cells; IL-4; PD-1 / PDCD1; PD-L1 / CD274; LAG-3; TIGIT; CD4; CD8; CD80; Ki-67; FOXP3; Cytotoxicity / cytolysis; T-cell receptor (TCR)", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10574", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "30 patients", "Male/Female": "23 male; 7 female", "Median_age/Range": "Median 62 years; range 47–80 years"}, {"study_type": "patient_studies", "ID": "CANIMM/2292", "Drug": "Pembrolizumab+stereotactic body radiation therapy (SBRT)", "Drug_category": "Others/combination", "Drugbank_ID": "DB09037", "Target/s_or_mechanism_of_action": "Binds PD-1 (PDCD1/CD279) and blocks its interaction with PD-L1 and PD-L2, releasing inhibitory checkpoint signaling and restoring T-cell effector activity", "KEGG_Drug__ID": null, "Pubchem_ID": "481101797", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "36252995", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Stage IV non-small cell lung cancer; adenocarcinoma, squamous cell carcinoma and large-cell neuroendocrine tumors", "System": null, "Dose": "Pembrolizumab 200 mg intravenously every 3 weeks; SBRT 8 Gy × 3 fractions on alternate days to one tumor site", "Technique": "Multiplex immunofluorescence for CD3, CD8, CD20, CD103 and FoxP3; pan-cytokeratin staining; HLA-ABC assessment", "Controlled_Technique": "Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "Total lymphocytes increased 2.29-fold at 6 weeks; cytotoxic T cells increased 2.80-fold; CD103+ cytotoxic T cells increased 4.87-fold; helper and other T-cell populations increased", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; Lymphocytes", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Regulatory T cells (Tregs); T cells; FOXP3", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10574", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "27 baseline tumor biopsies; 15 matched baseline/on-treatment biopsies and 3 on-treatment-only biopsies were adequate for analysis", "Male/Female": "16 male / 14 female", "Median_age/Range": "61 years (35–75)"}, {"study_type": "patient_studies", "ID": "CANIMM/2293", "Drug": "pembrolizumab + gemcitabine", "Drug_category": "Others/combination", "Drugbank_ID": "DB09037", "Target/s_or_mechanism_of_action": "Binds PD-1 (PDCD1/CD279) and blocks its interaction with PD-L1 and PD-L2, releasing inhibitory checkpoint signaling and restoring T-cell effector activity", "KEGG_Drug__ID": null, "Pubchem_ID": "481101797", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "42126144", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Previously treated advanced NSCLC", "System": null, "Dose": null, "Technique": "Multiplex immunofluorescence", "Controlled_Technique": "Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "Tumor inflammation score based on CD3+ T-cell density and spatial proximity to FOXP3+ Tregs was associated with progression-free survival", "Controlled_Terms_Function_enhanced_Number_increased": "Regulatory T cells (Tregs); T cells; CD3; FOXP3", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": "Peripheral-blood Treg frequency, PD-L1 expression", "Controlled_Terms_Unaffected": "Regulatory T cells (Tregs); PD-L1 / CD274", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Regulatory T cells (Tregs); T cells; CD3; FOXP3", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10574", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "16 patients enrolled; pretreatment tumor tissue available for 14", "Male/Female": null, "Median_age/Range": "Median 64 years; range 53–75 years"}, {"study_type": "patient_studies", "ID": "CANIMM/2294", "Drug": "Trametinib+ Pembrolizumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB08911", "Target/s_or_mechanism_of_action": "MEK1/MAP2K1 and MEK2/MAP2K2 inhibitor", "KEGG_Drug__ID": null, "Pubchem_ID": "11707110", "STR_LINK_(SMILES)": "CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Combination", "PMID": "40486486", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Advanced/stage IV non-small-cell lung cancer", "System": null, "Dose": "1.5 mg or 2 mg orally, days 1–10/according to dose level; RP2D 2 mg", "Technique": "Quantitative immunofluorescence, flow cytometry", "Controlled_Technique": "Flow cytometry; Immunofluorescence assay; Immunostaining/image