Genes up-regulated in pancreatic cancer cells grown in orthotopic xenograft tumors compared to those grown in vitro.
Genes down-regulated in pancreatic cancer cells grown in orthotopic xenograft tumors compared to those grown in vitro.
Top up-regulated genes in pediatric adrenocortical tumors (ACT) compared to the normal tissue.
Top down-regulated genes in pediatric adrenocortical tumors (ACT) compared to the normal tissue.
Genes up-regulated in head and neck tumor samples which clustered around known hypoxia genes.
Genes down-regulated in head and neck tumor samples which clustered around known hypoxia genes.
Genes up-regulated in HepaRG cells (liver cancer) expressing constituvely active form of MTOR [Gene ID=2475].
Genes down-regulated in HepaRG cells (liver cancer) expressing constituvely active form of MTOR [Gene ID=2475].
Up-regulated genes in cervical carcinoma and head and neck tumors positive for human papilloma virus (HPV) compared to those negative for HPV.
Down-regulated genes in cervical carcinoma and head and neck tumors positive for human papilloma virus (HPV) compared to those negative for HPV.
Up-regulated genes in peripheral zone of human pancreatic cancer growing in the pancreas of nude mice compared to that of the tumor from the central zone.
Down-regulated genes in peripheral zone of human pancreatic cancer growing in the pancreas of nude mice compared to that of the tumor from the central zone.
Up-regulated genes in angioimmunoblastic lymphoma (AILT) compared to normal T lymphocytes.
Down-regulated genes in angioimmunoblastic lymphoma (AILT) compared to normal T lymphocytes.
Genes up-regulated in endothelial cells derived from invasive ovarian cancer tissue.
Genes down-regulated in endothelial cells derived from invasive ovarian cancer tissue.
Genes from the 12p region that were up-regulated in embryonic carcinoma tumors compared to normal testis.
Genes from the 12p region that were down-regulated in embryonic carcinoma tumors compared to normal tissue.
Genes from the 12p region that up-regulated in teratoma cells compared to normal testis.
Genes from the 12p region that down-regulated in teratoma cells compared to normal testis.
Genes from the 12p region that were up-regulated in yolk sac tumor cells compared to normal testis.
Genes from the 12p region that were down-regulated in yolk sac tumor cells compared to normal testis.
Genes from the 12p region that were up-regulated in choriocarcinoma cells compared to normal testis.
Genes from the 12p region that were down-regulated in choriocarcinoma cells compared to normal testis.
Genes from the 12p region that were up-regulated in seminoma tumors compared to normal testis.
Genes from the 12p region that were down-regulated in seminoma tumors compared to normal testis.
Genes up-regulated in rectal cancer patients resistant to radiotherapy (non-responders) relative to the sensitive ones (responders).
Genes down-regulated in rectal cancer patients resistant to radiotherapy (non-responders) relative to the sensitive ones (responders).
Genes up-regulated in DLBCL (diffuse large B-cell lymphoma) cell lines sensitive to stimulation of CD40 [Gene ID=958] relative to the resistant ones.
Genes down-regulated in DLBCL (diffuse large B-cell lymphoma) cell lines sensitive to stimulation of CD40 [Gene ID=958] relative to the resistant ones.
Genes up-regulated in prostate cancer samples.
Genes down-regulated in prostate cancer samples.
Genes up-regulated in LNCaP cells (prostate cancer) by overexpression of SOX4 [Gene ID=6659] and down-regulated by its RNAi knockdown.
Genes down-regulated in LNCaP cells (prostate cancer) by overexpression of SOX4 [Gene ID=6659] and up-regulated by its RNAi knockdown.
Genes up-regulated in uveal melanoma: class 2 vs class 1 tumors.
Genes down-regulated in uveal melanoma: class 2 vs class 1 tumors.
Genes up-regulated in medullary breast cancer (MBC) relative to ductal breast cancer (DBD).
Genes down-regulated in medullary breast cancer (MBC) relative to ductal breast cancer (DBD).
Genes up-regulated in invasive ductal carcinoma (IDC) relative to ductal carcinoma in situ (DCIS, non-invasive).
Genes down-regulated in invasive ductal carcinoma (IDC) relative to ductal carcinoma in situ (DCIS, non-invasive).
'PAX-FKHR signature':  genes up-regulated by PAX3- or PAX7-FOXO1 [Gene ID=5081, 5077, 2308] fusion in primary alveolar rhabdomyosarcoma(ARMS) tumors.
'PAX-FKHR signature':  genes down-regulated by PAX3- or PAX7-FOXO1 [Gene ID=5081, 5077, 2308] fusion in primary alveolar rhabdomyosarcoma(ARMS) tumors.
Genes up-regulated early in HMEC cells (mammary epithelium) during acinar development in vitro.
Genes down-regulated early in HMEC cells (mammary epithelium) during acinar development in vitro.
Genes up-regulated late in HMEC cells (mammary epithelium) during acinar development in vitro.
Genes down-regulated late in HMEC cells (mammary epithelium) during acinar development in vitro.
Genes down-regulated in MDA-MB-231 cells (breast cancer) after knockdown of FXYD5 [Gene ID=53827] by RNAi.
Genes preferentially up-regulated in MCF-7 cells (breast cancer) by tamoxifen [PubChem=5376] but not by estradiol or fulvestrant (ICI 182780) [PubChem=5757, 3478439].
Genes preferentially down-regulated in MCF-7 cells (breast cancer) by tamoxifen [PubChem=5376] but not by estradiol or fulvestrant (ICI 182780) [PubChem=5757, 3478439].
Genes up-regulated in glioma cell lines treated with both decitabine [PubChem=451668] and TSA [PubChem=5562].
Genes down-regulated in glioma cell lines treated with both decitabine [PubChem=451668] and TSA [PubChem=5562].
Genes up-regulated in nsopharyngeal carcinoma relative to the normal tissue.
Genes down-regulated in nsopharyngeal carcinoma relative to the normal tissue.
Up-regulated genes discriminating between MSI (microsatellite instability) and MSS (microsatellite stability) colon cancers.
Down-regulated genes discriminating between MSI (microsatellite instability) and MSS (microsatellite stability) colon cancers.
Genes up-regulated in H1975 cells (non-small cell lung cancer, NSCLC) resistant to gefitinib [PubChem=123631] after treatment with EGFR inhibitor CL-387785 [PubChem=2776] for 6h.
Genes down-regulated in H1975 cells (non-small cell lung cancer, NSCLC) resistant to gefitinib [PubChem=123631] after treatment with EGFR inhibitor CL-387785 [PubChem=2776] for 6h.
Up-regulated genes whose expression correlated with histologic grade of invasive breast cancer tumors: comparison of grade 1 vs grade 3.
Down-regulated genes whose expression correlated with histologic grade of invasive breast cancer tumors: comparison of grade 1 vs grade 3.
Genes up-regulated in erythroid progenitor cells isolated from bone marrow of patients with Diamond-Blackfan anemia (DBA) and mutated RPS19 [Gene ID=6223].
Genes down-regulated in erythroid progenitor cells isolated from bone marrow of patients with Diamond-Blackfan anemia (DBA) and mutated RPS19 [Gene ID=6223].
Genes up-regulated in myeloid progenitor cells isolated from bone marrow of patients with Diamond-Blackfan anemia (DBA) and mutated RPS19 [Gene ID=6223].
Genes down-regulated in myeloid progenitor cells isolated from bone marrow of patients with Diamond-Blackfan anemia (DBA) and mutated RPS19 [Gene ID=6223].
Genes up-regulated in common hematopoietic progenitor cells isolated from bone marrow of patients with Diamond-Blackfan anemia (DBA) and mutated RPS19 [Gene ID=6223].
Genes down-regulated in common hematopoietic progenitor cells isolated from bone marrow of patients with Diamond-Blackfan anemia (DBA) and mutated RPS19 [Gene ID=6223].
Genes up-regulated in CD4+ [Gene ID=920] T lymphocytes after stimulation with prostaglandin E2 [PubChem=5280360].
Genes down-regulated in CD4+ [Gene ID=920] T lymphocytes after stimulation with prostaglandin E2 [PubChem=5280360].
Selected genes up-regulated in DU145 and PC-3 cells (prostate cancer) after treatment with the NSAID (non-steroid anti-inflammatory drug) sulindac [PubChem=5352].
Selected genes down-regulated in DU145 and PC-3 cells (prostate cancer) after treatment with the NSAID (non-steroid anti-inflammatory drug) sulindac [PubChem=5352].
Genes up-regulated in A549 cells (lung cancer) after knockdown of ATF4 [Gene ID=468] by RNAi.
Genes down-regulated in A549 cells (lung cancer) after knockdown of ATF4 [Gene ID=468] by RNAi.
Genes up-regulated in 3 out of 4 NSCLC cell lines (non-small cell lung cancer) after treatment with azacitidine [PubChem=9444] and TSA [PubChem=5562].
Genes down-regulated in 3 out of 4 NSCLC cell lines (non-small cell lung cancer) after treatment with azacitidine [PubChem=9444] and TSA [PubChem=5562].
Genes up-regulated in mARMS (molecular ARMS) compared to the mERMS (molecular ERMS) class of rhabdomyosarcoma tumors.
Genes down-regulated in mARMS (molecular ARMS) compared to the mERMS (molecular ERMS) class of rhabdomyosarcoma tumors.
Genes up-regulated in RD cells (embryonal rhabdomyosarcoma, ERMS) by expression of PAX3- or PAX7-FOXO1 [Gene ID=5077, 5081, 2308] fusions off retroviral vectors.
Genes down-regulated in RD cells (embryonal rhabdomyosarcoma, ERMS) by expression of PAX3- or PAX7-FOXO1 [Gene ID=5077, 5081, 2308] fusions off retroviral vectors.
Genes up-regulated in RMS cells (rhabdomyosarcoma) expressing PAX3 or PAX7 fusions with FOXO1 [Gene ID=5077, 5081, 2308] compared to the fusion negative cell lines.
Genes down-regulated in RMS cells (rhabdomyosarcoma) expressing PAX3 or PAX7 fusions with FOXO1 [Gene ID=5077, 5081, 2308] compared to the fusion negative cell lines.
Genes up-regulated in nasopharyngeal carcinoma (NPC) positive for LMP1 [Gene ID=9260], a latent gene of Epstein-Barr virus (EBV).
Genes down-regulated in nasopharyngeal carcinoma (NPC) positive for LMP1 [Gene ID=9260], a latent gene of Epstein-Barr virus (EBV).
Genes up-regulated in normal ductal and normal lobular breast cells.
Genes down-regulated in normal ductal and normal lobular breast cells.
Genes up-regulated in ductal carcinoma vs normal ductal breast cells.
Genes down-regulated in ductal carcinoma vs normal ductal breast cells.
Genes up-regulated in ductal carcinoma vs normal lobular breast cells.
Genes down-regulated in ductal carcinoma vs normal lobular breast cells.
Genes up-regulated in ductal vs lobular carcinoma breast tumor cells.
Genes down-regulated in ductal vs lobular carcinoma breast tumor cells.
Genes up-regulated in lobular carcinoma vs normal ductal breast cells.
Genes down-regulated in lobular carcinoma vs normal ductal breast cells.
Genes up-regulated in lobular carcinoma vs normal lobular breast cells.
Genes down-regulated in lobular carcinoma vs normal lobular breast cells.
Top 50 genes up-regulated in metastatic vs primary prostate cancer  tumors.
Top 50 genes down-regulated in metastatic vs primary prostate cancer  tumors.
Genes up-regulated in primary cultures of ovarian surface epithlium cells exposed to progesterone [PubChem=5994] for 5 days.
Genes down-regulated in primary cultures of ovarian surface epithlium cells exposed to progesterone [PubChem=5994] for 5 days.
Genes up-regulated in monocyte-derived dendritic cells (MDDC) after stimulation with galecin-1 (lectin, LGALS1) [Gene ID=3956] compared to that with bacterial lipopolysaccharide (LPS).
Genes down-regulated in monocyte-derived dendritic cells (MDDC) after stimulation with galecin-1 (lectin, LGALS1) [Gene ID=3956] compared to that with bacterial lipopolysaccharide (LPS).
Genes up-regulated in Daudi cells (B lymphocytes) stably expressing CD5 [Gene ID=921] off a plasmid vector.
Genes down-regulated in Daudi cells (B lymphocytes) stably expressing CD5 [Gene ID=921] off a plasmid vector.
Genes up-regulated in macrophage by live P.gingivalis.
Genes down-regulated in macrophage by live P.gingivalis.
Genes up-regulated in 293 cells (embryonic kidney) upon expression of KHSV (Kaposi sarcoma???associated herpesvirus) microRNAs.
Genes down-regulated in 293 cells (embryonic kidney) upon expression of KHSV (Kaposi sarcoma???associated herpesvirus) microRNAs.
Genes up-regulated in PC-3 cells (prostate cancer) stably expressing ST7 [Gene ID=7982] off a plasmid vector.
Genes down-regulated in PC-3 cells (prostate cancer) stably expressing ST7 [Gene ID=7982] off a plasmid vector.
Genes up-regulated in ACC3 cells (adenoid cystic carcinoma) after knockdown of SOX4 [Gene ID=6659] by RNAi.
Genes down-regulated in ACC3 cells (adenoid cystic carcinoma) after knockdown of SOX4 [Gene ID=6659] by RNAi.
Genes up-regulated in OV-90 cells (ovarian cancer) exposed to ascites which inhibited invasion.
Genes down-regulated in OV-90 cells (ovarian cancer) exposed to ascites which inhibited invasion.
Up-regulated genes in U87 cells (glioblastoma multiforme, GBM) engineered to stably express LGI1 [Gene ID=9211].
Down-regulated genes in U87 cells (glioblastoma multiforme, GBM) engineered to stably express LGI1 [Gene ID=9211].
Genes up-regulated in samples with systolic heart failure compared to normal hearts.
Genes down-regulated in samples with systolic heart failure compared to normal hearts.
Genes up-regulated in APL (acute promyeolocytic leukemia) blasts expressing PML-RARA fusion [Gene ID=5371, 5914] compared to normal promyeloblasts.
Genes down-regulated in APL (acute promyeolocytic leukemia) blasts expressing PML-RARA fusion [Gene ID=5371, 5914] compared to normal promyeloblasts.
Genes up-regulated in multiple myeloma (MM) bone marrow mesenchymal stem cells.
Genes down-regulated in multiple myeloma (MM) bone marrow mesenchymal stem cells.
Up-regulated genes in B-CLL (B-cell chronic leukemia) patients expressing high levels of ZAP70 and CD38 [Gene ID=7535, 952], which are associated with poor survival.
Down-regulated genes in B-CLL (B-cell chronic leukemia) patients expressing high levels of ZAP70 and CD38 [Gene ID=7535, 952], which are associated with poor survival.
Genes up-regulated in CD34+ [Gene ID=947] cells isolated from bone marrow of CML (chronic myelogenous leukemia) patients, compared to those from normal donors.
Genes down-regulated in CD34+ [Gene ID=947] cells isolated from bone marrow of CML (chronic myelogenous leukemia) patients, compared to those from normal donors.
