GS_ID NAME GS_SIZE ORGANISM DESCRIPTION LINK REFERENCE PUBMED_ID CATEGORY STATUS CURATOR CURATOR_CONTACT CONTRIBUTED_BY FLAG COCO_V2 GO_FLAG VERSION REF_OLD_ID ORIGINAL_ID RECORD_DATE SOURCE TYPE
FAX000843 Genes down-regulated in myometrial cells over-expressing a shortened splice form of ATF2 [GeneID=1386] gene. 179 Homo sapiens Human myometrial cells taken from biopsies of pre-menopausal non-cancerous non-pregnant uteri were cultured in complete MEM D-valine medium plus 10% FCS, and stably-transfected with the pcDNA3.1/V5-His TOPO vector (Invitrogen) harbouring ATF2-small gene or a control empty-vector. http://www.broadinstitute.org/gsea/msigdb/cards/ATF2_S_UP.V1_DN M2681 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 5.04972790453672 N 1.0 13-AUG-20 MSigDB A
FAX000844 Genes up-regulated in myometrial cells over-expressing a shortened splice form of ATF2 [GeneID=1386] gene. 182 Homo sapiens Human myometrial cells taken from biopsies of pre-menopausal non-cancerous non-pregnant uteri were cultured in complete MEM D-valine medium plus 10% FCS, and stably-transfected with the pcDNA3.1/V5-His TOPO vector (Invitrogen) harbouring ATF2-small gene or a control empty-vector. http://www.broadinstitute.org/gsea/msigdb/cards/ATF2_S_UP.V1_UP M2682 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 1.7671065735617801 N 1.0 13-AUG-20 MSigDB A
FAX000845 Genes down-regulated in myometrial cells over-expressing ATF2 [GeneID=1386] gene. 176 Homo sapiens Human myometrial cells taken from biopsies of pre-menopausal non-cancerous non-pregnant uteri were cultured in complete MEM D-valine medium plus 10% FCS, and stably-transfected with the pcDNA3.1/V5-His TOPO vector (Invitrogen) harbouring ATF2 gene or a control empty-vector. http://www.broadinstitute.org/gsea/msigdb/cards/ATF2_UP.V1_DN M2684 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 3.0752085933335604 N 1.0 13-AUG-20 MSigDB A
FAX000846 Genes up-regulated in myometrial cells over-expressing ATF2 [GeneID=1386] gene. 184 Homo sapiens Human myometrial cells taken from biopsies of pre-menopausal non-cancerous non-pregnant uteri were cultured in complete MEM D-valine medium plus 10% FCS, and stably-transfected with the pcDNA3.1/V5-His TOPO vector (Invitrogen) harbouring ATF2 gene or a control empty-vector. http://www.broadinstitute.org/gsea/msigdb/cards/ATF2_UP.V1_UP M2686 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 8.1591248833217 N 1.0 13-AUG-20 MSigDB A
FAX000851 Genes down-regulated in primary epithelial breast cancer cell culture over-expressing activated CTNNB1 [GeneID=1499] gene. 45 Homo sapiens RNA was extracted from human mammary epithelial cells expressing oncogenes (or GFP control) for gene array analysis. Experiment was performed in replicate. http://www.broadinstitute.org/gsea/msigdb/cards/BCAT_BILD_ET_AL_DN M2702 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 5.20073474965666 N 1.0 13-AUG-20 MSigDB A
FAX000852 Genes up-regulated in primary epithelial breast cancer cell culture over-expressing activated CTNNB1 [GeneID=1499] gene. 43 Homo sapiens RNA was extracted from human mammary epithelial cells expressing oncogenes (or GFP control) for gene array analysis. Experiment was performed in replicate. http://www.broadinstitute.org/gsea/msigdb/cards/BCAT_BILD_ET_AL_UP M2703 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 2.8475019010328 N 1.0 13-AUG-20 MSigDB A
FAX000859 Genes down-regulated in MCF10A cells (breast cancer) upon knockdown of BRCA1 [GeneID=672] gene by RNAi. 124 Homo sapiens MCF10A cells in 3-D culture for 15 h after treatment with BRCA1-RNAi vs Luc-RNAi adenovirus http://www.broadinstitute.org/gsea/msigdb/cards/BRCA1_DN.V1_DN M2747 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.0710474611939326 N 1.0 13-AUG-20 MSigDB A
FAX000860 Genes up-regulated in MCF10A cells (breast cancer) upon knockdown of BRCA1 [GeneID=672] gene by RNAi. 130 Homo sapiens MCF10A cells in 3-D culture for 15 h after treatment with BRCA1-RNAi vs Luc-RNAi adenovirus http://www.broadinstitute.org/gsea/msigdb/cards/BRCA1_DN.V1_UP M2748 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.0 N 1.0 13-AUG-20 MSigDB A