analysis", "Immune_System-Function_enhanced/numbers_increased": "TIL representing CD4+, CD8+, and CD20+ cells, ratio of CD8+ T-cells to Tregs", "Controlled_Terms_Function_enhanced_Number_increased": "Regulatory T cells (Tregs); CD8+ T cells; Tumor-infiltrating lymphocytes (TILs); CD4; CD8; CD20 / MS4A1", "Immune_System-Function_inhibited/numbers_decreased": "T-regulatory cells and MDSCs decreased with trametinib lead-in", "Controlled_Terms_Function_inhibited_Number_decreased": "Myeloid-derived suppressor cells (MDSCs)", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10175", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "15", "Male/Female": "6 M / 9 F", "Median_age/Range": "69 y (32–81)"}, {"study_type": "patient_studies", "ID": "CANIMM/2295", "Drug": "Brentuximab vedotin + Pembrolizumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB08870+DB09037", "Target/s_or_mechanism_of_action": "Binds PD-1 (PDCD1/CD279) and blocks its interaction with PD-L1 and PD-L2, releasing inhibitory checkpoint signaling and restoring T-cell effector activity", "KEGG_Drug__ID": null, "Pubchem_ID": "481101797", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "39786430", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Metastatic squamous or nonsquamous NSCLC without actionable genomic aberrations; primary or secondary refractory disease", "System": null, "Dose": "Brentuximab vedotin 1.8 mg/kg IV + pembrolizumab 200 mg IV every 3 weeks; maximum 35 cycles; drugs administered separately on day 1", "Technique": "flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "tumor CD8+ T-cell infiltration, especially in responders, ratio of CD8 to Tregs", "Controlled_Terms_Function_enhanced_Number_increased": "Regulatory T cells (Tregs); CD8+ T cells; T cells; CD8", "Immune_System-Function_inhibited/numbers_decreased": "Peripheral-blood regulatory T cells (Tregs)", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); T cells", "Immune_System_function_unaffected": "CD30+ CD8+ T cells", "Controlled_Terms_Unaffected": "CD8+ T cells; T cells; CD8", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09587+D10574", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "55 patients received at least one dose of the combination (12 primary refractory; 43 secondary refractory)", "Male/Female": "Male 35 / Female: 20", "Median_age/Range": "Median: 67 years; overall study age range: 23–86 years"}, {"study_type": "patient_studies", "ID": "CANIMM/2296", "Drug": "Pembrolizumab + chemotherapy (individual agents NR)", "Drug_category": "Others/combination", "Drugbank_ID": "DB09037", "Target/s_or_mechanism_of_action": "Pembrolizumab blocks PD-1 signaling; chemotherapy mechanism depends on the agents used", "KEGG_Drug__ID": null, "Pubchem_ID": "481101797", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "34866339", "Cancer_Type": "Lung Cancer", "Cancer_Type_Description": "Unresectable or recurrent non-small-cell lung cancer; first-line treatment", "System": null, "Dose": null, "Technique": "survival and tumor response analysis", "Controlled_Technique": "Clinical outcome/response assessment", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": "PD-1 inhibitory signaling blocked", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-1 / PDCD1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "49 patients", "Male/Female": null, "Median_age/Range": "68 years (range 52–81 years)"}, {"study_type": "patient_studies", "ID": "CANIMM/2297", "Drug": "Citarinostat + Oxaliplatin", "Drug_category": "Others/combination", "Drugbank_ID": "DB15449 + DB00526", "Target/s_or_mechanism_of_action": "HDAC6 inhibition/immunomodulation + platinum-mediated DNA damage", "KEGG_Drug__ID": null, "Pubchem_ID": "53340426 + 9887054", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "35223194", "Cancer_Type": "Lung Cancer; Adenocarcinoma", "Cancer_Type_Description": "NSCLC / lung adenocarcinoma", "System": null, "Dose": "Ex-vivo ACY241 + oxaliplatin, each at 10 µg/mL", "Technique": "Flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Enhanced CD8+ T-cell TNF-α/IFN-γ production", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells; TNF-α / TNF; CD8", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10918 + D01790", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "ex-vivo patient