Genes up-regulated in secondary APL (acute promyelocytic leukemia) compared to the de novo tumors.
Genes down-regulated in secondary APL (acute promyelocytic leukemia) compared to the de novo tumors.
Genes up-regulated in T-PLL cells (T-cell prolymphocytic leukemia) bearing the inv(14)/t(14:14) chromosomal aberration.
Genes down-regulated in T-PLL cells (T-cell prolymphocytic leukemia) bearing the inv(14)/t(14:14) chromosomal aberration.
Genes up-regulated in MCF-7 cells (breast cancer) by overexpression of CMYB [Gene ID=4602] off adenovirus vector.
Genes down-regulated in MCF-7 cells (breast cancer) by overexpression of CMYB [Gene ID=4602] off adenovirus vector.
Genes up-regulated in MCF-7 cells (breast cancer) by overexpression of v-MYB oncogenic varian of CMYB [Gene ID=4602] off adenovirus vector.
Gene in the opposite directions by v-MYB (UP) and c-MYB  (DN) variants of CMYB [Gene ID=4602] overexpressed in primary monocyte cultures off adenoviral vectors.
Gene in the opposite directions by v-MYB (DN) and c-MYB  (UP) variants of CMYB [Gene ID=4602] overexpressed in primary monocyte cultures off adenoviral vectors.
Genes up-regulated in luminal-like breast cancer cell lines compared to the basal-like ones.
Genes down-regulated in luminal-like breast cancer cell lines compared to the basal-like ones.
Genes up-regulated in luminal-like breast cancer cell lines compared to the mesenchymal-like ones.
Genes down-regulated in luminal-like breast cancer cell lines compared to the mesenchymal-like ones.
Genes up-regulated in basal-like breast cancer cell lines as compared to the mesenchymal-like ones.
Genes down-regulated in basal-like breast cancer cell lines as compared to the mesenchymal-like ones.
Genes up-regulated in ER(-) / PR(-) breast tumors (do not express ESR1 and PGR [Gene ID=2099, 5241]) with molecular similarity to ER(+) (class A) relative to the rest of the ER(-) / PR(-) samples (class B).
Genes down-regulated in ER(-) / PR(-) breast tumors (do not express ESR1 and PGR [Gene ID=2099, 5241]) with molecular similarity to ER(+) (class A) relative to the rest of the ER(-) / PR(-) samples (class B).
Genes up-regulated in MDA-MB-453 cells (class A ER(-) [Gene ID=2099] breast cancer) after exposure to the androgen R1881 [PubChem=13766].
Genes down-regulated in MDA-MB-453 cells (class A ER(-) [Gene ID=2099] breast cancer) after exposure to the androgen R1881 [PubChem=13766].
Genes changed in breast cancer samples according to the ESR1 [Gene ID=2099] status: ER positive vs ER negative tumors.
Genes changed in breast cancer samples according to the ESR1 [Gene ID=2099] status: ER positive vs ER negative tumors.
Genes up-regulated in LNCaP cells (prostate cancer) treated with synthetic androgen R1881 [PubChem=13766].
Genes up-regulated in LNCaP cells (prostate cancer) treated with forskolin [PubChem=47936], an activator of PKA pathway.
Genes down-regulated in LNCaP cells (prostate cancer) treated with forskolin [PubChem=47936], an activator of PKA pathway.
Genes down-regulated in SK-NEP-1 cells (Wilm's tumor ) stably expressing inactivated forms of STAT1 [Gene ID=6772] under growth stress (hypoxia or nutritional deprivation).
Genes up-regulated in serrated vs conventional colorectal carcinoma (CRC) samples.
Genes down-regulated in serrated vs conventional colorectal carcinoma (CRC) samples.
Genes up-regulated in biphasic (mixed) vs epithelial subtypes of malignant peritoneal mesothelioma.
Genes down-regulated in biphasic (mixed) vs epithelial subtypes of malignant peritoneal mesothelioma.
Genes up-regulated in blood vessel cells from wound site.
Genes down-regulated in blood vessel cells from wound site.
Genes up-regulated in Jurkat cells (transformed T lymphocytes) after knockdown of BCL11B [Gene ID=64919] by RNAi.
Genes down-regulated in Jurkat cells (transformed T lymphocytes) after knockdown of BCL11B [Gene ID=64919] by RNAi.
Genes up-regulated in Cockayne syndrome fibroblasts rescued by expression of ERCC6 [Gene ID=2074] off a plasmid vector.
Genes down-regulated in Cockayne syndrome fibroblasts rescued by expression of ERCC6 [Gene ID=2074] off a plasmid vector.
Genes up-regulated in primary endothelial cells (HUVEC) after knockdown of WTAP [Gene ID=9589] by RNAi.
Genes down-regulated in primary endothelial cells (HUVEC) after knockdown of WTAP [Gene ID=9589] by RNAi.
Genes up-regulated in leukemic stem cells (LSC), defined as CD34+CD38- [Gene ID=947, 952] cells from AML (acute myeloid leukemia patients) compared to the CD34+CD38+ cells.
Genes down-regulated in leukemic stem cells (LSC), defined as CD34+CD38- [Gene ID=947, 952] cells from AML (acute myeloid leukemia patients) compared to the CD34+CD38+ cells.
Genes down-regulated in adult T-cell leukemia (ATL), chronic vs acute clinical condition.
Genes up-regulated in SKOC-3 cells (ovarian cancer) after YB-1 (YBX1) [Gene ID=4904] knockdown by RNAi.
Genes down-regulated in SKOC-3 cells (ovarian cancer) after YB-1 (YBX1) [Gene ID=4904] knockdown by RNAi.
Cellular proliferation, growth, apoptosis and Wnt signaling genes up-regulated in SNU638 cells (gastric cancer) by overexpression of SFRP2 [Gene ID=6423] off a plasmid vector.
Cellular proliferation, growth, apoptosis and Wnt signaling genes up-regulated in SNU638 cells (gastric cancer) by overexpression of SFRP2 [Gene ID=6423] off a plasmid vector.
Genes positively correlated with the asbestos exposure of lung cancer patients.
Genes negatively correlated with the asbestos exposure of lung cancer patients.
Genes up-regulated in HCT8/S1 cells (colon cancer) which normally lack DCC [Gene ID=9423] compared to those stably expressing wild type DCC off a plasmid vector.
Genes down-regulated in HCT8/S1 cells (colon cancer) which normally lack DCC [Gene ID=9423] compared to those stably expressing wild type DCC off a plasmid vector.
Genes up-regulated in HCT8/S11 cells (colon cancer) engineered to stably express NTN1 [Gene ID=1630] off a plasmid vector.
Genes down-regulated in HCT8/S11 cells (colon cancer) engineered to stably express NTN1 [Gene ID=1630] off a plasmid vector.
Genes up-regulated in MCF7 cells (breast cancer) engineered to conditionally express LMO4 [Gene ID=8543] by a Tet Off system.
Genes down-regulated in MCF7 cells (breast cancer) engineered to conditionally express LMO4 [Gene ID=8543] by a Tet Off system.
Genes up-regulated in MCF7 cells (breast cancer) engineered to conditionally express a dominant negative form of CLIM2 [Gene ID=8861] by a Tet Off system.
Genes down-regulated in MCF7 cells (breast cancer) engineered to conditionally express a dominant negative form of CLIM2 [Gene ID=8861] by a Tet Off system.
Up-regulated genes distinguishing between two subtypes of gastric cancer: advanced (AGC) and early (EGC).
Down-regulated genes distinguishing between two subtypes of gastric cancer: advanced (AGC) and early (EGC).
Up-regulated genes distinguishing between early gastric cancer (EGC) and normal tissue samples.
Down-regulated genes distinguishing between early gastric cancer (EGC) and normal tissue samples.
Up-regulated genes from the 70-gene prognosis predictor for stage 2 colon cancer, based on non-neoplastic mucosa gene expression profiles.
Down-regulated genes from the 70-gene prognosis predictor for stage 2 colon cancer, based on non-neoplastic mucosa gene expression profiles.
Genes up-regulated in circulating endothelial cells (CEC) from cancer patients compared to those from healthy donors.
Genes down-regulated in circulating endothelial cells (CEC) from cancer patients compared to those from healthy donors.
Genes up-regulated in head and neck squamous cell carcinoma (HNSCC) samples positive for HPV compared to the HPV-negative tumors.
Genes up-regulated in metastases from malignant melanoma compared to the primary tumors.
Genes down-regulated in metastases from malignant melanoma compared to the primary tumors.
Genes up-regulated in blood samples from bladder cancer patients.
Genes down-regulated in blood samples from bladder cancer patients.
Genes up-regulated in non-metastatic breast cancer tumors having type 1 amplification in the 20q13 region; involves ZNF217 [Gene ID=7764] locus only.
Genes down-regulated in non-metastatic breast cancer tumors having type 1 amplification in the 20q13 region; involves ZNF217 [Gene ID=7764] locus only.
Genes up-regulated in metastatic breast cancer tumors having  type 2 amplification in the 20q13 region; involves MYBL2, STK6 and ZNF217 [Gene ID=4605, 6790, 7764]
Genes down-regulated in metastatic breast cancer tumors having  type 2 amplification in the 20q13 region; involves MYBL2, STK6 and ZNF217 [Gene ID=4605, 6790, 7764]
Genes up-regulated in hematopoietic stem cells (HSC, CD34+ [Gene ID=947]) cultured in a three-dimentional collagen gel compared to the cells grown in suspension.
Genes down-regulated in hematopoietic stem cells (HSC, CD34+ [Gene ID=947]) cultured in a three-dimentional collagen gel compared to the cells grown in suspension.
Genes from the yellow module which are up-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the yellow module which are down-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the turquoise module which are up-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphocholine (oxPAPC).
Genes from the turquoise module which are down-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphocholine (oxPAPC).
Genes from the red module which are up-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the red module which are down-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the magenta module which are up-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the magenta module which are down-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the lightyellow module which are up-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the lightyellow module which are down-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the green module which are up-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the green module which are down-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the blue module which are up-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the blue module which are down-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the black module which are up-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the black module which are down-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the grey module which are up-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Genes from the grey module which are down-regulated in HAEC cells (primary aortic endothelium) after exposure to the oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycerophosphorylcholine (oxPAPC).
Up-regulated genes detecting gender effects in global expression profiling studies.
Down-regulated genes detecting gender effects in global expression profiling studies.
Genes up-rgulated in CD34+ [Gene ID=947] hematopoetic cells by expression of NUP98-HOXA9 fusion [Gene ID=4928, 3205] off a retroviral vector at 6h.
Genes down-rgulated in CD34+ [Gene ID=947] hematopoetic cells by expression of NUP98-HOXA9 fusion [Gene ID=4928, 3205] off a retroviral vector at 6h.
Genes up-regulated in CD34+ [Gene ID=947] hematopoetic cells by expression of NUP98-HOXA9 fusion [Gene ID=4928, 3205] off a retroviral vector at 3 days after transduction.
Genes down-regulated in CD34+ [Gene ID=947] hematopoetic cells by expression of NUP98-HOXA9 fusion [Gene ID=4928, 3205] off a retroviral vector at 3 days after transduction.
Genes up-regulated in CD34+ [Gene ID=947] hematopoetic cells by expression of NUP98-HOXA9 fusion [Gene ID=4928, 3205] off a retroviral vector at 8 days after transduction.
Genes down-regulated in CD34+ [Gene ID=947] hematopoetic cells by expression of NUP98-HOXA9 fusion [Gene ID=4928, 3205] off a retroviral vector at 8 days after transduction.
Genes up-regulated in CD34+ [Gene ID=947] hematopoetic cells by expression of NUP98-HOXA9 fusion [Gene ID=4928, 3205] off a retroviral vector at 10 days after transduction.
Genes down-regulated in CD34+ [Gene ID=947] hematopoetic cells by expression of NUP98-HOXA9 fusion [Gene ID=4928, 3205] off a retroviral vector at 10 days after transduction.
Genes up-regulated in CD34+ [Gene ID=947] hematopoetic cells by expression of NUP98-HOXA9 fusion [Gene ID=4928, 3205] off a retroviral vector at 16 days after transduction.
Genes down-regulated in CD34+ [Gene ID=947] hematopoetic cells by expression of NUP98-HOXA9 fusion [Gene ID=4928, 3205] off a retroviral vector at 16 days after transduction.
Top genes higher expressed in short term mesothelioma survivors.
Top genes higher expressed in long term mesothelioma survivors.
Genes up-regulated in ALL (acute lymphoblastic leukemia) patients who developed t-ML (treatment related myeloid leukemia).
Genes down-regulated in ALL (acute lymphoblastic leukemia) patients who developed t-ML (treatment related myeloid leukemia).
Genes up-regulated in B-CLL (B-cell chronic leukemia) samples expressing high levels of LPL [Gene ID=4023] compared with those expressing low levels of the gene.
Genes down-regulated in B-CLL (B-cell chronic leukemia) samples expressing high levels of LPL [Gene ID=4023] compared with those expressing low levels of the gene.
Genes up-regulated in the common lymphoid progenitor (CLP, defined as CD34+CD38-CD7+ [Gene ID=947, 952, 924]) compared to a multipotent cord blood cell (defined as CD34+CD38+CD7-).
Genes down-regulated in the common lymphoid progenitor (CLP, defined as CD34+CD38-CD7+ [Gene ID=947, 952, 924]) compared to a multipotent cord blood cell (defined as CD34+CD38+CD7-).
Genes up-regulated in CD38+ [Gene ID=952] CLL (chronic lymphocytic leukemia) cells.
Genes down-regulated in CD38+ [Gene ID=952] CLL (chronic lymphocytic leukemia) cells.
Genes up-regulated in WE17/10 cells (CD4+ [Gene ID=920] T lymphocytes) infected by HTLV1 (and thus displaying low CD7 [Gene ID=924]) compared to the uninfected (i.e., CD7+) cells.
Genes down-regulated in WE17/10 cells (CD4+ [Gene ID=920] T lymphocytes) infected by HTLV1 (and thus displaying low CD7 [Gene ID=924]) compared to the uninfected (i.e., CD7+) cells.
Genes up-regulated in ALL (acute lymphoblastic leukemia) blasts after 1 week of treatment with glucocorticoids.
Genes down-regulated in ALL (acute lymphoblastic leukemia) blasts after 1 week of treatment with glucocorticoids.
The 'NPM1-mutated signature 1': genes up-regulated in pediatric AML (acute myeloid leukemia) samples with mutated NPM1 [Gene ID=4869] compared to all AML cases with the intact gene.
The 'NPM1-mutated signature 1': genes down-regulated in pediatric AML (acute myeloid leukemia) samples with mutated NPM1 [Gene ID=4869] compared to all AML cases with the intact gene.
The 'NPM1-mutated signature 2': genes up-regulated in pediatric AML (acute myeloid leukemia) samples with mutated NPM1 [Gene ID=4869] compared to the AML cases with the intact gene and without recurring cytogenetic anomalities or M7 phenotype.
The 'NPM1-mutated signature 2': genes down-regulated in pediatric AML (acute myeloid leukemia) samples with mutated NPM1 [Gene ID=4869] compared to the AML cases with the intact gene and without recurring cytogenetic anomalities or M7 phenotype.