FAX000867 YAP conserved signature. 53 Homo sapiens Cancer stem cells (CSCs) are proposed to drive tumor initiation and progression. Yet, our understanding of the cellular and molecular mechanisms that underlie CSC properties is limited. Here we show that the activity of TAZ, a transducer of the Hippo pathway, is required to sustain self-renewal and tumor-initiation capacities in breast CSCs. TAZ protein levels and activity are elevated in prospective CSCs and in poorly differentiated human tumors and have prognostic value. Gain of TAZ endows self-renewal capacity to non-CSCs. In epithelial cells, TAZ forms a complex with the cell-polarity determinant Scribble, and loss of Scribble--or induction of the epithelial-mesenchymal transition (EMT)--disrupts the inhibitory association of TAZ with the core Hippo kinases MST and LATS. This study links the CSC concept to the Hippo pathway in breast cancer and reveals a mechanistic basis of the control of Hippo kinases by cell polarity http://www.broadinstitute.org/gsea/msigdb/cards/CORDENONSI_YAP_CONSERVED_SIGNATURE M2871 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 128.390749794682 N 1.0 13-AUG-20 MSigDB A
FAX000876 Genes down-regulated in MCF10A cells (breast cancer) upon knockdown of RBBP8 [Gene ID=RBBP8] gene by RNAi. 123 Homo sapiens MCF10A cells in 3-D culture for 15 h after treatment with CtIP-RNAi vs Luc-RNAi adenovirus. http://www.broadinstitute.org/gsea/msigdb/cards/CTIP_DN.V1_DN M2751 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.0 N 1.0 13-AUG-20 MSigDB A
FAX000877 Genes up-regulated in MCF10A cells (breast cancer) upon knockdown of RBBP8 [Gene ID=RBBP8] gene by RNAi. 126 Homo sapiens MCF10A cells in 3-D culture for 15 h after treatment with CtIP-RNAi vs Luc-RNAi adenovirus. http://www.broadinstitute.org/gsea/msigdb/cards/CTIP_DN.V1_UP M2752 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 1.9477802192686902 N 1.0 13-AUG-20 MSigDB A
FAX000878 Genes down-regulated in MCF-7 cells (breast cancer) over-expressing a mutant K112E form of CCND1 [GeneID=595] gene. 185 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/CYCLIN_D1_KE_.V1_DN M2647 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 24.8716706370311 N 1.0 13-AUG-20 MSigDB A
FAX000879 Genes up-regulated in MCF-7 cells (breast cancer) over-expressing a mutant K112E form of CCND1 [GeneID=595] gene. 185 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/CYCLIN_D1_KE_.V1_UP M2648 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 19.281937826541103 N 1.0 13-AUG-20 MSigDB A
FAX000880 Genes down-regulated in MCF-7 cells (breast cancer) over-expressing CCND1 [GeneID=595] gene. 182 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/CYCLIN_D1_UP.V1_DN M2652 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 19.986238015173303 N 1.0 13-AUG-20 MSigDB A
FAX000881 Genes up-regulated in MCF-7 cells (breast cancer) over-expressing CCND1 [GeneID=595] gene. 182 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/CYCLIN_D1_UP.V1_UP M2654 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 16.648366487459302 N 1.0 13-AUG-20 MSigDB A
FAX000882 Genes down-regulated in A549 lung carcinoma and M059K glioblastoma cells treated with dichloroacetate [PubChem=6597]. 168 Homo sapiens Analysis of A549 lung carcinoma and M059K glioblastoma cells treated with dichloroacetate (DCA), an inhibitor of the mitochondrial pyruvate dehydrogenase kinase. DCA shifts metabolism from glycolysis to glucose oxidation and decreases mitochondrial membrane potential in cancer cells. http://www.broadinstitute.org/gsea/msigdb/cards/DCA_UP.V1_DN M2760 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.0 N 1.0 13-AUG-20 MSigDB A
FAX000883 Genes up-regulated in A549 lung carcinoma and M059K glioblastoma cells treated with dichloroacetate [PubChem=6597]. 173 Homo sapiens Analysis of A549 lung carcinoma and M059K glioblastoma cells treated with dichloroacetate (DCA), an inhibitor of the mitochondrial pyruvate dehydrogenase kinase. DCA shifts metabolism from glycolysis to glucose oxidation and decreases mitochondrial membrane potential in cancer cells. http://www.broadinstitute.org/gsea/msigdb/cards/DCA_UP.V1_UP M2762 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.0 N 1.0 13-AUG-20 MSigDB A