tissue culture", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2298", "Drug": "Sintilimab", "Drug_category": "Others/combination", "Drugbank_ID": "DB15765", "Target/s_or_mechanism_of_action": "Binds PD-1 (PDCD1/CD279) and blocks PD-1-mediated inhibitory signaling/checkpoint activity. P PubMed +1", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "38755119", "Cancer_Type": "Lymphoma", "Cancer_Type_Description": "Relapsed/refractory extranodal natural killer (NK)/T-cell lymphoma, nasal type", "System": null, "Dose": "200 mg IV every 21 days; fixed dose throughout study.", "Technique": "PD-L1 IHC; peripheral-blood flow cytometry for lymphocyte subsets; Th1/Th2 cytokine assay/FACS; plasma ctDNA/EBV-DNA; capture-based NGS. P PubMed Central (PMC)", "Controlled_Technique": "Flow cytometry; Next-generation sequencing (NGS); Immunohistochemistry (IHC); Cytokine/multiplex immunoassay", "Immune_System-Function_enhanced/numbers_increased": null, "Controlled_Terms_Function_enhanced_Number_increased": null, "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D12119", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "38 treated patients; baseline peripheral blood and pretreatment FFPE tumor samples were evaluated", "Male/Female": "28 male / 10 female (73.7% / 26.3%) P PubMed Central (PMC)", "Median_age/Range": "43 years (20–72) P PubMed Central (PMC)"}, {"study_type": "patient_studies", "ID": "CANIMM/2299", "Drug": "Pomalidomide + dexamethasone", "Drug_category": "Others/combination", "Drugbank_ID": "DB08910+DB01234", "Target/s_or_mechanism_of_action": "Pomalidomide binds CRBN and promotes IKZF1/IKZF3 degradation; dexamethasone activates the glucocorticoid receptor and has anti-inflammatory and antimyeloma effects", "KEGG_Drug__ID": null, "Pubchem_ID": "134780+5743", "STR_LINK_(SMILES)": "C1CC(=O)NC(=O)C1N2C(=O)C3=C(C2=O)C(=CC=C3)N and C[C@@H]1C[C@H]2[C@@H]3CCC4=CC(=O)C=C[C@@]4([C@]3([C@H](C[C@@]2([C@]1(C(=O)CO)O)C)O)F)C", "Single/Combination": "Combination", "PMID": "25869284", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Relapsed, lenalidomide-refractory multiple myeloma", "System": null, "Dose": "Pomalidomide: continuous 2 mg/day, days 1–28, or intermittent 4 mg/day, days 1–21 of each 28-day cycle; dexamethasone: 40 mg weekly (20 mg if age >70 years)", "Technique": "Multiparameter flow cytometry; gene expression profiling; immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC); Flow cytometry; Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "T-cell and NK-cell activation; interferon-γ, TNFα, IL2, and IL4 by CD4 and CD8 T cells and TNFα and IFNγ by NK cells; increased expression of cytolysis genes, granzymeB and perforin, by CD8 T cells, as well as NK cells; enhanced CD8+ T-cell activation, CD25hiFOXP3+ regulatory T cells, BTLA+ T cells and Tim-3+ NK cells", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; Regulatory T cells (Tregs); CD8+ T cells; T cells; IFN-γ; TNF-α / TNF; IL-2; IL-4; TIM-3; BTLA; CD4; CD8; Granzyme B / GZMB; Perforin / PRF1; Cytotoxicity / cytolysis", "Immune_System-Function_inhibited/numbers_decreased": "Dexamethasone blunts pomalidomide-mediated T-cell activation", "Controlled_Terms_Function_inhibited_Number_decreased": "T cells", "Immune_System_function_unaffected": "no change in PD1+ T cells", "Controlled_Terms_Unaffected": "T cells; PD-1 / PDCD1", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "NK cells; T cells; TIM-3; BTLA", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08976+D00292", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "39", "Male/Female": "22 male, 17 female (overall study population)", "Median_age/Range": "Overall median 61 years; range NR"}, {"study_type": "patient_studies", "ID": "CANIMM/2300", "Drug": "Durvalumab + pomalidomide", "Drug_category": "Others/combination", "Drugbank_ID": "DB11714+DB08910", "Target/s_or_mechanism_of_action": "Durvalumab blocks PD-L1; pomalidomide provides immunomodulatory and immune-stimulatory effects", "KEGG_Drug__ID": null, "Pubchem_ID": "319075068+134780", "STR_LINK_(SMILES)": "C1CC(=O)NC(=O)C1N2C(=O)C3=C(C2=O)C(=CC=C3)N", "Single/Combination": "Combination", "PMID": "34385543", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple myeloma", "System": null, "Dose": "Durvalumab 1500 mg IV on day 