The 'MLL signature 1': genes up-regulated in pediatric AML (acute myeloid leukemia) with rearranged MLL [Gene ID=4297] compared to all AML cases with the intact gene.
The 'MLL signature 1': genes down-regulated in pediatric AML (acute myeloid leukemia) with rearranged MLL [Gene ID=4297] compared to all AML cases with the intact gene.
The 'MLL signature 2': genes up-regulated in pediatric AML (acute myeloid leukemia) with rearranged MLL [Gene ID=4297] compared to the AML cases with intact MLL and NPM1 [Gene ID=4869].
The 'MLL signature 2': genes down-regulated in pediatric AML (acute myeloid leukemia) with rearranged MLL [Gene ID=4297] compared to the AML cases with intact MLL and NPM1 [Gene ID=4869].
The 'NPM1 signature 3': genes up-regulated in pediatric AML (acute myeloid leukemia) with mutated NPM1 [Gene ID=4869] compared to the AML cases with intact NPM1 and MLL [[Gene ID=4297].
The 'NPM1 signature 3': genes down-regulated in pediatric AML (acute myeloid leukemia) with mutated NPM1 [Gene ID=4869] compared to the AML cases with intact NPM1 and MLL [[Gene ID=4297].
Genes up-regulated by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion protein in normal hematopoietic progenitors; their expression was sustained in subsequently developing granulocytes.
Genes down-regulated by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion protein in normal hematopoietic progenitors; their expression was sustained in subsequently developing granulocytes.
Genes up-regulated in normal hematopoietic progenitors by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion.
Genes down-regulated in normal hematopoietic progenitors by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion.
Genes up-regulated in granulocytes by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion.
Genes down-regulated in granulocytes by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion.
Genes up-regulated in monocytes by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion.
Genes down-regulated in monocytes by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion.
Genes up-regulated in erythroid lineage cells by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion .
Genes down-regulated in erythroid lineage cells by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion .
Genes up-regulated by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion protein in normal hematopoietic progenitors; their expression was sustained in subsequently developing monocytes.
Genes down-regulated by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion protein in normal hematopoietic progenitors; their expression was sustained in subsequently developing monocytes.
Genes up-regulated by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion protein in normal hematopoietic progenitors; their expression was sustained in subsequently developing erythroid lineage.
Genes down-regulated by RUNX1-RUNX1T1 [Gene ID=861, 862] fusion protein in normal hematopoietic progenitors; their expression was sustained in subsequently developing erythroid lineage.
Genes higher expressed in the worst 25 mesothelioma survivors compared to the 25 best ones.
Genes higher expressed in the best 25 mesothelioma survivors compared to the 25 worst ones.
Genes up-regulated in unstable ateroslerotic plaques compared to the stable ones.
Genes down-regulated in unstable ateroslerotic plaques compared to the stable ones.
Genes up-regulated in MDA-MB-231 cells (breast cancer) after knockdown of PTHLH [Gene ID=5744] by RNAi.
Genes down-regulated in MDA-MB-231 cells (breast cancer) after knockdown of PTHLH [Gene ID=5744] by RNAi.
Genes up-regulated in HeLa cells after knockdown of MED1 [Gene ID=5469] by RNAi.
Genes down-regulated in HeLa cells after knockdown of MED1 [Gene ID=5469] by RNAi.
Genes up-regulated in P493-6 cells (B lymphocyte) upon knockdown of TFRC [Gene ID=7037] by RNAi.
Genes dpwn-regulated in P493-6 cells (B lymphocyte) upon knockdown of TFRC [Gene ID=7037] by RNAi.
Genes up-regulated in P493-6 cells (B lymphocyte) by MYC [Gene ID=4609] and down-regulated by RNAi knockdown of TFRC [Gene ID=7037].
Genes down-regulated in P493-6 cells (B lymphocyte) by MYC [Gene ID=4609] and up-regulated by RNAi knockdown of TFRC [Gene ID=7037].
Genes up-regulated in U2OS cells (osteosarcoma) upon knockdown of HDAC1 [Gene ID=3065] by RNAi.
Genes down-regulated in U2OS cells (osteosarcoma) upon knockdown of HDAC1 [Gene ID=3065] by RNAi.
Genes up-regulated in U2OS cells (osteosarcoma) upon knockdown of both HDAC1 and HDAC2 [Gene ID=3065, 3066] by RNAi.
Genes down-regulated in U2OS cells (osteosarcoma) upon knockdown of both HDAC1 and HDAC2 [Gene ID=3065, 3066] by RNAi.
Genes up-regulated in U2OS cells (osteosarcoma) upon knockdown of HDAC2 [Gene ID=3066] by RNAi.
Genes down-regulated in U2OS cells (osteosarcoma) upon knockdown of HDAC2 [Gene ID=3066] by RNAi.
Genes up-regulated in U2OS cells (osteosarcoma) upon knockdown of HDAC3 [Gene ID=8841] by RNAi.
Genes down-regulated in U2OS cells (osteosarcoma) upon knockdown of HDAC3 [Gene ID=8841] by RNAi.
Genes up-regulated in the neural crest stem cells (NCS), defined as p75+/HNK1+ [Gene ID=4804, 27087].
Genes down-regulated in the neural crest stem cells (NCS), defined as p75+/HNK1+ [Gene ID=4804, 27087].
Up-regulated genes constituting the molecular signature of Burkitt 's lymphoma.
Down-regulated genes constituting the molecular signature of Burkitt 's lymphoma.
Genes up-regulated in Caco-2 cells (intestinal epithelium) after coculture with the probiotic bacteria L. casei for 2h.
Genes down-regulated in Caco-2 cells (intestinal epithelium) after coculture with the probiotic bacteria L. casei for 2h.
Genes up-regulated in Caco-2 cells (intestinal epithelium) after coculture with the probiotic bacteria L. casei for 6h.
Genes down-regulated in Caco-2 cells (intestinal epithelium) after coculture with the probiotic bacteria L. casei for 6h.
Genes up-regulated in Caco-2 cells (intestinal epithelium) after coculture with the probiotic bacteria L. casei for 24h.
Genes down-regulated in Caco-2 cells (intestinal epithelium) after coculture with the probiotic bacteria L. casei for 24h.
Genes up-regulated in macrophages by P.gingivalis FimA pathogen.
Genes down-regulated in macrophages by P.gingivalis FimA pathogen.
Genes up-regulated in macrophages by P.gingivalis LPS (lipopolysaccharide).
Genes down-regulated in macrophages by P.gingivalis LPS (lipopolysaccharide).
Genes up-regulated in TC71 and EWS502 cells (Ewing's sarcoma) upon knockdown of the EWSR1-FLII fusion [Gene ID=2130, 2314].
Genes down-regulated in TC71 and EWS502 cells (Ewing's sarcoma) upon knockdown of the EWSR1-FLII fusion [Gene ID=2130, 2314].
A selection of genes whose expression displayed significant positive correlation with size of colorectal adenoma.
A selection of genes whose expression displayed significant negative correlation with size of colorectal adenoma.
Genes up-regulated in colorectal adenoma compared to normal mucosa samples.
Genes down-regulated in colorectal adenoma compared to normal mucosa samples.
Genes up-regulated in HB2 cells (mammary epithelium) upon expression of KDM5B [Gene ID=10765] off an adenoviral vector.
Genes down-regulated in HB2 cells (mammary epithelium) upon expression of KDM5B [Gene ID=10765] off an adenoviral vector.
Genes up-regulated in MCF7 cells (breast cancer) after stimulation with NRG1 [Gene ID=3084].
Genes down-regulated in MCF7 cells (breast cancer) after stimulation with NRG1 [Gene ID=3084].
Genes up-regulated in MCF7 cells (breast cancer) after stimulation with EGF [Gene ID=1950].
Genes up-regulated in UB27 cells (osteosarcoma) at any time point after inducing the expression of a mutant form of WT1 [Gene ID=7490].
Genes down-regulated in UB27 cells (osteosarcoma) at any time point after inducing the expression of a mutant form of WT1 [Gene ID=7490].
Genes up-regulated in UB27 cells (osteosarcoma) at 8 hr after inducing the expression of a mutant form of WT1 [Gene ID=7490].
Genes down-regulated in UB27 cells (osteosarcoma) at 8 hr after inducing the expression of a mutant form of WT1 [Gene ID=7490].
Genes up-regulated in UB27 cells (osteosarcoma) at 12 hr after inducing the expression of a mutated form of WT1 [Gene ID=7490].
Genes down-regulated in UB27 cells (osteosarcoma) at 12 hr after inducing the expression of a mutated form of WT1 [Gene ID=7490].
Genes up-regulated in MCF7 cells (breast cancer) under hypoxia conditions.
Genes down-regulated in MCF7 cells (breast cancer) under hypoxia conditions.
Genes up-regulated in MCF7 cells (breast cancer) treated with hypoxia mimetic DMOG [PubChem=3080614].
Genes down-regulated in MCF7 cells (breast cancer) treated with hypoxia mimetic DMOG [PubChem=3080614].
Genes up-regulated in MCF7 cells (breast cancer) after knockdown of HIF1A [Gene ID=3091] by RNAi.
Genes down-regulated in MCF7 cells (breast cancer) after knockdown of HIF1A [Gene ID=3091] by RNAi.
Genes up-regulated in MCF7 cells (breast cancer) after knockdown of HIF2A [Gene ID=2034] by RNAi.
Genes up-regulated in MCF7 cells (breast cancer) after knockdown of both HIF1A and HIF2A [Gene ID=3091, 2034] by RNAi.
Genes down-regulated in MCF7 cells (breast cancer) after knockdown of both HIF1A and HIF2A [Gene ID=3091, 2034] by RNAi.
Genes up-regulated in CD133+ [Gene ID=8842] cells (hematopoietic stem cells, HSC) compared to the CD133- cells.
Genes up-regulated in CD133+ [Gene ID=8842] cells (hematopoietic stem cells, HSC) compared to the CD133- cells.
Genes up-regulated in FSHD (facioscapulohumeral muscular dystrophy) mesoangioblasts.
Genes down-regulated in FSHD (facioscapulohumeral muscular dystrophy) mesoangioblasts.
Genes up-regulated in quiescent (G0) vs dividing (M) CD34+ [Gene ID=8842] cells isolated from peripheral blood of CML (chronic myeloid leukemia) patients.
Genes down-regulated in quiescent (G0) vs dividing (M) CD34+ [Gene ID=8842] cells isolated from peripheral blood of CML (chronic myeloid leukemia) patients.
Genes up-regulated in quiescent (G0) CD34+ [Gene ID=8842] cells isolated from peripheral blood of CML (chronic myeloid leukemia) patients compared to the quiescent cells from normal donors.
Genes down-regulated in quiescent (G0) CD34+ [Gene ID=8842] cells isolated from peripheral blood of CML (chronic myeloid leukemia) patients compared to the quiescent cells from normal donors.
Genes up-regulated in quescent CD34+ [Gene ID=8842] cells isolated from peripheral blood of CML (chronic myeloblastic leukemia) patients compared to the dividing cells from normal donors.
Genes down-regulated in quescent CD34+ [Gene ID=8842] cells isolated from peripheral blood of CML (chronic myeloblastic leukemia) patients compared to the dividing cells from normal donors.
Genes up-regulated in dividing CD34+ [Gene ID=8842] cells isolated from peripheral blood of CML (chronic myeloid leukemia) patients compared to the dividing cells from normal donors.
Genes down-regulated in dividing CD34+ [Gene ID=8842] cells isolated from peripheral blood of CML (chronic myeloid leukemia) patients compared to the dividing cells from normal donors.
Genes up-regulated in quiescent CD34+ [Gene ID=8842] cells isolated from peripheral blood of normal donors compared to the dividing cells from CML (chronic myeloid leukemia) patients.
Genes down-regulated in quiescent CD34+ [Gene ID=8842] cells isolated from peripheral blood of normal donors compared to the dividing cells from CML (chronic myeloid leukemia) patients.
Genes up-regulated in quiescent vs dividing CD34+ [Gene ID=8842] cells isolated from peripheral blood of normal donors.
Genes down-regulated in quiescent vs dividing CD34+ [Gene ID=8842] cells isolated from peripheral blood of normal donors.
Genes up-regulated in endometroid endometrial tumors from patients with lymph node metastases compared to those without the metastases.
Genes down-regulated in endometroid endometrial tumors from patients with lymph node metastases compared to those without the metastases.
Genes up-regulated in mucinous ovarian carcinoma tumors of low malignant potential (LMP) compared to normal ovarian surface epithelium tissue.
Genes down-regulated in mucinous ovarian carcinoma tumors of low malignant potential (LMP) compared to normal ovarian surface epithelium tissue.
Genes up-regulated in mucinous ovarian carcinoma tumors of grades 1 and 2 compared to the normal ovarian survace epithelium tissue.
Genes down-regulated in mucinous ovarian carcinoma tumors of grades 1 and 2 compared to the normal ovarian survace epithelium tissue.
Genes up-regulated in H720 cells (lung cancer) after treatment with L663536 (MK886) [PubChem=105049], an inhibitor of leukotriene biosynthesis.
Genes down-regulated in H720 cells (lung cancer) after treatment with L663536 (MK886) [PubChem=105049], an inhibitor of leukotriene biosynthesis.
Genes up-regulated in non-neoplastic rectal mucosa samples from patients having cancer associated with ulcerative collitis, compared to those who did not have the cancer.
Genes down-regulated in non-neoplastic rectal mucosa samples from patients having cancer associated with ulcerative collitis, compared to those who did not have the cancer.
Genes up-regulated in nasopharyngeal carcinoma (NPC) compared to the normal tissue.
Genes down-regulated in nasopharyngeal carcinoma (NPC) compared to the normal tissue.
Genes up-regulated in poorly differentiated thyroid carcinoma (PDTC) compared to normal thyroid tissue.
Genes down-regulated in poorly differentiated thyroid carcinoma (PDTC) compared to normal thyroid tissue.
Genes up-regulated in anaplastic thyroid carcinoma (ATC) compared to normal thyroid tissue.
Genes down-regulated in anaplastic thyroid carcinoma (ATC) compared to normal thyroid tissue.
Genes up-regulated in poorly differentiated thyroid carcinoma (PDTC) compared to anaplastic thyroid carcinoma (ATC).
Genes down-regulated in poorly differentiated thyroid carcinoma (PDTC) compared to anaplastic thyroid carcinoma (ATC).
Genes up-regulated in TMX2-28 cells (breast cancer) which do not express ESR1 [Gene ID=2099]) compared to the parental MCF7 cells which do.
Genes down-regulated in TMX2-28 cells (breast cancer) which do not express ESR1 [Gene ID=2099]) compared to the parental MCF7 cells which do.
Genes up-regulated in monocytes isolated from peripheral blood samples of Sezary syndrom patients compared to those from healthy normal donors.
Genes down-regulated in monocytes isolated from peripheral blood samples of Sezary syndrom patients compared to those from healthy normal donors.