FAX000886 Genes down-regulated in primary epithelial breast cancer cell culture over-expressing E2F3 [GeneID=1871] gene. 142 Homo sapiens RNA was extracted from human mammary epithelial cells expressing oncogenes (or GFP control) for gene array analysis. Experiment was performed in replicate. http://www.broadinstitute.org/gsea/msigdb/cards/E2F3_UP.V1_DN M2704 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.0 N 1.0 13-AUG-20 MSigDB A
FAX000887 Genes up-regulated in primary epithelial breast cancer cell culture over-expressing E2F3 [GeneID=1871] gene. 175 Homo sapiens RNA was extracted from human mammary epithelial cells expressing oncogenes (or GFP control) for gene array analysis. Experiment was performed in replicate. http://www.broadinstitute.org/gsea/msigdb/cards/E2F3_UP.V1_UP M2706 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.8079663838455821 N 1.0 13-AUG-20 MSigDB A
FAX000888 Genes down-regulated in MCF-7 cells (breast cancer) positive for ESR1 [GeneID=2099] and engineered to express ligand-activatable EGFR [GeneID=1956]. 168 Homo sapiens Profiling of MCF-7 cell lines stably overexpressing ligand-activatable EGFR as models of overexpressed growth factor signaling, as well as control vector transfected cells (coMCF-7) and control vector transfected cells long-term adapted for estrogen-independent growth (coMCF-7/lt-E2). http://www.broadinstitute.org/gsea/msigdb/cards/EGFR_UP.V1_DN M2633 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 4.41687582370726 N 1.0 13-AUG-20 MSigDB A
FAX000889 Genes up-regulated in MCF-7 cells (breast cancer) positive for ESR1 [GeneID=2099] and engineered to express ligand-activatable EGFR [GeneID=1956]. 180 Homo sapiens Profiling of MCF-7 cell lines stably overexpressing ligand-activatable EGFR as models of overexpressed growth factor signaling, as well as control vector transfected cells (coMCF-7) and control vector transfected cells long-term adapted for estrogen-independent growth (coMCF-7/lt-E2). http://www.broadinstitute.org/gsea/msigdb/cards/EGFR_UP.V1_UP M2634 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 16.7315423583952 N 1.0 13-AUG-20 MSigDB A
FAX000892 Genes down-regulated in MCF-7 cells (breast cancer) positive for ESR1 [GeneID=2099] and engineered to express ligand-activatable ERBB2 [GeneID=2064]. 178 Homo sapiens Profiling of MCF-7 cell lines stably overexpressing constitutively active c-erbB-2 as well as control vector transfected cells (coMCF-7) and control vector transfected cells long-term adapted for estrogen-independent growth (coMCF-7/lt-E2). http://www.broadinstitute.org/gsea/msigdb/cards/ERB2_UP.V1_DN M2635 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 82.94228743645591 N 1.0 13-AUG-20 MSigDB A
FAX000893 Genes up-regulated in MCF-7 cells (breast cancer) positive for ESR1 [GeneID=2099] and engineered to express ligand-activatable ERBB2 [GeneID=2064]. 178 Homo sapiens Profiling of MCF-7 cell lines stably overexpressing constitutively active c-erbB-2 as well as control vector transfected cells (coMCF-7) and control vector transfected cells long-term adapted for estrogen-independent growth (coMCF-7/lt-E2). http://www.broadinstitute.org/gsea/msigdb/cards/ERB2_UP.V1_UP M2636 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 2.76794388076439 N 1.0 13-AUG-20 MSigDB A
FAX000922 Genes down-regulated in four lineages of epithelial cell lines over-expressing an oncogenic form of KRAS [GeneID=3845]. 135 Homo sapiens The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. A complementary strategy for targeting KRAS is to identify gene products that, when inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkappaB kinase TBK1 was selectively essential in cells that contain mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF-kappaB anti-apoptotic signals involving c-Rel and BCL-XL (also known as BCL2L1) that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations indicate that TBK1 and NF-kappaB signalling are essential in KRAS mutant tumours, and establish a general approach for the rational identification of co-dependent pathways in cancer. http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.300_UP.V1_DN M2874 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 8.45843776318209 N 1.0 13-AUG-20 MSigDB A