1; pomalidomide 4 mg orally daily on days 1–21", "Technique": "Flow cytometry, RNA sequencing, T-cell receptor sequencing, multiplex immunofluorescence and electrochemiluminescence assay", "Controlled_Technique": "Flow cytometry; Gene expression/sequencing analysis; Immunofluorescence assay; Enzyme-linked immunosorbent assay (ELISA); T-cell receptor sequencing", "Immune_System-Function_enhanced/numbers_increased": "150–500% increases in proportions of proliferating CD4+ T cells, CD8+ T cells and NK cells; increased CD4+ ICOS+ helper T cells; inferred increases in CD8+ T cells, increase in genes from dendritic cells, monocytes, and macrophages, in addition to CD8 + T cells and Tregs upregulation of IL1B, CXCL1, CXCL9 and inflammatory genes such as TNF, PD-L1 (CD274), and PD-1 (PDCD1), CXCR3, Tim-3 (HAVCR2), and IL7", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; T cells; CD8+ T cells; Regulatory T cells (Tregs); CD4+ T cells; Dendritic cells; Macrophages; Monocytes; TNF-α / TNF; IL-1 family; IL-7; PD-1 / PDCD1; PD-L1 / CD274; TIM-3; CD4; CD8; CXCL9", "Immune_System-Function_inhibited/numbers_decreased": "Reduced B-cell-related gene signatures, including CD19, CD79B and BLK", "Controlled_Terms_Function_inhibited_Number_decreased": "CD19", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Regulatory T cells (Tregs); CD4; FOXP3", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10808+D08976", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "7", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2301", "Drug": "Durvalumab + pomalidomide + dexamethasone", "Drug_category": "Others/combination", "Drugbank_ID": "DB11714+DB08910+DB01234", "Target/s_or_mechanism_of_action": "Durvalumab blocks PD-L1; pomalidomide provides immunomodulatory and immune-stimulatory effects", "KEGG_Drug__ID": null, "Pubchem_ID": "134780+5743", "STR_LINK_(SMILES)": "C1CC(=O)NC(=O)C1N2C(=O)C3=C(C2=O)C(=CC=C3)N and C[C@@H]1C[C@H]2[C@@H]3CCC4=CC(=O)C=C[C@@]4([C@]3([C@H](C[C@@]2([C@]1(C(=O)CO)O)C)O)F)C", "Single/Combination": "Combination", "PMID": "34385543", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Multiple myeloma", "System": null, "Dose": "Durvalumab 1500 mg IV on day 1; pomalidomide 4 mg orally daily on days 1–21; dexamethasone 40 mg/day for patients aged 75 or younger, or 20 mg/day for those older than 75, on days 1, 8, 15 and 22", "Technique": "Flow cytometry, RNA sequencing, T-cell receptor sequencing, multiplex immunofluorescence and electrochemiluminescence assay", "Controlled_Technique": "Flow cytometry; Gene expression/sequencing analysis; Immunofluorescence assay; Enzyme-linked immunosorbent assay (ELISA); T-cell receptor sequencing", "Immune_System-Function_enhanced/numbers_increased": "Increases in proliferating CD4+ T cells, CD8+ T cells and NK cells; increased CD4+ and CD8+ ICOS+ subsets and effector-memory T cells; increase in genes from dendritic cells, monocytes, and macrophages, in addition to CD8 + T cells and Tregs; increased IFN-γ 4-gene signature; upregulated IL1B, CXCL1, CXCL9, TNF, CXCR3, HAVCR2 (TIM-3) and IL7; increased T-cell clonality and clonal expansion", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; T cells; CD8+ T cells; Regulatory T cells (Tregs); CD4+ T cells; Dendritic cells; Macrophages; Monocytes; TNF-α / TNF; IL-1 family; IL-7; TIM-3; CD4; CD8; CXCL9; T-cell clonal expansion", "Immune_System-Function_inhibited/numbers_decreased": "Approximately 50% decreases in absolute naive CD8+ T-cell counts and in naive/central-memory CD4+ T-cell populations; Reduced B-cell-related gene signatures, including CD19, CD79B and BLK", "Controlled_Terms_Function_inhibited_Number_decreased": "CD4+ T cells; CD8+ T cells; T cells; CD4; CD8; CD19", "Immune_System_function_unaffected": "IFN-γ", "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Regulatory T cells (Tregs); CD4; FOXP3", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10808+D08976+D00292", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "73", "Male/Female": "AN", "Median_age/Range": "AN"}, {"study_type": "patient_studies", "ID": "CANIMM/2302", "Drug": "Pomalidomide+Dexamethasone+Daratumumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB01234+DB01234+DB09331", "Target/s_or_mechanism_of_action": "Binds cereblon (CRBN), promoting