Genes up-regulated in lesional skin biopsies from mycosis fundoides patients compared to the normal skin samples.
Genes down-regulated in lesional skin biopsies from mycosis fundoides patients compared to the normal skin samples.
Genes up-regulated in T helper cells (defines as CD4+) isolated from patients with mucosis fungoides compared to those from normal control donors.
Genes down-regulated in T helper cells (defines as CD4+) isolated from patients with mucosis fungoides compared to those from normal control donors.
Genes up-regulated in monocytes isolated from peripheral blood samples of patients with mucosis fungoides compared to those from normal healthy donors.
Genes down-regulated in monocytes isolated from peripheral blood samples of patients with mucosis fungoides compared to those from normal healthy donors.
Genes up-regulated in polysomal and total RNA samples from SW480 cells (primary colorectal carcinoma, CRC) compared to the SW620 cells (lymph node metastasis from the same individual).
Genes down-regulated in polysomal and total RNA samples from SW480 cells (primary colorectal carcinoma, CRC) compared to the SW620 cells (lymph node metastasis from the same individual).
Genes up-regulated in MCF7 cells (breast cancer) by IGF1 and IGF2 [Gene ID=3479, 3481].
Genes up-regulated in HET1A cells (esophagus epithelium) engineered to stably express CDX2 [Gene ID=1045].
Genes down-regulated in HET1A cells (esophagus epithelium) engineered to stably express CDX2 [Gene ID=1045].
Genes up-regulated in NSCLC (non-small cell lung carcinoma) cell lines resistant to gefitinib [PubChem=123631] compared to the sensitive ones.
Genes down-regulated in NSCLC (non-small cell lung carcinoma) cell lines resistant to gefitinib [PubChem=123631] compared to the sensitive ones.
Genes up-regulated in MEWO cells (melanoma) after 48h of methionine [PubChem=876] deprivation.
Genes down-regulated in MEWO cells (melanoma) after 48h of methionine [PubChem=876] deprivation.
Genes up-regulated in MEWO cells (melanoma) after 96 h of methionine [PubChem=876] deprivation.
Genes down-regulated in MEWO cells (melanoma) after 96 h of methionine [PubChem=876] deprivation.
Genes up-regulated in K562 (chronic myelogenous leukemia, CML) cells engineered to stably express RIZ1 [Gene ID=7799].
Genes down-regulated in K562 (chronic myelogenous leukemia, CML) cells engineered to stably express RIZ1 [Gene ID=7799].
Genes up-regulated in C666-1 cells (nasopharyngeal carcinoma) by stable expression of RASSF1 [Gene ID=11186].
Genes down-regulated in C666-1 cells (nasopharyngeal carcinoma) by stable expression of RASSF1 [Gene ID=11186].
Genes up-regulated in epidermis after to UVB irradiation.
Genes down-regulated in epidermis after to UVB irradiation.
Genes up-regulated in NHEK cells (normal epidermal keratinocytes) after UVB irradiation.
Genes down-regulated in NHEK cells (normal epidermal keratinocytes) after UVB irradiation.
Genes up-regulated in preneoplastic mammary tissues and whose expression is maintained in tumors.
Genes down-regulated in preneoplastic mammary tissues and whose expression is maintained in tumors.
Genes down-regulated in MEF cells (embryonic fibroblasts) with TERT [Gene ID=7015] knockout, after expression of the gene off a retroviral vector.
Transcription factors down-regulated in LNCaP cells (prostate cancer) by expression of GR [Gene ID=2908] off a lentiviral vector.
Genes up-regulated by UV-irradiation in cervical cancer cells after knockdown of CDKN2A [Gene ID=1029].
Genes down-regulated by UV-irradiation in cervical cancer cells after knockdown of CDKN2A [Gene ID=1029].
Genes up-regulated in papillary thyroid carcinoma (PTC) compared to normal tissue.
Genes down-regulated in papillary thyroid carcinoma (PTC) compared to normal tissue.
Genes up-regulated in NIH3T3 cells (fibroblasts) transformed by activated KRAS [Gene ID=3845] vs those reverted to normal cells upon over-expression of a dominant negative form of CDC25 [Gene ID=5923].
Genes down-regulated in NIH3T3 cells (fibroblasts) transformed by activated KRAS [Gene ID=3845] vs those reverted to normal cells upon over-expression of a dominant negative form of CDC25 [Gene ID=5923].
Genes up-regulated in transformed NIH3T3 cells (fibroblasts transformed by activated KRAS [Gene ID=3845]) vs normal cells.
Genes down-regulated in transformed NIH3T3 cells (fibroblasts transformed by activated KRAS [Gene ID=3845]) vs normal cells.
Genes up-regulated in reverted NIH3T3 cells (fibroblasts transformed by activated KRAS [Gene ID=3845] which then reverted to normal cells upon stable over-expression of a dominant negative form of CDC25 [Gene ID=5923]) vs normal fibroblasts.
Genes down-regulated in reverted NIH3T3 cells (fibroblasts transformed by activated KRAS [Gene ID=3845] which then reverted to normal cells upon stable over-expression of a dominant negative form of CDC25 [Gene ID=5923]) vs normal fibroblasts.
Genes up-regulated in MEF cells (embryonic fibroblast) isolated from HRAS [Gene ID=3265] knockout mice.
Genes down-regulated in MEF cells (embryonic fibroblast) isolated from HRAS [Gene ID=3265] knockout mice.
Genes up-regulated in MEF cells (embryonic fibroblasts) isolated from HRAS [Gene ID=3265] and NRAS [Gene ID=4893] double knockout mice.
Genes down-regulated in MEF cells (embryonic fibroblasts) isolated from HRAS [Gene ID=3265] and NRAS [Gene ID=4893] double knockout mice.
Genes up-regulated in MEF cells (embryonic fibroblast) isolated from NRAS [Gene ID=4893] knockout mice.
Genes down-regulated in MEF cells (embryonic fibroblast) isolated from NRAS [Gene ID=4893] knockout mice.
Genes up-regulated in follicular epithelial stem cells after transgenic expression of GR [Gene ID=2908] under control of the keratin5 (K5) [Gene ID=3852] promoter.
Genes down-regulated in follicular epithelial stem cells after transgenic expression of GR [Gene ID=2908] under control of the keratin5 (K5) [Gene ID=3852] promoter.
Genes up-regulated in NIH3T3 cells (fibroblasts) after treatment with Y27632 [PubChem=123862], an inhibitor of ROCK proteins; the changes did not depend on expression of constitutively active (Q63L) form of RHOA [Gene ID=387].
Genes down-regulated in NIH3T3 cells (fibroblasts) after treatment with Y27632 [PubChem=123862], an inhibitor of ROCK proteins; the changes did not depend on expression of constitutively active (Q63L) form of RHOA [Gene ID=387].
Genes up-regulated in NIH3T3 cells (fibroblasts) transformed by  expression of contitutively active (Q63L) form of RHOA [Gene ID=387] off plasmid vector; their expression reverted completely after treatment with Y27632 [PubChem=123862], an inhibitor of ROCK proteins.
Genes down-regulated in NIH3T3 cells (fibroblasts) transformed by  expression of contitutively active (Q63L) form of RHOA [Gene ID=387] off plasmid vector; their expression reverted completely after treatment with Y27632 [PubChem=123862], an inhibitor of ROCK proteins.
Genes whose expression profile is specific to Custer I of urothelial cell carcinoma (UCC) tumors.
Genes whose expression profile is specific to Custer I of urothelial cell carcinoma (UCC) tumors.
Genes whose expression profile is specific to Cluster IIa of urothelial cell carcinoma (UCC) tumors.
Genes whose expression profile is specific to Cluster IIa of urothelial cell carcinoma (UCC) tumors.
Genes whose expression profile is specific to Cluster III of urothelial cell carcinoma (UCC) tumors.
Genes whose expression profile is specific to Cluster III of urothelial cell carcinoma (UCC) tumors.
Genes down-regulated in colorectal carcinoma samples positive for MSI (microsatellite instability) compared to the MSI negative ones.
Genes in the AKT1 [Gene ID=207] pathway which are independent of MTOR [Gene ID=2475], insensitive to RAD001 (everolimus) [PubChem=6442177].
Genes in the AKT1 [Gene ID=207] pathway which depend on MTOR [Gene ID=2475], sensitive to RAD001 (everolimus) [PubChem=6442177].
Up-regulated genes in the breast cancer prognostic signature of 70 genes that significantly correlated with survival.
Down-regulated genes in the breast cancer prognostic signature of 70 genes that significantly correlated with survival.
Genes up-regulated in MEF cells (embryonic fibroblasts) isolated from RB1 [Gene ID=5925] knockout mice: chronic loss of function (LOF) of RB1.
Genes down-regulated in MEF cells (embryonic fibroblasts) isolated from RB1 [Gene ID=5925] knockout mice: chronic loss of function (LOF) of RB1.
Genes up-regulated in adult fibroblasts with inactivated RB1 [Gene ID=5925] by Cre-lox: acute loss of function (LOF) of RB1.
Genes down-regulated in adult fibroblasts with inactivated RB1 [Gene ID=5925] by Cre-lox: acute loss of function (LOF) of RB1.
Genes from common regions of gains observed in more than 15% of 148 primary breast cancer tumors.
Genes from common regions of losses observed in more than 15% of 148 primary breast cancer tumors.
Genes up-regulated in uterine fibroids vs normal myometrium samples.
Genes down-regulated in uterine fibroids vs normal myometrium samples.
Genes up-regulated in uterine fibroids with deletions in the 7q region vs those without the deletion.
Genes down-regulated in uterine fibroids with deletions in the 7q region vs those without the deletion.
The 65 most significantly changed (p<0.01) genes out of the 324 genes identified by two analytical methods in the mammary tumors induced by transgenic expression of ERBB2 [Gene ID=2064].
The 65 most significantly changed (p<0.01) genes out of the 324 genes identified by two analytical methods in the mammary tumors induced by transgenic expression of ERBB2 [Gene ID=2064].
The 82 genes out of the 324-gene signature that changed in  the pre-neoplastic tissue adjacent to the mammary tumors induced by transgenic expression of ERBB2 [Gene ID=2064].
The 82 genes out of the 324-gene signature that changed in  the pre-neoplastic tissue adjacent to the mammary tumors induced by transgenic expression of ERBB2 [Gene ID=2064].
Genes up-regulated in SH-SY5Y cells (neuroblastoma) after treatment with epoxomicin [PubChem=3035402], a protease inhibitor causing apoptosis.
Genes down-regulated in SH-SY5Y cells (neuroblastoma) after treatment with epoxomicin [PubChem=3035402], a protease inhibitor causing apoptosis.
Up-regulated genes in the signature set for lymph node metastasis in head and neck squamous cell carcinoma (HNSCC).
Down-regulated genes in the signature set for lymph node metastasis in head and neck squamous cell carcinoma (HNSCC).
Up-regulated genes from the set B (Fig. 5a): specific signature shared by cells expressing either AF4-MLL or MLL-AF4 [Gene ID=4299, 4297] fusion proteins.
Down-regulated genes from the set B (Fig. 5a): specific signature shared by cells expressing either AF4-MLL or MLL-AF4 [Gene ID=4299, 4297] fusion proteins.
Up-regulated genes from the set D (Fig. 5a): specific signature shared by cells expressing MLL-AF4 [Gene ID=4297, 4299] alone and those expressing both MLL-AF4 and AF4-MLL fusion proteins.
Down-regulated genes from the set D (Fig. 5a): specific signature shared by cells expressing MLL-AF4 [Gene ID=4297, 4299] alone and those expressing both MLL-AF4 and AF4-MLL fusion proteins.
Up-regulated genes from the set E (Fig. 5a): specific signature shared by cells expressing either MLL-AF4 [Gene ID=4297, 4299] or AF4-MLL fusion proteins alone, and those expressing both fusion proteins.
Down-regulated genes from the set E (Fig. 5a): specific signature shared by cells expressing either MLL-AF4 [Gene ID=4297, 4299] or AF4-MLL fusion proteins alone, and those expressing both fusion proteins.
Up-regualted genes from the set F (Fig. 5a): specific signature shared by cells expressing AF4-MLL [Gene ID=4299, 4297] alone and those expressing both AF4-MLL and MLL-AF4 fusion proteins.
Down-regualted genes from the set F (Fig. 5a): specific signature shared by cells expressing AF4-MLL [Gene ID=4299, 4297] alone and those expressing both AF4-MLL and MLL-AF4 fusion proteins.
Up-regulated genes from the set G (Fig. 5a): specific to cells expressing both MLL-AF4 [Gene ID=4297, 4299] and AF4-MLL fusion proteins.
Down-regulated genes from the set G (Fig. 5a): specific to cells expressing both MLL-AF4 [Gene ID=4297, 4299] and AF4-MLL fusion proteins.
Genes up-regulated in NIH3T3 cells (fibroblasts) transfrormed by expression of constitutively active (Q63L) form of RHOA [Gene ID=387] off plasmid vector; their expression did NOT reverted completely after treatment with Y27632 [PubChem=123862], an inhibitor of ROCK proteins.
Genes down-regulated in NIH3T3 cells (fibroblasts) transfrormed by expression of constitutively active (Q63L) form of RHOA [Gene ID=387] off plasmid vector; their expression did NOT reverted completely after treatment with Y27632 [PubChem=123862], an inhibitor of ROCK proteins.
Genes up-regulated in epithelial ovarian cancer (EOC) biopsies: invasive (TOV) vs low malignant potential (LMP) tumors.
Genes down-regulated in epithelial ovarian cancer (EOC) biopsies: invasive (TOV) vs low malignant potential (LMP) tumors.
The 324 genes identified by two analytical methods as changed in the mammary tumors induced by transgenic expression of ERBB2 [Gene ID=2064].
The 324 genes identified by two analytical methods as changed in the mammary tumors induced by transgenic expression of ERBB2 [Gene ID=2064].
Up-regulated genes in non-neoplastic mucosa samples from colon cancer patients who developed recurrence of the disease.
Down-regulated genes in non-neoplastic mucosa samples from colon cancer patients who developed recurrence of the disease.
Up-regulated genes in tumor samples from colon cancer patients who developed recurrence of the disease.
Down-regulated genes in tumor samples from colon cancer patients who developed recurrence of the disease.
Genes up-regulated in oncocytic follicular carcinoma (FTC) vs mitochondrial-rich papillary carcinoma (PTC) types of thyroid cancer.
Genes down-regulated in oncocytic follicular carcinoma (FTC) vs mitochondrial-rich papillary carcinoma (PTC) types of thyroid cancer.
Genes up-regulated in NIH3T3 cells (fibroblasts) transformed by  expression of contitutively active (Q63L) form of RHOA [Gene ID=387] off plasmid vector.
Genes down-regulated in NIH3T3 cells (fibroblasts) transformed by  expression of contitutively active (Q63L) form of RHOA [Gene ID=387] off plasmid vector.
Candidate genes in the regions of copy number gain in gastric cancer cell lines.
Candidate genes in the regions of copy number loss in gastric cancer cell lines.
Genes up-regulated in esophageal adenocarcinoma (EAC) and Barret's esophagus (BE) relative to normal esophagi.