FAX000926 Genes down-regulated in epithelial lung and breast cancer cell lines over-expressing an oncogenic form of KRAS [GeneID=3845] gene. 266 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.600.LUNG.BREAST_UP.V1_DN M2885 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.7189160104551909 N 1.0 13-AUG-20 MSigDB A
FAX000927 Genes up-regulated in epithelial lung and breast cancer cell lines over-expressing an oncogenic form of KRAS [GeneID=3845] gene. 275 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.600.LUNG.BREAST_UP.V1_UP M2886 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 14.250934199431699 N 1.0 13-AUG-20 MSigDB A
FAX000930 Genes down-regulated in epithelial lung cancer cell lines over-expressing KRAS [GeneID=3845] gene. 129 Homo sapiens Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression. The purpose of the dataset is to analyze expression of genes induced by KRAS and regulated by TBK1. The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF-kappaB anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. Knock out of TBK1 in the contect of KRAS activation (mutant) and control (WT). http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.AMP.LUNG_UP.V1_DN M2859 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 1.0219927371140798 N 1.0 13-AUG-20 MSigDB A
FAX000931 Genes up-regulated in epithelial lung cancer cell lines over-expressing KRAS [GeneID=3845] gene. 130 Homo sapiens Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression. The purpose of the dataset is to analyze expression of genes induced by KRAS and regulated by TBK1. The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF-kappaB anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. Knock out of TBK1 in the contect of KRAS activation (mutant) and control (WT). http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.AMP.LUNG_UP.V1_UP M2860 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 1.25921071448133 N 1.0 13-AUG-20 MSigDB A
FAX000932 Genes down-regulated in epithelial breast cancer cell lines over-expressing an oncogenic form of KRAS [GeneID=3845] gene. 135 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.BREAST_UP.V1_DN M2887 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.0 N 1.0 13-AUG-20 MSigDB A
FAX000933 Genes up-regulated in epithelial breast cancer cell lines over-expressing an oncogenic form of KRAS [GeneID=3845] gene. 134 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.BREAST_UP.V1_UP M2888 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 3.35960915075887 N 1.0 13-AUG-20 MSigDB A
FAX000934 Genes down-regulated in epithelial lung cancer cell lines over-expressing an oncogenic form of KRAS [GeneID=3845] gene. 182 Homo sapiens Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression. The purpose of the dataset is to analyze expression of genes induced by KRAS and regulated by TBK1. The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF-kappaB anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. Knock out of TBK1 in the contect of KRAS activation (mutant) and control (WT). http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.DF.V1_DN M2861 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 1.41096758590366 N 1.0 13-AUG-20 MSigDB A
FAX000935 Genes up-regulated in epithelial lung cancer cell lines over-expressing an oncogenic form of KRAS [GeneID=3845] gene. 183 Homo sapiens Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression. The purpose of the dataset is to analyze expression of genes induced by KRAS and regulated by TBK1. The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF-kappaB anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. Knock out of TBK1 in the contect of KRAS activation (mutant) and control (WT). http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.DF.V1_UP M2863 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 7.824780185846372 N 1.0 13-AUG-20 MSigDB A