degradation of IKZF1 and IKZF3; immunomodulatory and antimyeloma effects+Glucocorticoid-receptor agonist; anti-inflammatory, immunosuppressive, and antimyeloma activity+Binds CD38 and mediates tumor-cell killing; depletes CD38-expressing immune-cell populations", "KEGG_Drug__ID": null, "Pubchem_ID": "134780+5743", "STR_LINK_(SMILES)": "C1CC(=O)NC(=O)C1N2C(=O)C3=C(C2=O)C(=CC=C3)N and C[C@@H]1C[C@H]2[C@@H]3CCC4=CC(=O)C=C[C@@]4([C@]3([C@H](C[C@@]2([C@]1(C(=O)CO)O)C)O)F)C", "Single/Combination": "Combination", "PMID": "32928795", "Cancer_Type": "Myeloma", "Cancer_Type_Description": "Relapsed/refractory multiple myeloma (RRMM)", "System": null, "Dose": "Once daily, days 1–21 of each 28-day cycle; verify exact protocol", "Technique": "Longitudinal flow cytometry and immune phenotyping", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "Combination-associated increases in proliferating and activated T cells, CD8⁺ T cells, effector-memory T cells, ICOS⁺ T cells, and proliferating NK cells, Activated CD4+ and CD8+ T-cell frequencies increased after treatment", "Controlled_Terms_Function_enhanced_Number_increased": "NK cells; CD4+ T cells; CD8+ T cells; T cells; CD4; CD8", "Immune_System-Function_inhibited/numbers_decreased": "Approximately 80% reduction in total NK cells after initial administration; decreased CD19⁺ B cells and depletion of CD38-expressing T-cell subsets; decreased Lin−CD14+HLA−DR−/CD33+CD11b+ M-MDSCs", "Controlled_Terms_Function_inhibited_Number_decreased": "B cells; Myeloid-derived suppressor cells (MDSCs); Monocytic myeloid-derived suppressor cells (M-MDSCs); NK cells; T cells; CD14; CD19; CD38", "Immune_System_function_unaffected": "Treg numbers broadly stable; no significant increase in T-cell exhaustion during the first two cycles", "Controlled_Terms_Unaffected": "Regulatory T cells (Tregs); T cells", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "Myeloid-derived suppressor cells (MDSCs); Regulatory T cells (Tregs); Monocytic myeloid-derived suppressor cells (M-MDSCs)", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D08976+D00292+NA", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Peripheral blood; 110 patients in immune-biomarker subgroup", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2303", "Drug": "Pembrolizumab + XL888", "Drug_category": "Others/combination", "Drugbank_ID": "DB09037", "Target/s_or_mechanism_of_action": "Binds PD-1 (PDCD1/CD279) and blocks its interaction with PD-L1 and PD-L2, releasing inhibitory checkpoint signaling and restoring T-cell effector activity", "KEGG_Drug__ID": null, "Pubchem_ID": "481101797", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "41448449", "Cancer_Type": "Pancreas Cancer", "Cancer_Type_Description": "Advanced metastatic, mismatch repair-proficient PDAC; combination treatment following initial 21-day cycle", "System": null, "Dose": "Pembrolizumab 200 mg IV every 21 days + XL888 90 mg orally twice weekly; combination continued after cycle 1 until progression or toxicity", "Technique": "Multiplex assay (48-plex); CyTOF mass cytometry; liver-biopsy immune profiling; multiplex immunohistochemistry", "Controlled_Technique": "Immunohistochemistry (IHC); Cytokine/multiplex immunoassay; Mass cytometry (CyTOF); Tumor tissue/biopsy assessment", "Immune_System-Function_enhanced/numbers_increased": "monocytic cells (CD14+) and polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) (CD14+CD33+CD11b+) , Increase in circulating Th1-associated cytokines/chemokines, including IL-15, IL-1β, IL-12p40, IL-12p70, IL-27, CXCL9, CXCL10 and CCL3; CD8+ T cells (CD3+CD8+CCR7−CD27−) and CD4+ regulatory (CD3+CD4+CD25+CD127−CCR4+) T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells; Myeloid-derived suppressor cells (MDSCs); Granulocytic myeloid-derived suppressor cells (G-MDSCs); CD4+ T cells; IL-1 family; IL-15; CD3; CD4; CD8; CD14; CD25 / IL2RA; CCL3 / MIP-1α; CXCL9; CXCL10 / IP-10", "Immune_System-Function_inhibited/numbers_decreased": "CD8+:Treg ratio remained unchanged; no significant overall changes in liver-biopsy immune-cell frequencies; no significant treatment-related changes across most tumor microenvironment measures", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); CD8", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10574", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "17", "Male/Female": "8 