Genes down-regulated in esophageal adenocarcinoma (EAC) and Barret's esophagus (BE) relative to normal esophagi.
Genes genes up-regulated in NT2/D1 cells (embryonal carcinoma) in response to treatment with cisplatin [PubChem=2767].
Genes genes down-regulated in NT2/D1 cells (embryonal carcinoma) in response to treatment with cisplatin [PubChem=2767].
Genes up-regulated in PaCa44 and CFPAC1 cells (pancreatic cancer) after treatment with decitabine [PubChem=451668], a DNA hypomethylating agent similar to azacitidine [PubChem=9444].
Genes down-regulated in PaCa44 and CFPAC1 cells (pancreatic cancer) after treatment with decitabine [PubChem=451668], a DNA hypomethylating agent similar to azacitidine [PubChem=9444].
Genes up-regulated in WI-38 cells (senescent primary fibroblasts) after inactivation of TP53 [Gene ID=7157] by GSE56 polypeptide.
Genes down-regulated in WI-38 cells (senescent primary fibroblasts) after inactivation of TP53 [Gene ID=7157] by GSE56 polypeptide.
Genes up-regulated in Barrett's esophagus compared to the normal tissue.
Genes down-regulated in Barrett's esophagus compared to the normal tissue.
Genes specific to esophageal adenocarcinoma (EAC) relative to normal tissue.
Genes specific to esophageal adenocarcinoma (EAC) relative to normal tissue.
Candidate progression biomarkers up-regulated in transition from non-tumor-risk associated to tumor-risk associated Barrett's esophagus and then to esophageal adenocarcinoma (EAC).
Genes bound by EWSR1-FLT1 [Gene ID=2130, 2321] fusion and whose expression changed in STA-ET-7.2 cells (Ewing's sarcoma) after knockdown of EWSR1-FLT1 by RNAi.
Genes bound by EWSR1-FLT1 [Gene ID=2130, 2321] fusion and whose expression changed in STA-ET-7.2 cells (Ewing's sarcoma) after knockdown of EWSR1-FLT1 by RNAi.
Genes in discrete regions of gain within 16q region detected in individual invasive breast cancer tumors.
Genes in discrete regions of loss within 16q region detected in individual invasive breast cancer tumors.
Genes up-regulated during pubertal mammary gland development between weeks 3 and 4.
Genes down-regulated during pubertal mammary gland development between weeks 3 and 4.
Genes up-regulated during pubertal mammary gland development between week 4 and 5.
Genes down-regulated during pubertal mammary gland development between week 4 and 5.
Genes up-regulated during pubertal mammary gland development between week 5 and 6.
Genes down-regulated during pubertal mammary gland development between week 5 and 6.
Genes up-regulated during pubertal mammary gland development between week 6 and 7.
Genes down-regulated during pubertal mammary gland development between week 6 and 7.
Genes up-regulated in MDA-MB-231 cells (breast cancer) after knockdown of PRKCA and ETS1 [Gene ID=5578, 2113] by RNAi.
Genes down-regulated in MDA-MB-231 cells (breast cancer) after knockdown of PRKCA and ETS1 [Gene ID=5578, 2113] by RNAi.
Genes up-regulated in Kasumi-1 cells (acute myeloid leukaemia (AML) with the t(8;21) translocation) after knockdown of the AML1 MTG8 fusion [Gene ID=861, 862] by RNAi.
Genes down-regulated in Kasumi-1 cells (acute myeloid leukaemia (AML) with the t(8;21) translocation) after knockdown of the AML1 MTG8 fusion [Gene ID=861, 862] by RNAi.
Top genes distinguishing between follicular thyroid carcinoma (FTC) samples by the presence or absence of the PAX8-PPARG [Gene ID=7849, 5468] fusion protein.
Top genes distinguishing between follicular thyroid carcinoma (FTC) samples by the presence or absence of the PAX8-PPARG [Gene ID=7849, 5468] fusion protein.
Genes up-regulated in T1 cells (primary melanoma, sensitive to TRAIL [Gene ID=8743]) compared to G1 cells (metastatic melanoma, resistant to TRAIL).
Genes down-regulated in T1 cells (primary melanoma, sensitive to TRAIL [Gene ID=8743]) compared to G1 cells (metastatic melanoma, resistant to TRAIL).
Genes up-regulated in pirmary cultures of epithelial ovarian cancer (EOC): invasive (TOV) vs low malignant potential (LMP) tumors.
Genes down-regulated in pirmary cultures of epithelial ovarian cancer (EOC): invasive (TOV) vs low malignant potential (LMP) tumors.
Genes up-regulated in Tet-On HEK293 cells (embryonic kidney) by expression of HNF4A [Gene ID=3172].
Genes down-regulated in Tet-On HEK293 cells (embryonic kidney) by expression of HNF4A [Gene ID=3172].
Genes up-regulated in MZ128 cells (Wilms tumor with mutated WT1 [Gene ID=7490]) after treatment with 10 microM tretinoin (ATRA) [PubChem=5538] for 24 h.
Genes down-regulated in MZ128 cells (Wilms tumor with mutated WT1 [Gene ID=7490]) after treatment with 10 microM tretinoin (ATRA) [PubChem=5538] for 24 h.
Genes up-regulated in MS427 cells (Wilms tumor with normal WT1 [Gene ID=7490]) after treatment with 10 microM tretinoin (ATRA) [PubChem=5538] for 24 h.
Genes down-regulated in MS427 cells (Wilms tumor with normal WT1 [Gene ID=7490]) after treatment with 10 microM tretinoin (ATRA) [PubChem=5538] for 24 h.
Genes up-regulated in MCF10A cells (breast cancer) by expression of LSM1 [Gene ID=27257] off a letiviral vector.
Genes down-regulated in MCF10A cells (breast cancer) by expression of LSM1 [Gene ID=27257] off a letiviral vector.
Genes up-regulated in LNCaP cells (prostate cancer) after knockdown of SAM68 [Gene ID=10657] by RNAi.
Genes down-regulated in LNCaP cells (prostate cancer) after knockdown of SAM68 [Gene ID=10657] by RNAi.
Genes changed in U373-MG cells (malignant glioma) upon treatment with arsenic trioxide [PubChem=14888], a chemical that can cause autophagic cell death.
Genes up-regulated in K562 cells (bone marrow) after treatment with dasatinib [PubChem=3062316] or imatinib [PubChem=5291].
Genes down-regulated in K562 cells (bone marrow) after treatment with dasatinib [PubChem=3062316] or imatinib [PubChem=5291].
Top genes up-regulated in the GIST (gastrointestinal stromal tumor) cell line resistant to imatinib [PubChem=5291] compared to the parental cell line sensitive to the drug.
Top genes down-regulated in the GIST (gastrointestinal stromal tumor) cell line resistant to imatinib [PubChem=5291] compared to the parental cell line sensitive to the drug.
Up-regulated genes associated with the acquision of metastatic potential in LNM35 cells (large cell lung cancer).
Down-regulated genes associated with the acquision of metastatic potential in LNM35 cells (large cell lung cancer).
Cancer motility and invasion genes up-regulated by the AP-1 transcription factor.
Proteins implicated in prostate carcinogenesis.
Up-regulated genes that separate angiogenic from non-angiogenic non-small cell lung carcinoma (NSCLC) samples.
Down-regulated genes that separate angiogenic from non-angiogenic non-small cell lung carcinoma (NSCLC) samples.
Genes up-regulated in SaOS-2 cells (osteosarcoma) upon expression of PAX3-FOXO1 [Gene ID=5077, 2308] fusion protein off an adenoviral vector.
Genes down-regulated in SaOS-2 cells (osteosarcoma) upon expression of PAX3-FOXO1 [Gene ID=5077, 2308] fusion protein off an adenoviral vector.
Genes up-regulated in A375 and 397 cells (melanoma) by forced expression of PLZF [Gene ID=7704] off adenovirus vector.
Genes down-regulated in A375 and 397 cells (melanoma) by forced expression of PLZF [Gene ID=7704] off adenovirus vector.
Genes up-regulated in the 5637 cell line (bladder cancer) after knockdown of E2F3 [Gene ID=1871] by RNAi.
Genes down-regulated in the 5637 cell line (bladder cancer) after knockdown of E2F3 [Gene ID=1871] by RNAi.
Genes whose transcription is altered by histone deacetylase inhibitors.
Genes whose transcription is altered by histone deacetylase inhibitors.
Acute stage-specific genes for adult T cell leukemia (ATL).
Genes used to predict the clinical stages of acute T-cell leukemia (ATL): chronic vs acute.
Genes up-regulated in cancer endometrium samples compared to the normal endometrium.
Genes down-regulated in cancer endometrium samples compared to the normal endometrium.
Genes down-regulated in late stage (stage 3) endometrial cancers compared to the earlier stages (stage 1 and 2).
Genes down-regulated in the RCC4 cells (renal cell carcinoma, RCC) expressing VHL [Gene ID=7428] mutants Type 1 and 2B (associated with RCC) but not those of Type 2A and 2C (not associated with RCC).
Genes with hypermethylated DNA in all four esophageal squamous cell carcinoma (ESCC) lines analyzed.
RB1 [Gene ID=5925] target genes involved in cell cycle regulation: genes down-regulated by doxorubicin [PubChem=31703] only in cells expressing RB1.
Genes mutated in colon cancer cell lines, identified using the GINI method described in the paper.
Genes whose promoters bound AR [Gene ID=367] in LNCaP cells (prostate cancer) after exposure to the synthetic androgen R1881 [PubChem=13766], based on ChIP-chip analysis.
Selected gradually up-regulated genes in the TLX1 [Gene ID=3195] Tet On iEBHX15-4 cells (pro-erythroblasts).
Selected gradually up-regulated genes whose expression profile follows that of CCNE1 [Gene ID=898] in the TLX1 [Gene ID=3195] Tet On iEBHX15-4 cells (pro-erythroblasts).
Selected gradually up-regulated genes whose expression profile follows that of HBZ [Gene ID=3050] in the TLX1 [Gene ID=3195] Tet On iEBHX15-4 cells (pro-erythroblasts).
List of the transcription factors up-regulated 1 hr after wounding HDF cells (dermal fibroblasts).
Genes with copy number gains in primary neuroblastoma tumors.
Genes with copy number losses in primary neuroblastoma tumors.
Genes up-regulated in short-term cultured glioblastomas after azacitidine [PubChem=9444] treatment.
Selected gradually up-regulated genes whose expression profile follows that of HEMGN [Gene ID=55363] in the TLX1 [Gene ID=3195] Tet On iEBHX15-4 cells (pro-erythroblasts).
Selected genes whose expression profile follows that of APOBEC2 [Gene ID=10930] in the TLX1 [Gene ID=3195] Tet On iEBHX15-4 cells (pro-erythroblasts).
Selected genes down-regulated in the TLX1 [Gene ID=3195] Tet On iEBHX15-4 cells (pro-erythroblasts) at 6 h time point.
Selected genes down-regulated in the TLX1 [Gene ID=3195] Tet On iEBHX15-4 cells (pro-erythroblasts) at 12 h time point.
Genes up-regulated in Rh4 cells (alveolar rhabdomyosarcoma, ARMS) after knockdown of the PAX3-FOXO1 [Gene iD=5077, 2308] fusion protein by RNAi for 72 hr.
Genes up-regulated in the HMEC cells (primary mammary epithelium) upon expression of TP53 [Gene ID=7157] off adenoviral vector.
Genes up-regulated in the HMEC cells (primary mammary epithelium) upon expression of the transcriptionally active isoform of TP63 [Gene ID=8626] off adenoviral vector.
Genes up-regulated in HMEC cells (primary mammary epithelium) upon expression of both of TP53 [Gene ID=7157] and the transcriptionally active isoform of TP63 [Gene ID=8626] off adenoviral vectors.
DNA repair genes whose promoters contain putative ZNF143 [Gene ID=7702] binding sites.
Genes down-regulated in HCT8/S11 cells (colon cancer) which lack DCC [Gene ID=9423] and stably express NTN1 [Gene ID=1630].
Genes exclusively up-regulated in fibroblasts expressing the XP/CS mutant form of ERCC3 [Gene ID=2071] after high dose UVC irradiation.
Genes exclusively down-regulated in fibroblasts expressing the XP/CS mutant form of ERCC3 [Gene ID=2071] after high dose UVC irradiation.
Genes exclusively up-regulated in fibroblasts expressing the TTD mutant form of ERCC3 [Gene ID=2071], after UVC irradiation.
Genes exclusively down-regulated in fibroblasts expressing the TTD mutant form of ERCC3 [Gene ID=2071], after UVC irradiation.
Examples of transcription factors whose activities are regulated by MAPK1 and MAPK3 [Gene ID=5594, 5595] phosphorylation.
Examples of transcription factors whose activities are regulated by MAPK8 and MAPK9 [Gene ID=5599, 5601].
Examples of transcription factors whose activities are regulated by MAPK7 [Gene ID=5598] phosphorylation.
Examples of transcription factors whose activities are regulated by MAPK11 [Gene ID=5600] phosphorylation.
Examples of transcription factors whose activities are regulated by MAPK14 [Gene ID=1432] phosphorylation.
Genes up-regulated in the GIST (gastrointestinal stromal tumor) cell line resistant to imatinib [PubChem=5291] that may correlate with the morphological switch in these cells.
Top genes up-regulated in the GIST (gastrointestinal stromal tumor) cell line sensitive to imatinib [PubChem=5291] after treatment with MP470, a protein kinase inhibitor.
Top genes up-regulated in the GIST (gastrointestinal stromal tumor) cell line resistant to imatinib [PubChem=5291] after treatment with MP470, a protein kinase inhibitor.
Genes up-regulated in A2780 cells (ovarian carcinoma) exposed to fenretinide [PubChem=1744].
Genes down-regulated in A2780 cells (ovarian carcinoma) exposed to fenretinide [PubChem=1744].
Composition of the 2 MDa human TFTC complex containing KAT2A [Gene ID=2648].
Composition of the 2 MDa human STAGA complex containing KAT2A [Gene ID=2648].
Composition of the 2 MDa human PCAF complex.
Genes down-regulated both in vivo and in vitro upon activation of MET [Gene ID=4233] signaling.
Selected genes specifically expressed in gastric cancer.
Genes up-regulated in BJ cells (forskin fibroblasts) upon overexpression of the most abundant alternative splicing forms of MDM2 [Gene ID=4193], HDM2-A and HDM2-B, off a retroviral vector.
Growth factor signaling components up-regulated  in hepatocellular carcinoma (HCC).
Genes up-regulated in lung adenocarcinoma cell lines and not expressed in non-cancerous lung epithelial cells.
Proteins that permeabilize mitochondria.
Genes with the highest differential expression in primary tissue cultures of high grade glioma: responders vs non-responders to imatinib [PubChem=5291] treatment.
Genes identified with the Fanconi anemia (FA) and the FA pathway.
Candidate genes in genomic amplification regions in hepatocellular carcinoma (HCC) samples.
Genes encoding the NF-kB core signaling proteins.
Genes encoding substrates of IkappaB kinase (IKK) complex.