FAX000936 Genes down-regulated in epithelial kidney cancer cell lines over-expressing an oncogenic form of KRAS [GeneID=3845] gene. 131 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.KIDNEY_UP.V1_DN M2889 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 13.248981823004902 N 1.0 13-AUG-20 MSigDB A
FAX000937 Genes up-regulated in epithelial kidney cancer cell lines over-expressing an oncogenic form of KRAS [GeneID=3845] gene. 138 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.KIDNEY_UP.V1_UP M2892 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 19.260942306402303 N 1.0 13-AUG-20 MSigDB A
FAX000938 Genes down-regulated in epithelial breast cancer cell lines over-expressing an oncogenic form of KRAS [Gene ID=3845 gene]. 135 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.LUNG.BREAST_UP.V1_DN M2898 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 1.5204784540017098 N 1.0 13-AUG-20 MSigDB A
FAX000939 Genes up-regulated in epithelial lung and breast cancer cell lines over-expressing an oncogenic form of KRAS [GeneID=3845] gene. 139 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.LUNG.BREAST_UP.V1_UP M2900 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 17.4316744679415 N 1.0 13-AUG-20 MSigDB A
FAX000940 Genes down-regulated in epithelial lung cancer cell lines over-expressing an oncogenic form of KRAS [GeneID=3845] gene. 135 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.LUNG_UP.V1_DN M2893 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 4.422896210290969 N 1.0 13-AUG-20 MSigDB A
FAX000941 Genes up-regulated in epithelial lung cancer cell lines over-expressing an oncogenic form of KRAS [GeneID=3845] gene. 132 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.LUNG_UP.V1_UP M2897 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 3.0952390828409504 N 1.0 13-AUG-20 MSigDB A
FAX000942 Genes down-regulated in epithelial prostate cancer cell lines over-expressing an oncogenic form of KRAS [GeneID=3845] gene. 138 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.PROSTATE_UP.V1_DN M2901 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 4.4585625905129005 N 1.0 13-AUG-20 MSigDB A
FAX000943 Genes up-regulated in epithelial prostate cancer cell lines over-expressing an oncogenic form of KRAS [GeneID=3845] gene. 129 Homo sapiens http://www.broadinstitute.org/gsea/msigdb/cards/KRAS.PROSTATE_UP.V1_UP M2902 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.5258013197290979 N 1.0 13-AUG-20 MSigDB A
FAX000946 Genes down-regulated in MCF-7 cells (breast cancer) positive for ESR1 [GeneID=2099] MCF-7 cells (breast cancer) and long-term adapted for estrogen-independent growth. 182 Homo sapiens Profiling of control vector transfected cells (coMCF-7) and control vector transfected cells long-term adapted for estrogen-independent growth (coMCF-7/lt-E2). http://www.broadinstitute.org/gsea/msigdb/cards/LTE2_UP.V1_DN M2721 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 253.598873906732 N 1.0 13-AUG-20 MSigDB A
FAX000947 Genes up-regulated in MCF-7 cells (breast cancer) positive for ESR1 [GeneID=2099] MCF-7 cells (breast cancer) and long-term adapted for estrogen-independent growth. 177 Homo sapiens Profiling of control vector transfected cells (coMCF-7) and control vector transfected cells long-term adapted for estrogen-independent growth (coMCF-7/lt-E2). http://www.broadinstitute.org/gsea/msigdb/cards/LTE2_UP.V1_UP M2723 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 1.15172358633928 N 1.0 13-AUG-20 MSigDB A
FAX000948 Genes down-regulated in MCF-7 cells (breast cancer) positive for ESR1 [GeneID=2099] MCF-7 cells (breast cancer) stably over-expressing constitutively active MAP2K1 [GeneID=5604] gene. 170 Homo sapiens Profiling of MCF-7 cell lines stably overexpressing constitutively active MEK as a model of overexpressed growth factor signaling, as well as control vector transfected cells (coMCF-7). http://www.broadinstitute.org/gsea/msigdb/cards/MEK_UP.V1_DN M2724 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 121.770560144345 N 1.0 13-AUG-20 MSigDB A