male, 9 female", "Median_age/Range": "median 68 years (range: 55–70)"}, {"study_type": "patient_studies", "ID": "CANIMM/2304", "Drug": "Dabrafenib+trametinib", "Drug_category": "Others/combination", "Drugbank_ID": "DB08912, DB08911", "Target/s_or_mechanism_of_action": "suppresses MAPK/RAF–MEK–ERK signaling, Inhibits MEK1 and MEK2, suppressing downstream MAPK/ERK signaling", "KEGG_Drug__ID": null, "Pubchem_ID": "44462760, 11707110", "STR_LINK_(SMILES)": "CC(C)(C)C1=NC(=C(S1)C2=NC(=NC=C2)N)C3=C(C(=CC=C3)NS(=O)(=O)C4=C(C=CC=C4F)F)F  and CC1=C2C(=C(N(C1=O)C)NC3=C(C=C(C=C3)I)F)C(=O)N(C(=O)N2C4=CC=CC(=C4)NC(=O)C)C5CC5", "Single/Combination": "Combination", "PMID": "33275172", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Nonresectable metastatic, BRAF V600E-mutant melanoma", "System": null, "Dose": "150 mg orally twice daily", "Technique": "Multiplex immunofluorescence, T-cell receptor β-chain sequencing", "Controlled_Technique": "Immunofluorescence assay", "Immune_System-Function_enhanced/numbers_increased": "increased CD4+ T-cell infiltration in all 4 patients; increased CD8+ T-cell infiltration in 2/4;Induction of TCF7 and T-bet was associated with expansion and persistence of antitumor T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD4+ T cells; CD8+ T cells; T cells; CD4; CD8", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D10064, D10175", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Tumor biopsies from 4 patients, collected before and during therapy", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2305", "Drug": "Domatinostat + pembrolizumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB17521", "Target/s_or_mechanism_of_action": "Domatinostat modulates tumor immune microenvironment and antigen presentation; pembrolizumab blocks PD-1 signaling", "KEGG_Drug__ID": null, "Pubchem_ID": "15985904", "STR_LINK_(SMILES)": "CN1C=C(C=N1)C2=CC=C(C=C2)S(=O)(=O)N3C=CC(=C3)/C=C/C(=O)NC4=CC=CC=C4N", "Single/Combination": "Combination", "PMID": "31703604", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Advanced unresectable/metastatic cutaneous melanoma", "System": null, "Dose": "Domatinostat 100 mg once daily + pembrolizumab", "Technique": "Tumor biopsy; RNA-seq/gene-expression analysis", "Controlled_Technique": "Gene expression/sequencing analysis; Tumor tissue/biopsy assessment", "Immune_System-Function_enhanced/numbers_increased": "IFNG/IFN-gamma response increased in several patients; antigen-processing machinery/MHC expression increased; cytolytic activity increased; pembrolizumab-response signature increased", "Controlled_Terms_Function_enhanced_Number_increased": "IFN-γ; Antigen presentation; Cytotoxicity / cytolysis", "Immune_System-Function_inhibited/numbers_decreased": "PD-1-mediated inhibitory signaling blocked", "Controlled_Terms_Function_inhibited_Number_decreased": "PD-1 / PDCD1", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": "PD-1 / PDCD1", "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": null, "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "6", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2306", "Drug": "Ipilimumab (anti-CTLA-4) + Nivolumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB06186", "Target/s_or_mechanism_of_action": "Blocks CTLA-4-mediated inhibitory signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "30753825", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Metastatic melanoma", "System": null, "Dose": null, "Technique": "Transcriptomic profiling; immune-cell population analysis", "Controlled_Technique": "Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "Anti-tumor T-cell responses associated with treatment response, Intratumoral densities of CD8 and PD-L1 , peritumoral CD8 and PD-1 , intratumoral and peritumoral FOXP3 densities, CD45RO, EOMES, and TBET densities, Granzyme B. CD8+/CD4+EOMES+CD69+CD45RO+ memory T cell phenotype", "Controlled_Terms_Function_enhanced_Number_increased": "CD4+ T cells; CD8+ T cells; T cells; PD-1 / PDCD1; PD-L1 / CD274; CD4; CD8; FOXP3; Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": "CTLA-4-mediated inhibitory signaling