NF-kB target genes involved in the regulation of programmed cell death.
NF-kB-driven pro-inflammatory genes that are  negatively regulated by glucocorticoids.
Genes in the most frequently homozygous deleted loci in a panel of glioma cell lines.
Genes changed in xenograft tumors formed by DLD-1 or DKO-4 cells (colon cancer) overexpressing MET [Gene ID=4233].
Genes identified by subtractive hybridization comparing malignant and benign components of a hepatocellular carcinoma (HCC) in a pre-existing liver adenoma in a morphologically normal liver.
Genes changed in pre-B lymphoblastic leukemia cells with BCR-ABL1 fusion [Gene ID=613, 25] vs normal pre-B lymphocytes.
Genes in the most frequently heterozygous deleted loci of a panel of glioma cell lines.
Genes in the most frequently gained loci in a panel of glioma cell lines.
Cluster 1: ATM [Gene ID=472] dependent genes induced at 30 min after ionizing radiation treatment.
Cluster 2: late ATM [Gene ID=472] dependent genes induced by ionizing radiation treatment.
Cluster 3: genes activated by ionizing radiation regardless of ATM [Gene ID=472] status.
Cluster 4: genes repressed by ionizing radiation regardless of ATM [Gene ID=472] status.
Cluster 5: early responding genes activated in ATM [Gene ID=472] deficient but not in the wild type tissues.
Cluster 6: late responding genes activated in ATM [Gene ID=472] deficient but not in the wild type tissues.
Genes up-regulated in MDA-MB-231 cells (breast cancer) after knockdown of ZEB1 [Gene ID=6935] by RNAi.
High-level amplifications detected in oral squamous cell carcinoma (OSCC) lines by array-CGH analysis.
Interaction partners of class IIa histone deacetylases (HDAC).
Genes co-amplified within MYCN [Gene ID=4613] in primary neuroblastoma tumors.
Proteins showing significant overexpression in lung cancer cell lines  relative to normal bronchial epithelial cell lines.
Genes with increased copy number that correlates with increased expression across six different lung adenocarcinoma cell lines.
Genes specifically up-regulated in Cluster IIb of urothelial cell carcinom (UCC) tumors.
Genes up-regulated among the high recurrence rate urothelial cell carcinoma (UCC) tumors.
Genes down-regulated in urothelial cell carcinoma (UCC) tumors with LOH on 9q as compared to the tumors showing retention.
Candidate lung adenocarcinoma tumor markers.
Differentiation markers for normal alveolar epithelium cells.
Differentiation markers for normal bronchiolar and bronchial epithelial cells.
14 candidate differentiation markers in lung adenocarcinoma cells, noncancerous lung cells and peripheral blood cells.
Proteins acting on mitochondria to prevent membrane permeabilization.
Amplification hot spot 17: colocalized fragile sites and cancer genes in the 1q11-q44 region.
Amplification hot spot 24: colocalized fragile sites and cancer genes in the 1q21-q24 region.
Amplification hot spot 25: colocalized fragile sites and cancer genes in the 2q13-q36 region.
Amplification hot spot 7: colocalized fragile sites and cancer genes in the 3q26.3-q29 region.
Amplification hot spot 27: colocalized fragile sites and cancer genes in the 5p15.3-p15.1; 5p12-q35 region.
Amplification hot spot 15: colocalized fragile sites and cancer genes in the 6p25-p11.1 region.
Amplification hot spot 29: colocolized fragile sites and cancer genes in the 7p22-p13 region.
Amplification hot spot 9: colocolized fragile sites and cancer genes in the 8p23-q12; 8q23 region.
Amplification hot spot 16: colocolized fragile sites and cancer genes in the 8q11.1-q24.3 region.
Amplification hot spot 14: colocolized fragile sites and cancer genes in the 8q24.1-q24.3 region.
Genes down-regulated in Rh4 cells (alveolar rhabdomyosarcoma, ARMS) after knockdown of the PAX3-FOXO1 [Gene iD=5077, 2308] fusion protein by RNAi for 72 hr.
Muscle development genes up-regulated in Rh4 cells (alveolar rhabdomyosarcoma, ARMS) but not in the RD cells (embryonal rhabdomyosarcoma, ERMS) after knockdown of PAX3-FOXO1 [Gene ID=5077, 2308] fusion by RNAi for 72 hr.
Genes up-regulated by TP53 [Gene ID=7157]  and down-regulated by an isoform of TP63 [Gene ID=8626] in primary HEK cells (epidermal keratinocytes).
Amplification hot spot 8: colocolized fragile sites and cancer genes in the 9q11-34 region.
Amplification hot spot 23: colocolized fragile sites and cancer genes in the 11q12-q25 region.
Amplification hot spot 11: colocolized fragile sites and cancer genes in the 11q3 region.
Amplification hot spot 21: colocolized fragile sites and cancer genes in the 12q13-q21 region.
Amplification hot spot 30: colocolized fragile sites and cancer genes in the 12q21-q24.3 region.
Amplification hot spot 3: colocolized fragile sites and cancer genes in the 15q21-q26 region.
Amplification hot spot 12: colocolized fragile sites and cancer genes in the 17q11.1-q21; 17q25 region.
Genes changed in MGUS (monoclonal gammopathy of undetermined significance) compared to PCL (plasma cell leukemia) samples.
Genes distinguishing between MGUS (monoclonal gammopathy of undetermined significance) and multiple myeloma (MM) samples.
Genes which best discriminate between two groups of breast cancer according to the status of ESR1 and AR [Gene ID=2099, 367]: apocrine (ESR1- AR+) and luminal (ESR1+ AR+).
Genes which best discriminate between two groups of breast cancer according the status of ESR1 and AR [Gene ID=2099, 367]: apocrine (ESR1- AR+) vs basal (ESR1- AR-).
Genes which best discriminated between two groups of breast cancer according to the status of ESR1 and AR [Gene ID=2099, 367]: basal (ESR1- AR-) and luminal (ESR1+ AR+).
Amplification hot spot 5: colocolized fragile sites and cancer genes in the 17q22-q25 region.
Amplification hot spot 18: colocolized fragile sites and cancer genes in the 18q11.2-q23 region.
Cluster 1: genes with similar expression profiles across follicular thyrorid carcinoma (FTC) samples.
Cluster 2: genes with similar expression profiles across follicular thyroid carcinoma (FTC) samples.
Cluster 3: genes with similar expression profiles across follicular thyrorid carcinoma (FTC) samples; genes in this cluster correlated well with the presence of PAX8-PPARG [Gene ID=7849, 5468] fusion protein.
Cluster 4: genes with similar expression profiles across follicular thyroid carcinoma (FTC) samples.
Cluster 5: genes with similar expression profiles across follicular thyroid carcinoma (FTC) samples.
Amplification hot spot 22: colocolized fragile sites and cancer genes in the 22q11.1-q13s region.
Amplification hot spot 1: colocolized fragile sites and cancer genes in the Xp22.3-p11.1 region.
Amplification hot spot 13: colocolized fragile sites and cancer genes in the Xq12-q28 region.
Genes changed in retinoblastoma tumors with respect to chromosome 6p amplifications.
Genes down-regulated in follicular thyroid carcinoma (FTC) samples that bear PAX8-PPARG [Gene ID=7849, 5468] fusion protein.
Cluster 1: genes up-regulated in B493-6 cells (B lymphocytes) upon serum stimulation but not by affected by MYC [Gene ID=4609].
Cluster 2: genes up-regulated in B493-6 cells (B lymphocytes) by serum alone or in combination with MYC [Gene ID=4609] but not by MYC alone.
Cluster 3: genes strongly up-regulated in B493-6 cells (B lymphocytes) by a combination of MYC [Gene ID=4609] and serum but not by each of them alone.
Cluster 7: genes up-regulated in B493-6 cells (B lymphocytes) by MYC [Gene ID=4609] and down-regulated by the combination of MYC and serum.
Cluster 6: genes down-regulated in B493-6 cells (B lymphocytes) by MYC [Gene ID=4609] in combination with serum but not affected by serum alone; they are also up-regulated by MYC alone.
Cluster 5: genes up-regulated in B493-6 cells (B lymphocytes) by MYC [Gene ID=4609] alone or in combination with serum but not by serum alone.
Cluster 4: genes down-regulated in B493-6 cells (B lymphocytes) upon serum stimulation but not affected by MYC [Gene ID=4609].
Genes differentially expressed in multiple myeloma (MM) patients: comparison of MGUS-like vs PCL-like samples; MGUS=monoclonal gammopathy of undetermined significance, PCL=plasma cell leukemia.
Genes expressed in multiple myeloma (MM) patients carrying specific translocations involving the immunoglobulin heavy chain (IGH) locus at 14q32.
Cluster 1: interferon, T and B lymphocyte genes clustered together across breast cancer samples.
Cluster 8: selected ERBB2 [Gene ID=2064] amplicon genes clustered together across breast cancer samples.
Cluster 7: selected apocrine and luminal genes clustered together across breast cancer samples.
Cluster 6: selected luminal genes clustered together across breast cancer samples.
Cluster 5: selected 17q21_23 amplicon genes clustered together across breast cancer samples.
Cluster 4: selected stromal genes clustered together across breast cancer samples.
Cluster 2: selected proliferation and 8q amplicon genes clustered together across breast cancer samples.
The 'Cervical Cancer Proliferation Cluster' (CCPC): genes whose expression in cervical carcinoma positively correlates with that of the HPV E6 and E7 oncogenes; they are also differentially expressed according to disease outcome.
Genes encoding IkappaB kinase (IKK) interacting proteins.
Genes whose expression was increased due to copy number gain in laryngeal cancer tumors (both in primary cultures and cell lines).
Genes from selected recurrently amplified regions in soft tissue tumors with supernumerary  ring chromosomes.
Genes from selected recurrently amplified regions in bone tissue tumors with supernumerary  ring chromosomes.
Candidate substrate proteins of AURKB [Gene ID=9212].
Genes up-regulated in MM-LH cells (malignant melanoma) after treatment with the HDAC inhibitor romidepsin (FK228) [PubChem=5352062].
Genes changed in H1299 cells (non-small cell lung cancer, NSCLC) transiently transfected to express the TP63 [Gene ID=8626] gamma splice variant.
Genes up-regulated in FE-8 cells (fibroblasts) upon treatment with azacitidine [PubChem=9444].
Genes distinguishing between breast cancer tumors bearing mutations in BRCA1 [Gene ID=672] and those with mutated BRCA2 [Gene ID=675].
Genes up-regulated in DU145-RD cells (prostate cancer) resistant to docetaxel [PubChem=148124] vs the parental, docetaxel-sensitive cells.
Genes up-regulated by growing HMEC-E6 cells (mammary epithelial cells damaged by expression of HPV-16 E6 [Gene ID=1489078]) in extracellular matrix (ECM).
Genes up-regulated  by tamoxifen [PubChem=5376] in HMEC-E6 cells (mammary epithelial cells damaged by expression of HPV-16 E6 [Gene ID=1489078]).
Genes up-regulated in T47D cells (breast cancer) after COBRA1 [Gene ID=25920] knockdown by RNAi.
Genes down-regulated in T47D cells (breast cancer) after COBRA1 [Gene ID=25920] knockdown by RNAi.
Genes consistently down-regulated in ACRP cells (ovarian cancer, resistant to cisplatin [PubChem=2767]) compared to the parental sensitive A2780 cells, regardless of cisplatin exposure.
Genes consistently up-regulated in ACRP cells (ovarian cancer, resistant to cisplatin [PubChem=2767]) compared to the parental sensitive A2780 cells, regardless of cisplatin exposure.
Genes changed similarly in DU-145 cells (prostate cancer) in the absence and presence of a dominant negative form of AKT1 [Gene ID=207] upon exposure to HGF [Gene ID=3082] for 6 hr.
Genes changed in DU-145 cells (prostate cancer) in the absence but not presence of a dominant negative form of AKT1 [Gene ID=207] upon exposure to HGF [Gene ID=3082] for 6 hr.
Genes up-regulated in DU-145 cells (prostate cancer) in the absence and presence of a dominant negative form of AKT1 [Gene ID=207] upon exposure to HGF [Gene ID=3082] for 48 hr.
Genes down-regulated in DU-145 cells (prostate cancer) in the absence and presence of a dominant negative form of AKT1 [Gene ID=207] upon exposure to HGF [Gene ID=3082] for 48 hr.
Genes up-regulated in DU-145 cells (prostate cancer) in the absence but not in the presence of a dominant negative form of AKT1 [Gene ID=207] upon exposure to HGF [Gene ID=3082] for 48 hr.
Genes down-regulated in DU-145 cells (prostate cancer) in the absence but not in the presence of a dominant negative form of AKT1 [Gene ID=207] upon exposure to HGF [Gene ID=3082] for 48 hr.
Genes up-regulated in DU-145 cells (prostate cancer) in the presence but not in the absence of a dominant negative form of AKT1 [Gene ID=207] upon exposure to HGF [Gene ID=3082] for 48 hr.
Genes down-regulated in DU-145 cells (prostate cancer) in the presence but not in the absence of a dominant negative form of AKT1 [Gene ID=207] upon exposure to HGF [Gene ID=3082] for 48 hr.
Genes up-regulated in DU-145 cells (prostate cancer) expressing a dominant negative form of AKT1 [Gene ID=207] upon sham-treatment for 6 hr (as a control for the HGF [Gene ID=3082] experiments).
Genes up-regulated in DU-145 cells (prostate cancer) expressing a dominant negative form of AKT1 [Gene ID=207] upon sham-treatment for 48 hr (as a control for the HGF [Gene ID=3082] experiments).
Genes up-regulated in glioma cell lines after knockdown of SPARC [Gene ID=6678] by RNAi.
Genes down-regulated in glioma cell lines after knockdown of SPARC [Gene ID=6678] by RNAi.
Subunits of the anaphase promoting complex (APC).
Angiogenic and metastatic genes changed in RKO cells (colorectal cancer) upon perturbation of key components of AKT pathway.
Genes up-regulated in acute myeloid leukemia (AML) samples with constitutively activated FLT3 [Gene ID=2322] or with activating point mutations within NRAS [Gene ID=4893].
Genes down-regulated in acute myeloid leukemia (AML) samples with constitutively activated FLT3 [Gene ID=2322] or with activating point mutations within NRAS [Gene ID=4893].
Clusters 1 and 2: genes up-regulated in B2264-19/3 cells (primary B lymphocytes) within 30-60 min after activation of LMP1 (an oncogene encoded by Epstein???Barr virus, EBV).
A gene expression signature found in a subset of cancer patients suggestive of a deregulated immune or inflammatory response.
Genes discriminating TP53 [Gene ID=7157] status across various genotoxic stress agents.
Genes from the recurrent amplicons in 89 samples of oral squamous cell carcinoma (SCC).
Genes within the smallest region of consistend deletion (SRD) within 1p36.3 area across a large collection of neuroblastoma cell lines and biopsy samples.
Genes up-regulated in SaOS-2 cells (osteosarcoma) upon expression of PAX3-FOXO1 [Gene ID=5077, 2308] but down-regulated by PAX3 expression off adenoviral vectors.