FAX000949 Genes up-regulated in MCF-7 cells (breast cancer) positive for ESR1 [GeneID=2099] MCF-7 cells (breast cancer) stably over-expressing constitutively active MAP2K1 [GeneID=5604] gene. 181 Homo sapiens Profiling of MCF-7 cell lines stably overexpressing constitutively active MEK as a model of overexpressed growth factor signaling, as well as control vector transfected cells (coMCF-7). http://www.broadinstitute.org/gsea/msigdb/cards/MEK_UP.V1_UP M2725 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 5.02213514822205 N 1.0 13-AUG-20 MSigDB A
FAX000956 Genes down-regulated in primary epithelial breast cancer cell culture over-expressing MYC [GeneID=4609] gene. 149 Homo sapiens RNA was extracted from human mammary epithelial cells expressing oncogenes (or GFP control) for gene array analysis. Experiment was performed in replicate. http://www.broadinstitute.org/gsea/msigdb/cards/MYC_UP.V1_DN M2708 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.317925653508505 N 1.0 13-AUG-20 MSigDB A
FAX000957 Genes up-regulated in primary epithelial breast cancer cell culture over-expressing MYC [GeneID=4609] gene. 157 Homo sapiens RNA was extracted from human mammary epithelial cells expressing oncogenes (or GFP control) for gene array analysis. Experiment was performed in replicate. http://www.broadinstitute.org/gsea/msigdb/cards/MYC_UP.V1_UP M2711 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 43.626773919376 N 1.0 13-AUG-20 MSigDB A
FAX000963 Genes down-regulated in NCI-60 panel of cell lines with mutated TP53 [GeneID=7157]. 185 Homo sapiens We examined gene expression patterns from the NCI-60 collection of cancer cell lines. We sought to use these data to identify targets of the transcription factor p53, which regulates gene expression in response to various signals of cellular stress. The mutational status of the p53 gene has been reported for 50 of the NCI-60 cell lines, with 17 being classified as normal and 33 as carrying mutations in the gene. http://www.broadinstitute.org/gsea/msigdb/cards/P53_DN.V1_DN M2697 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 15.716365201109099 N 1.0 13-AUG-20 MSigDB A
FAX000964 Genes up-regulated in NCI-60 panel of cell lines with mutated TP53 [GeneID=7157]. 186 Homo sapiens We examined gene expression patterns from the NCI-60 collection of cancer cell lines. We sought to use these data to identify targets of the transcription factor p53, which regulates gene expression in response to various signals of cellular stress. The mutational status of the p53 gene has been reported for 50 of the NCI-60 cell lines, with 17 being classified as normal and 33 as carrying mutations in the gene. http://www.broadinstitute.org/gsea/msigdb/cards/P53_DN.V1_UP M2698 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 20.705763509220894 N 1.0 13-AUG-20 MSigDB A
FAX000987 Genes down-regulated in MCF-7 cells (breast cancer) positive for ESR1 [GeneID=2099] MCF-7 cells (breast cancer) stably over-expressing constitutively active RAF1 [GeneID=5894] gene. 180 Homo sapiens Profiling of MCF-7 cell lines stably overexpressing constitutively active Raf-1 as a model of overexpressed growth factor signaling, as well as control vector transfected cells (coMCF-7). http://www.broadinstitute.org/gsea/msigdb/cards/RAF_UP.V1_DN M2726 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 9.28177113631339 N 1.0 13-AUG-20 MSigDB A
FAX000988 Genes up-regulated in MCF-7 cells (breast cancer) positive for ESR1 [GeneID=2099] MCF-7 cells (breast cancer) stably over-expressing constitutively active RAF1 [GeneID=5894] gene. 183 Homo sapiens Profiling of MCF-7 cell lines stably overexpressing constitutively active Raf-1 as a model of overexpressed growth factor signaling, as well as control vector transfected cells (coMCF-7). http://www.broadinstitute.org/gsea/msigdb/cards/RAF_UP.V1_UP M2728 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 5.63457543635564 N 1.0 13-AUG-20 MSigDB A