blocked", "Controlled_Terms_Function_inhibited_Number_decreased": "CTLA-4", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04603", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Tumor biopsy specimens", "Male/Female": "57", "Median_age/Range": "64"}, {"study_type": "patient_studies", "ID": "CANIMM/2307", "Drug": "Ipilimumab (anti-CTLA-4) +Pembrolizumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB06186", "Target/s_or_mechanism_of_action": "Blocks CTLA-4-mediated inhibitory signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "30753825", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Metastatic melanoma", "System": null, "Dose": null, "Technique": "Transcriptomic profiling; immune-cell population analysis", "Controlled_Technique": "Gene expression/sequencing analysis", "Immune_System-Function_enhanced/numbers_increased": "Anti-tumor T-cell responses associated with treatment response, Intratumoral densities of CD8 and PD-L1 , peritumoral CD8 and PD-1 , intratumoral and peritumoral FOXP3 densities, CD45RO, EOMES, and TBET densities, Granzyme B. CD8+/CD4+EOMES+CD69+CD45RO+ memory T cell phenotype", "Controlled_Terms_Function_enhanced_Number_increased": "CD4+ T cells; CD8+ T cells; T cells; PD-1 / PDCD1; PD-L1 / CD274; CD4; CD8; FOXP3; Granzyme B / GZMB", "Immune_System-Function_inhibited/numbers_decreased": "CTLA-4-mediated inhibitory signaling blocked", "Controlled_Terms_Function_inhibited_Number_decreased": "CTLA-4", "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04603", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Tumor biopsy specimens", "Male/Female": "57", "Median_age/Range": "64"}, {"study_type": "patient_studies", "ID": "CANIMM/2308", "Drug": "Ipilimumab (anti-CTLA-4) + Nivolumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB06186", "Target/s_or_mechanism_of_action": "Blocks CTLA-4-mediated inhibitory signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "25539810", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Patients receiving concurrent or sequential anti-CTLA-4 and anti-PD-1 therapy", "System": null, "Dose": null, "Technique": "Flow cytometry; mass cytometry (CyTOF); Affymetrix Human Transcriptome 2.0 microarray; qPCR; Luminex cytokine analysis", "Controlled_Technique": "Flow cytometry; Reverse transcription PCR (RT-PCR/qRT-PCR); Polymerase chain reaction (PCR/qPCR); Gene expression/sequencing analysis; Cytokine/multiplex immunoassay; Mass cytometry (CyTOF)", "Immune_System-Function_enhanced/numbers_increased": "plasma soluble IL-2 receptor and CXCL10; increased IL-1α; increased IFN-γ production by tumor-infiltrating T cells", "Controlled_Terms_Function_enhanced_Number_increased": "T cells; IL-2; CXCL10 / IP-10", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04603", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "12", "Male/Female": null, "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2309", "Drug": "Brentuximab vedotin + Pembrolizumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB08870+DB09037", "Target/s_or_mechanism_of_action": "Binds PD-1 (PDCD1/CD279) and blocks its interaction with PD-L1 and PD-L2, releasing inhibitory checkpoint signaling and restoring T-cell effector activity", "KEGG_Drug__ID": null, "Pubchem_ID": "481101797", "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "39786430", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Primary or secondary refractory metastatic cutaneous melanoma after progression on PD-1 inhibitor therapy", "System": null, "Dose": "Brentuximab vedotin 1.8 mg/kg IV + pembrolizumab 200 mg IV every 3 weeks; maximum 35 cycles; drugs administered separately on day 1", "Technique": "flow cytometry", "Controlled_Technique": "Flow cytometry", "Immune_System-Function_enhanced/numbers_increased": "tumor CD8+ T-cell infiltration, especially in responders, ratio of CD8 to Tregs", "Controlled_Terms_Function_enhanced_Number_increased": "Regulatory T cells (Tregs); CD8+ T cells; T cells; CD8", "Immune_System-Function_inhibited/numbers_decreased": "Peripheral-blood regulatory T cells (Tregs)", "Controlled_Terms_Function_inhibited_Number_decreased": "Regulatory T cells (Tregs); T cells", "Immune_System_function_unaffected": "CD30+ CD8+ T cells", "Controlled_Terms_Unaffected": "CD8+ T cells; T cells; CD8", "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D09587+D10574", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "58 