Genes bound by EWSR1-FLT1 [Gene ID=2130, 2321] fusion but whose expression did not change in STA-ET-7.2 cells (Ewing's sarcoma) after knockdown of EWSR1-FLT1 by RNAi.
Top 50 genes up-regulated in A549 cells (lung cancer) expressing STAT3 [Gene ID=6774] off an adenovirus vector.
Top 50 genes down-regulated in A549 cells (lung cancer) expressing STAT3 [Gene ID=6774] off an adenovirus vector.
Genes predicting the embryonic carcinoma (EC) subtype of nonseminomatous male germ cell tumors (NSGCT).
Genes predicting the teratoma (T) subtype of nonseminomatous male germ cell tumors (NSGCT).
Genes predicting the yolk sac tumor (YS) subtype of nonseminomatous male germ cell tumors (NSGCT).
Genes predicting the choriocarcinoma (CC) of nonseminomatous male germ cell tumors (NSGCT).
Genes up-regulated in MDA468 cells (breast cancer) vs DU99 cells (normal breast) after treatment with azacytidine [PubChem=9444].
Genes amplified and up-regulated more than twofold in at least two out of 10 pancreatic cancer cell lines studied.
Genes down-regulated in Kelly cells (neuroblastoma) by overexpressing INHBA [Gene ID=3624] off a plasmid vector.
Genes up-regulated in CT60/4 cells (breast cancer reverted to normal by transfer of chromosome 8p region) vs parental MDA-MB-231 cells (deleted chromosome 8p).
Genes down-regulated in CT60/4 cells (breast cancer reverted to normal by transfer of chromosome 8p region) vs parental MDA-MB-231 cells (deleted chromosome 8p).
Genes up-regulated in gastrointestinal stromal tumors (GIST) with PDGFRA [Gene ID=5156] mutations.
Genes up-regulated in low grade (LMP and G1) serous ovarian carcinomas vs the higher grade invasive tumors (G2 and G3).
Genes down-regulated in low grade (LMP and G1) serous ovarian carcinomas vs the higher grade invasive tumors (G2 and G3).
Genes up-regulated in fibroblasts expressing different mutant forms of ERCC3 [Gene ID=2071]: XP/CS (xeroderma pigmentosum (XP) and Cockraine's syndrome (CS)) vs TTD (trichothiodystrophy).
Genes down-regulated in fibroblasts expressing different mutant forms of ERCC3 [Gene ID=2071]: XP/CS (xeroderma pigmentosum (XP) and Cockraine's syndrome (CS)) vs TTD (trichothiodystrophy).
Genes up-regulated in fibroblasts expressing the XP/CS mutant form of ERCC3 [Gene ID=2071], after low dose UVC irradiation.
Genes down-regulated in fibroblasts expressing the XP/CS mutant form of ERCC3 [Gene ID=2071], after low dose UVC irradiation.
Genes up-regulated in fibroblasts expressing mutant forms of ERCC3 [Gene ID=2071] after UV irradiation.
Genes down-regulated in fibroblasts expressing mutant forms of ERCC3 [Gene ID=2071] after UV irradiation.
Common down-regulated transcripts in fibroblasts expressing either XP/CS or TDD mutant forms of ERCC3 [Gene ID=2071], after UVC irradiation.
Cluster 3: genes up-regulated in B2264-19/3 cells (primary B lymphocytes) within 60-180 min after activation of LMP1 (an oncogene encoded by Epstein???Barr virus, EBV).
Cluster 4: genes down-regulated in B2264-19/3 cells (primary B lymphocytes) within 60-180 min after activation of LMP1 (an oncogene encoded by Epstein???Barr virus, EBV).
Up-regulated genes whose expression is associated with amplification of the 8q24 chromosome region in pancreatic cancer cell lines.
Down-regulated genes whose expression is associated with amplification of the 8q24 chromosome region in pancreatic cancer cell lines.
Up-regulated genes whose expression is associated with amplification of the 12p11-12 chromosome in pancreatic cancer cell lines.
Down-regulated genes whose expression is associated with amplification of the 12p11-12 chromosome in pancreatic cancer cell lines.
Genes discriminating genotoxic (DNA damaging) agents from other kinds of stresses.
Genes discriminating responses to sodium arsenite [PubChem ID=26435] from other stresses.
Genes up-regulated by IL2 [Gene ID=3558] in T1 cells (primary thymocytes immortalized by Tax, an HTLV-1 encoded gene).
Genes up-regulated by IL2 [Gene ID=3558] in both primary thymocytes and T1 cells (primary thymocytes immortalized by Tax, an HTLV-1 encoded gene).
Genes with putative STAT5 [Gene ID=6777] binding sites; up-regulated by IL2 [Gene ID=3558] only in T1 cells (primary thymocytes immortalized by Tax, an HTLV-1 encoded gene).
Genes with putative STAT5 [Gene ID=6777] binding sites; up-regulated by IL2 [Gene ID=3558] in both primary thymocytes and T1 cells (primary thymocytes immortalized by Tax, an HTLV-1 encoded gene).
Human environmental stress response (H-ESR, ESR) signature: genes up-regulated in young donors after all of the stress types tested.
Subset C (Fig 2c): genes changed upon exposure to the carcinogen 4-nitroquinoline-1-oxide (4NQO) [PubChem=5955].
Subset D (Fig 2d): genes changed in response to gamma radiation.
Subset E (Fig 2e): genes changed in response to UV radiation.
Subset F (Fig. 2f): genes changed upon exposure to the carcinogen 4-nitroquinoline-1-oxide (4NQO) and in response to gamma radiation but not to UV.
Subset H (Fig. 2h): genes changed in response to UV and gamma radiation but not upon exposure to the carcinogen 4-nitroquinoline-1-oxide (4NQO) [PubChem=5955].
Subset G (fig 2g): genes changed upon exposure to the carcinogen 4-nitroquinoline-1-oxide (4NQO) [PubChem=5955] and in response to UV and but not to gamma irradiation.
Genes up-regulated in DLD1 cells (colon cancer) by p73 beta [Gene ID=7161] or by and p63 gamma [Gene ID=8626] but not by p53 [Gene ID=7157].
Genes down-regulated in U2-OS Tet-On cells (osteosarcoma) after induction of ESX1 [Gene ID=80712] expression.
Genes most up-regulated in hypoxia tolerant NCI H460 cells (lung cancer).
Genes most down-regulated in hypoxia tolerant NCI H460 cells (lung cancer).
Genes up-regulated in bladder cancer cells resistant to cisplatin [PubChem=2767] compared to the parental cells sensitive to the drug.
Genes down-regulated in bladder cancer cells resistant to cisplatin [PubChem=2767] compared to the parental cells sensitive to the drug.
Genes up-regulated by hypoxia in RCC4 cells (renal cell carcinoma) engineered to stably express VHL [Gene ID=7428] off a plasmid vector.
Genes up-regulated in apoptotic tissues (neuroepithelium) after MDM4 [Gene ID=4194] knockout.
Genes down-regulated in apoptotic tissues (neuroepithelium) after MDM4 [Gene ID=4194] knockout.
Genes up-regulated in non-apoptotic tissues (fetal liver) after MDM4 [Gene ID=4194] knockout.
Genes down-regulated in non-apoptotic tissues (fetal liver) after MDM4 [Gene ID=4194] knockout.
Genes up-regulated in HCT116 cells (colon cancer) after treatment with amifostine [PubChem=2141] depending on the presence of TP53 [Gene ID=7157]: TP53-positive vs TP53-null cells.
Genes down-regulated in HCT116 cells (colon cancer) after treatment with amifostine [PubChem=2141] depending on the presence of TP53 [Gene ID=7157]: TP53-positive vs TP53-null cells.
Genes up-regulated in the UMUC-3 cells (bladder cancer) after knockdown of both RALA and RALB [Gene ID=5898, 5899] by RNAi.
Genes up-regulated between two breast carcinoma subtypes: metaplastic (MCB) and ductal (DCB).
Genes down-regulated between two breast carcinoma subtypes: metaplastic (MCB) and ductal (DCB).
Genes up-regulated in the Ad/AH cells (adenocarcinoma) engineered to stably express the Epstein-Barr virus (EBV) gene EBNA1.
Genes down-regulated in the Ad/AH cells (adenocarcinoma) engineered to stably express the Epstein-Barr virus (EBV) gene EBNA1.
Up-regulated in MCF7 cells (breast cancer) by TLX1 (HOX11) [Gene ID=3195].
Down-regulated in MCF7 cells (breast cancer) by TLX1 (HOX11) [Gene ID=3195].
Genes up-regulated in non-spontaneously immortalizing (NSI) primary breast cancer tumor cultures upon expression of TERT [Gene ID=7015] off a retroviral vector.
Genes down-regulated in non-spontaneously immortalizing (NSI) primary breast cancer tumor cultures upon expression of TERT [Gene ID=7015] off a retroviral vector.
Selected genes up-regulated in WT-A10 cells (gastric epithelium) expressing the H. pilori virulence gene CagA.
Genes with the high-CpG-density promoters (HCP) that were up-regulated in 1542-CP3TX cells (prostate cancer) compared to 1542-NPTX (normal prostate).
Genes up-regulated in RCC4 cells (renal cell carcinoma) engineered to stably express VHL [Gene ID=7428] off a plasmid vector.
Genes down-regulated in RCC4 cells (renal cell carcinoma) engineered to stably express VHL [Gene ID=7428] off a plasmid vector.
Genes up-regulated in pancreatic ductal adenocarcinoma (PDAC) identified in a meta analysis across four independent studies.
Genes down-regulated in pancreatic ductal adenocarcinoma (PDAC) identified in a meta analysis across four independent studies.
Genes up-regulated in PANC-1-puro cells (pancreatic cancer) stimulated by TGF1B [Gene ID=7040] for 2 h.
Genes down-regulated in PANC-1-puro cells (pancreatic cancer) stimulated by TGF1B [Gene ID=7040] for 2 h.
Genes up-regulated in PANC-1-S4KD cells (pancreatic cancer; SMAD4 [Gene ID=4089] knocked down by RNAi) after stimulation by TGF1B [Gene ID=7040] for 2 h.
Genes down-regulated in PANC-1-S4KD cells (pancreatic cancer; SMAD4 [Gene ID=4089] knocked down by RNAi) after stimulation by TGF1B [Gene ID=7040] for 2 h.
Genes up-regulated in HFK cells (primary keratinocytes) in response to UVB irradiation.
Genes down-regulated in HFK cells (primary keratinocytes) in response to UVB irradiation.
Genes down-regulated in response to UVB radiation in HFK cells (keratinocytes) immortalized by overexpression of HPV E6 and E7 viral oncogenes.
Up-regulated genes characteristic for autonomous thyroid adenoma.
Down-regulated genes characteristic for autonomous thyroid adenoma.
Cluster 3: selected apocrine, basal and hypoxia genes clustered together across breast cancer samples.
Genes positively correlated with amplifications of MYC [Gene ID=4609] in SCLC (small cell lung cancer) cell lines.
Genes negatively correlated with amplifications of MYC [Gene ID=4609] in SCLC (small cell lung cancer) cell lines.
Genes positively  correlated with amplifications of MYCN  [Gene ID=4613] in the SCLC (small cell lung cancer) cell lines.
Genes negatively  correlated with amplifications of MYCN  [Gene ID=4613] in the SCLC (small cell lung cancer) cell lines.
Genes positively correlated with amplifications of MYCL1 [Gene ID=4610] in SCLC (small cell lung cancer) cell lines.
Genes negatively correlated with amplifications of MYCL1 [Gene ID=4610] in SCLC (small cell lung cancer) cell lines.
Genes up-regulated in TK6, WTK1, and NH32 cell lines (lymphoblast) in response to ionizing radiation.
Genes up-regulated in early primary breast tumors expressing ESR1 [Gene ID=2099] vs the ESR1 negative ones.
Genes down-regulated in early primary breast tumors expressing ESR1 [Gene ID=2099] vs the ESR1 negative ones.
Genes up-regulated in laser microdissected (LCM) samples of early primary breast tumors expressing ESR1 [Gene ID=2099] vs the ESR1 negative ones.
Genes down-regulated in laser microdissected (LCM) samples of early primary breast tumors expressing ESR1 [Gene ID=2099] vs the ESR1 negative ones.
Genes up-regulated in bulk samples from early primary breast tumors expressing ESR1 [Gene ID=2099] vs the ESR1 negative samples.
Genes down-regulated in bulk samples from early primary breast tumors expressing ESR1 [Gene ID=2099] vs the ESR1 negative samples.
Genes down-regulated in SK-N-DZ cells (neuroblastoma) after knockdown of MIF [Gene ID=4282] by antisense RNA.
Genes up-regulated in H1299 cells (non-small cell lung cancer, NSCLC) expressing the Y144F mutant form of FHIT [Gene ID=2272].
Genes down-regulated in H1299 cells (non-small cell lung cancer, NSCLC) expressing the Y144F mutant form of FHIT [Gene ID=2272].
Genes up-regulated in SiHa cells (cervical carcinoma) by stable expression of NOL7 [Gene ID=51406] off a plasmid vector.
Genes down-regulated in SiHa cells (cervical carcinoma) by stable expression of NOL7 [Gene ID=51406] off a plasmid vector.
Genes up-regulated in HSC-2/8 cells (chondrosarcoma) under hypoxic conditions.
Genes with hypermethylated DNA in lung cancer samples.
Genes with unmethylated DNA in lung cancer samples.
Genes up-regulated in neuroblastoma xenografts: sensitive vs resistant to the topoisomerase inhibitor irinotecan [Gene ID=3750].
Genes up-regulated in neuroblastoma xenografts: resistant vs those that reverted to be sensitive to the topoisomerase inhibitor irinotecan [PubChem=3750].
Genes up-regulated in PCI-35 cells (pancreatic cancer, lack endogenous DUSP6 [Gene ID=1848]) upon expression of DUSP6 off an adenoviral vector.
Genes down-regulated in PCI-35 cells (pancreatic cancer, lack endogenous DUSP6 [Gene ID=1848]) upon expression of DUSP6 off an adenoviral vector.
Genes specifically up-regulated via JNK (MAPK8) [Gene ID=5599] signaling pathway activated by paclitaxel [PubChem=4666] in BR cells (ovarian cancer).
Genes up-regulated by TGFB1 [Gene ID=7040] in MCF10A cells (breast cancer): both wild-type and those lacking p21 [Gene ID=1026].
Genes up-regulated in metaplastic carcinoma of the breast (MCB) subclass 2 compared to the MCB subclass 1.
Genes up-regulated in prostate cancer vs benign prostate tissue, based on a meta-analysis of five gene expression profiling studies.
Genes down-regulated in prostate cancer vs benign prostate tissue, based on a meta-analysis of five gene expression profiling studies.
Top genes up-regulated in hormone refractory metastatic prostate cancer compared to localized prostate cancer.
Top genes down-regulated in hormone refractory metastatic prostate cancer compared to localized prostate cancer.
Genes up-regulated in LSK cells (bone marrow) as a function of a QTL for the size of hematopoietic stem cell (HSC) population: comparison of congenic B.D. chr3 (BD, large HSC size) vs parental B6 strain (tiny HSC size).