FAX001001 Genes defining the KRAS [GeneID=3845] dependency signature. 18 Homo sapiens K-ras mutations occur frequently in epithelial cancers. Using short hairpin RNAs to deplete K-Ras in lung and pancreatic cancer cell lines harboring K-ras mutations, two classes were identified-lines that do or do not require K-Ras to maintain viability. Comparing these two classes of cancer cells revealed a gene expression signature in K-Ras-dependent cells, associated with a well-differentiated epithelial phenotype, which was also seen in primary tumors. Several of these genes encode pharmacologically tractable proteins, such as Syk and Ron kinases and integrin beta6, depletion of which induces epithelial-mesenchymal transformation (EMT) and apoptosis specifically in K-Ras-dependent cells. These findings indicate that epithelial differentiation and tumor cell viability are associated, and that EMT regulators in K-Ras-addicted cancers represent candidate therapeutic targets. http://www.broadinstitute.org/gsea/msigdb/cards/SINGH_KRAS_DEPENDENCY_SIGNATURE_ M2851 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 2.93452844894778 N 1.0 13-AUG-20 MSigDB A
FAX001006 Genes down-regulated in primary epithelial breast cancer cell culture over-expressing SRC [GeneID=6714] gene. 157 Homo sapiens RNA was extracted from human mammary epithelial cells expressing oncogenes (or GFP control) for gene array analysis. Experiment was performed in replicate. http://www.broadinstitute.org/gsea/msigdb/cards/SRC_UP.V1_DN M2713 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 9.141975560405411 N 1.0 13-AUG-20 MSigDB A
FAX001007 Genes up-regulated in primary epithelial breast cancer cell culture over-expressing SRC [GeneID=6714] gene. 156 Homo sapiens RNA was extracted from human mammary epithelial cells expressing oncogenes (or GFP control) for gene array analysis. Experiment was performed in replicate. http://www.broadinstitute.org/gsea/msigdb/cards/SRC_UP.V1_UP M2714 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.0 N 1.0 13-AUG-20 MSigDB A
FAX001014 Genes down-regulated in epithelial lung cancer cell lines upon over-expression of an oncogenic form of KRAS [GeneID=3845] gene and knockdown of TBK1 [GeneID=29110] gene by RNAi. 263 Homo sapiens Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression. The purpose of the dataset is to analyze expression of genes induced by KRAS and regulated by TBK1. The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF-kappaB anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. Knock out of TBK1 in the contect of KRAS activation (mutant) and control (WT). http://www.broadinstitute.org/gsea/msigdb/cards/TBK1.DF_DN M2864 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 6.934291282870281 N 1.0 13-AUG-20 MSigDB A
FAX001015 Genes up-regulated in epithelial lung cancer cell lines upon over-expression of an oncogenic form of KRAS [GeneID=3845] gene and knockdown of TBK1 [GeneID=29110] gene by RNAi. 266 Homo sapiens Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression. The purpose of the dataset is to analyze expression of genes induced by KRAS and regulated by TBK1. The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF-kappaB anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. Knock out of TBK1 in the contect of KRAS activation (mutant) and control (WT). http://www.broadinstitute.org/gsea/msigdb/cards/TBK1.DF_UP M2867 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 1.0419829346176 N 1.0 13-AUG-20 MSigDB A
FAX001016 Genes down-regulated in epithelial lung cancer cell lines upon over-expression of an oncogenic form of KRAS [GeneID=3845] gene and knockdown of TBK1 [GeneID=29110] gene by RNAi. 49 Homo sapiens Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression. The purpose of the dataset is to analyze expression of genes induced by KRAS and regulated by TBK1. The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF-kappaB anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. Knock out of TBK1 in the contect of KRAS activation (mutant) and control (WT). http://www.broadinstitute.org/gsea/msigdb/cards/TBK1.DN.48HRS_DN M2868 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 14.183066336054402 N 1.0 13-AUG-20 MSigDB A