patients received at least one dose of the combination (17 primary refractory; 41 secondary refractory)", "Male/Female": "Male: 36 / Female: 22", "Median_age/Range": "Median: 64.5 years; overall study age range: 23–86 years"}, {"study_type": "patient_studies", "ID": "CANIMM/2310", "Drug": "Ipilimumab (anti-CTLA-4) + Nivolumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB06186", "Target/s_or_mechanism_of_action": "Blocks CTLA-4-mediated inhibitory signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "31636098", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Metastatic melanoma", "System": null, "Dose": null, "Technique": "Cytokine analysis", "Controlled_Technique": "Cytokine analysis", "Immune_System-Function_enhanced/numbers_increased": "expression of CXCL9, CXCL10, and CXCL11; increased numbers of intratumoral CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells; CD8; CXCL9; CXCL10 / IP-10; CXCL11", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04603", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Tumor biopsy specimens", "Male/Female": "72", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2311", "Drug": "Ipilimumab (anti-CTLA-4) +Pembrolizumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB06186", "Target/s_or_mechanism_of_action": "Blocks CTLA-4-mediated inhibitory signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "31636098", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Metastatic melanoma", "System": null, "Dose": null, "Technique": "Cytokine analysis", "Controlled_Technique": "Cytokine analysis", "Immune_System-Function_enhanced/numbers_increased": "expression of CXCL9, CXCL10, and CXCL11; increased numbers of intratumoral CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells; CD8; CXCL9; CXCL10 / IP-10; CXCL11", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04603", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Tumor biopsy specimens", "Male/Female": "72", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2312", "Drug": "Ipilimumab (anti-CTLA-4) + Nivolumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB06186", "Target/s_or_mechanism_of_action": "Blocks CTLA-4-mediated inhibitory signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "31636098", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Metastatic melanoma", "System": null, "Dose": null, "Technique": "Cytokine analysis", "Controlled_Technique": "Cytokine analysis", "Immune_System-Function_enhanced/numbers_increased": "expression of CXCL9, CXCL10, and CXCL11; increased numbers of intratumoral CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells; CD8; CXCL9; CXCL10 / IP-10; CXCL11", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04603", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Tumor biopsy specimens", "Male/Female": "56", "Median_age/Range": null}, {"study_type": "patient_studies", "ID": "CANIMM/2313", "Drug": "Ipilimumab (anti-CTLA-4) +Pembrolizumab", "Drug_category": "Others/combination", "Drugbank_ID": "DB06186", "Target/s_or_mechanism_of_action": "Blocks CTLA-4-mediated inhibitory signaling", "KEGG_Drug__ID": null, "Pubchem_ID": null, "STR_LINK_(SMILES)": null, "Single/Combination": "Combination", "PMID": "31636098", "Cancer_Type": "Skin cancer", "Cancer_Type_Description": "Metastatic melanoma", "System": null, "Dose": null, "Technique": "Cytokine analysis", "Controlled_Technique": "Cytokine analysis", "Immune_System-Function_enhanced/numbers_increased": "expression of CXCL9, CXCL10, and CXCL11; increased numbers of intratumoral CD8+ T cells", "Controlled_Terms_Function_enhanced_Number_increased": "CD8+ T cells; T cells; CD8; CXCL9; CXCL10 / IP-10; CXCL11", "Immune_System-Function_inhibited/numbers_decreased": null, "Controlled_Terms_Function_inhibited_Number_decreased": null, "Immune_System_function_unaffected": null, "Controlled_Terms_Unaffected": null, "Negative_Immune_System_regulation_-Function_enhanced/numbers_in": null, "Controlled_Terms_Negative_Regulation": null, "KEGG_Drug_ID": "D04603", "Drug_Pubchem": null, "Animal_Strain_used": null, "Cell_line_used_to_induce_tumor_in_mice": null, "Patient_Sample": "Tumor biopsy specimens", "Male/Female": "56", "Median_age/Range": null}]