FAX001017 Genes up-regulated in epithelial lung cancer cell lines upon over-expression of an oncogenic form of KRAS [GeneID=3845] gene and knockdown of TBK1 [GeneID=29110] gene by RNAi. 49 Homo sapiens Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression. The purpose of the dataset is to analyze expression of genes induced by KRAS and regulated by TBK1. The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF-kappaB anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. Knock out of TBK1 in the contect of KRAS activation (mutant) and control (WT). http://www.broadinstitute.org/gsea/msigdb/cards/TBK1.DN.48HRS_UP M2869 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 10.7432995291561 N 1.0 13-AUG-20 MSigDB A
FAX001024 Genes down-regulated in MCF10A cells (breast cancer) over-expressing YAP1 [GeneID=10413] gene. 40 Homo sapiens MCF10A cells were infected with retrovirus constructs (vector or YAP) and puromycin was used to select for transduced cells. Cells were split and grown to ~60-75%% confluency at which point they were harvested for RNA. Vector vs. YAP comparison was done in duplicate. http://www.broadinstitute.org/gsea/msigdb/cards/YAP1_DN M2841 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.0 N 1.0 13-AUG-20 MSigDB A
FAX001025 Genes up-regulated in MCF10A cells (breast cancer) over-expressing YAP1 [GeneID=10413] gene. 37 Homo sapiens MCF10A cells were infected with retrovirus constructs (vector or YAP) and puromycin was used to select for transduced cells. Cells were split and grown to ~60-75%% confluency at which point they were harvested for RNA. Vector vs. YAP comparison was done in duplicate. http://www.broadinstitute.org/gsea/msigdb/cards/YAP1_UP M2845 C6: oncogenic signatures PAGER curation team PAGER-contact@googlegroups.com Pablo Tamayo (Broad Institute) CURRENT 0.936378466557912 N 1.0 13-AUG-20 MSigDB A
FAX001070 Genes down-regulated in comparison of macrophages treated with control (hIgG1) versus those treated with TNFRSF6B [GeneID=8771]. 163 Homo sapiens Decoy receptor 3 (DcR3) is a member of the TNF receptor superfamily and is up-regulated in tumors that originate from a diversity of lineages. DcR3 is capable of promoting angiogenesis, inducing dendritic cell apoptosis, and modulating macrophage differentiation. Since tumor-associated macrophages (TAMs) are the major infiltrating leukocytes in most malignant tumors, we used microarray technology to investigate whether DcR3 contributes to the development of TAMs. Among the DcR3-modulated genes expressed by TAMs, those that encode proteins involved in MHC class II (MHC-II)-dependent antigen presentation were down-regulated substantially, together with the master regulator of MHC-II expression (the class II transactivator, CIITA). The ERK- and JNK-induced deacetylation of histones associated with the CIITA promoters was responsible for DcR3-mediated down-regulation of MHC-II expression. Furthermore, the expression level of DcR3 in cancer cells correlated inversely with HLA-DR levels on TAMs and with the overall survival time of pancreatic cancer patients. The role of DcR3 in the development of TAMs was further confirmed using transgenic mice over-expressing DcR3. This elucidates the molecular mechanism of impaired MHC-II-mediated antigen presentation by TAMs, and raises the possibility that subversion of TAM-induced immunosuppression via inhibition of DcR3 expression might represent a target for the design of new therapeutics. http://www.broadinstitute.org/gsea/msigdb/cards/GSE10856_CTRL_VS_TNFRSF6B_IN_MACROPHAGE_DN M3101 C7: immunologic signatures PAGER curation team PAGER-contact@googlegroups.com Jernej Godec (Nick Haining lab (DFCI)) CURRENT 2.6137730855794703 N 1.0 13-AUG-20 MSigDB A
FAX001071 Genes up-regulated in comparison of macrophages treated with control (hIgG1) versus those treated with TNFRSF6B [GeneID=8771]