Genes down-regulated in LSK cells (bone marrow) as a function of a QTL for the size of hematopoietic stem cell (HSC) population: comparison of congenic B.D. chr3 (BD, large HSC size) vs parental B6 strain (tiny HSC size).
Genes up-regulated in LSK cells (bone marrow) as a function of a QTL for the size of hematopoietic stem cell (HSC) population: comparison of congenic D.B. Chr 3 (DB, small HSC population) vs parental D2 strain (huge HSC population).
Genes down-regulated in LSK cells (bone marrow) as a function of a QTL for the size of hematopoietic stem cell (HSC) population: comparison of congenic D.B. Chr 3 (DB, small HSC population) vs parental D2 strain (huge HSC population).
Genes up-regulated more than two-fold in lymphoblastoid cell lines from European population compared to those from Asian population.
Genes down-regulated more than two-fold in lymphoblastoid cell lines from European population compared to those from Asian population.
Genes up-regulated in lymphoblastoid cells from the European population compared to those from the Asian population.
Genes down-regulated in lymphoblastoid cells from the European population compared to those from the Asian population.
Candidate genes in the pericentromeric microdeletion in 16p11.2-p12.2 associated with developmental disabilities.
Genes expressed in normal colon; they undergo down-regulation in tumors through DNA methylation.
Genes mapped to core duplicons - elements shared by a majority of segmental duplication blocks.
Genes constituting the LIT-Int network of proteins interacting with breast cancer reference proteins BRCA1, BRCA2, ATM, and CHEK2 [Gene ID=672, 675, 472, 11200]; the interactions were manually curated from the literature.
Genes constituting the XPRSS-Int network: intersection of genes whose expression correlates with BRCA1, BRCA2, ATM, and CHEK2 [Gene ID=672, 675, 472, 11200] in a compendium of normal tissues.
Genes constituting the BRCA1-PCC network of transcripts whose expression positively correlated (Pearson correlation coefficient, PCC >= 0.4) with that of BRCA1 [Gene ID=672] across a compendium of normal tissues.
Genes constituting the BRCA2-PCC network of transcripts whose expression positively correlated (Pearson correlation coefficient, PCC >= 0.4) with that of BRCA2 [Gene ID=675] across a compendium of normal tissues.
Genes constituting the ATM-PCC network of transcripts whose expression positively correlated (Pearson correlation coefficient, PCC >= 0.4) with that of ATM [Gene ID=472] across a compendium of normal tissues.
Genes constituting the CHEK2-PCC network of transcripts whose expression positively correlates (Pearson correlation coefficient, PCC >= 0.4) with that of CHEK2 [Gene ID=11200].
Genes constituting the BRCA-centered network (BCN).
Genes bearing the H3K27me3 mark in normal cells; their DNA is methylated in cancer cells.
Genes bearing H3K27me3 mark or whose promoters are bound by the polycomb proteins SUZ12 or EED [Gene ID=23512, 8726]; their DNA is methylated de novo in cancer.
Top scoring cis-regulated QTL (quantitative trait loci) influencing blood levels of high-density lipoprotein (HDL) cholesterol.
Top scoring trans-regulated expression quantitative trait loci (eQTL) influencing blood levels of high-density lipoprotein (HDL) cholesterol.
Retinoic acid-responsive genes up-regulated in hepatocellular carcinoma (HCC) samples of TRIM24 [Gene ID=8805] knockout mice.
Retinoic acid-responsive genes down-regulated in hepatocellular carcinoma (HCC) samples of TRIM24 [Gene ID=8805] knockout mice.
Genes showing frequent DNA methylation and which are silenced in adult cancers but remain unmethylated in embryonic carcinoma and embryonic stem (ES) cells.
Genes with a high basal transcription state in undifferentiated embryonic carcinoma cells.
Genes with low to medium basal transcription state in undifferentiated embryonic carcinoma cells.
Genes able to induce cell death in an expression cDNA library screen.
Genes in the smallest region of deletion (SRD) in 1p36.3 area in neuroblastoma samples.
Genes down-regulated by MYCN [Gene ID=4613] but not by its transactivation-defficient, trunkated form N-Myc-delta-73.
Genes that distinguish normal from cancer (lung adenocarcinoma) samples and smokers from non-smoking subjects.
Potential targets of MIR125B1 [Gene ID=406911] microRNA which are up-regulated in prostate cancer.
DNA repair and replication genes up-regulated in melanoma patients who will relapse vs patients who will not.
DNA repair and replication genes down-regulated in melanoma patients who will relapse vs patients who will not.
The 'ER-alpha profile': genes up-regulated in T47D cells (breast cancer, ESR2 [Gene ID=2100] Tet-Off) upon activation of ESR1 [Gene ID=2099] by estradiol (E2) [PubChem=5757].
The 'ER-alpha profile': genes down-regulated in T47D cells (breast cancer, ESR2 [Gene ID=2100] Tet-Off) upon activation of ESR1 [Gene ID=2099] by estradiol (E2) [PubChem=5757].
Genes uniquely up-regulated in T47D cells (breast cancer) by induction of ESR2 [Gene ID=2100] expression in the Tet-Off system.
Genes uniquely down-regulated in T47D cells (breast cancer) by induction of ESR2 [Gene ID=2100] expression in the Tet-Off system.
Genes up-regulated in PC3 cells (prostate cancer) after knockdown of NIPP1 [Gene ID=5511] by RNAi.
Genes down-regulated in PC3 cells (prostate cancer) after knockdown of NIPP1 [Gene ID=5511] by RNAi.
Genes up-regulated in PC3 cells (prostate cancer) after knockdown of EZH2 [Gene ID=2146] by RNAi.
Genes down-regulated in PC3 cells (prostate cancer) after knockdown of EZH2 [Gene ID=2146] by RNAi.
Genes up-regulated in T24 (bladder cancer) cells in response to the photodynamic therapy (PDT) stress.
Genes down-regulated in T24 (bladder cancer) cells in response to the photodynamic therapy (PDT) stress.
Genes up-regulated in genomically unstable Ewing's sarcoma tumors compared to the stable ones.
Genes down-regulated in genomically unstable Ewing's sarcoma tumors compared to the stable ones.
Genes down-regulated in ST1 cells (adult T-cell leukemia, ATL) after knockdown of FRA2 [Gene ID=2355] by RNAi.
Genes up-regulated in HeLa cells (cervical cancer) after simultaneus knockdown of all three MBD (methyl-CpG binding domain) proteins MeCP2, MBD1 and MBD2 [Gene ID=4204, 4152, 8932] by RNAi.
X chromosome and imprinted genes up-regulated in HeLa cells (cervical cancer) after knockdown of the MBD (methyl-CpG binding domain) proteins by RNAi.
Genes up-regulated genes in cell lines with HDAC2 [Gene ID=3066] loss of function (LOS).
Genes up-regulated in constitutively invasive HT-29 5M21 cells (colon cancer) vs the parental non-invasive cells.
Low abundance transcripts specific to hepatocellular carcinoma (HCC).
Low abundance transcripts specific for breast cancer.
Low abundance transcripts specific to nasopharyngeal carcinoma (NPC).
Low abundance transcripts common to nasopharyngeal carcinoma (NPC), breast and liver tumors.
Overexpressed genes with amplified copy number across 27 non-small cell lung cancer (NSCLC) cell lines.
Genes down-regulated in H1703 cells (non-small cell lung cancer, NSCLC) after knockdown of PRKCI [Gene ID=5584] by RNAi.
Potential direct target genes for MIR34A [Gene ID=407040] microRNA in IMR32 cells (neuroblastoma).
Genes whose promoters contain E-box motifs and whose expression changed in MYCN-3 cells (neuroblastoma) upon induction of MYCN [Gene ID=4613].
Genes up-regulated in the samples with intrahepatic metastatic hepatocellular carcinoma (HCC) vs primary HCC that also have putative binding sites for SOX4 [Gene ID=6659].
Genes up-regulated in the samples with intrahepatic metastatic hepatocellular carcinoma (HCC) vs primary HCC.
Proteins that interact with PTTG1 [Gene ID=9232], based on protein array.
Cell cycle genes changed in H1299 cells (lung cancer) after overexpression of either P53 [Gene ID=7157] or P73 [Gene ID=7161].
Cell cycle genes changed in H1299 cells (lung cancer) after overexpression of either P53 [Gene ID=7157] or P73 [Gene ID=7161].
Genes that were inversely correlated in H1299 cells (lung cancer), either up-regulated by P53 [Gene ID=7157] and down-regulated by P73 [Gene ID=7161] or vice versa.
Genes that were inversely correlated in H1299 cells (lung cancer), either up-regulated by P53 [Gene ID=7157] and down-regulated by P73 [Gene ID=7161] or vice versa.
Genes up-regulated in glioblastoma cell lines displaying spherical growth (cluster-1) compared to those displaying semiadherent or adherent growth phenotype (cluster-2).
Genes down-regulated in glioblastoma cell lines displaying spherical growth (cluster-1) compared to those displaying semiadherent or adherent growth phenotype (cluster-2).
Genes up-regulated in 293 cells (embryonic kidney) expressing the polymorphic variant S427G [SNP ID=rs2070235] of BMYB [Gene ID=4605].
Genes down-regulated in 293 cells (embryonic kidney) expressing the polymorphic variant S427G [SNP ID=rs2070235] of BMYB [Gene ID=4605].
Genes up-regulated in 293 cells (embryonic kidney) expressing the polymorphic variant I624M (SNP ID=rs11556379] of BMYB [Gene ID=4605].
Genes down-regulated in 293 cells (embryonic kidney) expressing the polymorphic variant I624M (SNP ID=rs11556379] of BMYB [Gene ID=4605].
Genes up-regulated in constitutively invasive HT-29 5M21 cells (colon cancer) vs those expressing functionally inactive TATI [Gene ID=6690].
Genes down-regulated in constitutively invasive HT-29 5M21 cells (colon cancer) vs those expressing functionally inactive TATI [Gene ID=6690].
Genes up-regulated in EVSA-T cells (breast cancer) treated THC (delta-9-tetrahydrocannabinol) [PubChem=6610319].
Genes down-regulated in EVSA-T cells (breast cancer) treated THC (delta-9-tetrahydrocannabinol) [PubChem=6610319].
Genes up-regulated in EVSA-T cells (breast cancer) treated with 5 micromolar THC (delta-9-tetrahydrocannabinol) [PubChem=6610319] for 8 h.
Genes down-regulated in EVSA-T cells (breast cancer) treated with 5 micromolar THC (delta-9-tetrahydrocannabinol) [PubChem=6610319] for 8 h.
Genes down-regulated in EVSA-T cells (breast cancer) treated with 3 micromolar THC (delta-9-tetrahydrocannabinol) [PubChem=6610319] for 8 h.
Genes up-regulated in EVSA-T cells (breast cancer) after treatment with 3 micromolar THC (delta-9-tetrahydrocannabinol) [PubChem=6610319] for 24 h.
Genes down-regulated in EVSA-T cells (breast cancer) after treatment with 3 micromolar THC (delta-9-tetrahydrocannabinol) [PubChem=6610319] for 24 h.
Genes up-regulated in EVSA-T cells (breast cancer) treated with 5 micromolar THC (delta-9-tetrahydrocannabinol) [PubChem=6610319] for 24 h.
Genes down-regulated in EVSA-T cells (breast cancer) treated with 5 micromolar THC (delta-9-tetrahydrocannabinol) [PubChem=6610319] for 24 h.
Genes up-regulated in the invasive ductal carcinoma (IDC) compared to the invasive lobular carcinoma (ILC), the two major pathological types of breast cancer.
Genes down-regulated in the invasive ductal carcinoma (IDC) compared to the invasive lobular carcinoma (ILC), the two major pathological types of breast cancer.
Genes whose expression positively correlates with that of both ID1 [Gene ID=3397] and ID2 [Gene ID=3398] genes in a cohort of 285 patients with primaly AML (acule myelogenous leukemia) [PMID=15084694].
Common target genes regulated by all three Runx family members (RUNX1, RUNX2, and RUNX3 [Gene ID=861, 860, 864]) in MEF cells (embryonic fibroblasts).
Common target genes regulated by all three Runx family members (RUNX1, RUNX2, and RUNX3 [Gene ID=861, 860, 864]) in MEF cells (embryonic fibroblasts).
Genes up-regulated in the A673 cells (Ewing sarcoma) after double knockdown of both FLI1 and DAX1 [Gene ID=2313, 190] by RNAi.
Genes down-regulated in the A673 cells (Ewing sarcoma) after double knockdown of both FLI1 and DAX1 [Gene ID=2313, 190] by RNAi.
Up-regulated genes that vary between HNSCC (head and neck squamous cell carcinoma) groups formed on the basis of their level of pathological differentiation: well vs poorly differentiated tumors.
Down-regulated genes that vary between HNSCC (head and neck squamous cell carcinoma) groups formed on the basis of their level of pathological differentiation: well vs poorly differentiated tumors.
Up-regulated genes that vary between HNSCC (head and neck squamous cell carcinoma) groups formed on the basis of their level of pathological differentiation: well vs moderately differentiated tumors.
Down-regulated genes that vary between HNSCC (head and neck squamous cell carcinoma) groups formed on the basis of their level of pathological differentiation: well vs moderately differentiated tumors.
Up-regulated genes that vary between HNSCC (head and neck squamous cell carcinoma) groups formed on the basis of their level of pathological differentiation: moderately vs poorly differentiated tumors.
Down-regulated genes that vary between HNSCC (head and neck squamous cell carcinoma) groups formed on the basis of their level of pathological differentiation: moderately vs poorly differentiated tumors.
Genes up-regulated in metastatic vs non-metastatic HNSCC (head and neck squamous cell carcinoma) samples.
Genes down-regulated in metastatic vs non-metastatic HNSCC (head and neck squamous cell carcinoma) samples.
Genes up-regulated in senescent cells.
Genes down-regulated in senescent cells.
Genes down-regulated in immortalized cell lines.
Genes up-regulated in NCI-H1299 cells (large cell neuroendocrine carcinoma) stably expressing SEMA3B [Gene ID=7869].
Genes down-regulated in NCI-H1299 cells (large cell neuroendocrine carcinoma) stably expressing SEMA3B [Gene ID=7869].
Cluster a: genes identifying an intrinsic group in head and neck squamous cell carcinoma (HNSCC).
Cluster b: genes identifying an intrinsic group in head and neck squamous cell carcinoma (HNSCC).
Cluster c: genes identifying an intrinsic group in head and neck squamous cell carcinoma (HNSCC).
Cluster d: genes identifying an intrinsic group in head and neck squamous cell carcinoma (HNSCC).
Cluster e: genes identifying an intrinsic group in head and neck squamous cell carcinoma (HNSCC).
Cluster f: genes identifying an intrinsic group in head and neck squamous cell carcinoma (HNSCC).
Genes associated with migration rate of 40 human bladder cancer cells.
Genes that cooperate with MYC [Gene ID=4609] and TBX2 [Gene ID=6909] to transform MEF cells (embryo fibroblasts).
Genes up-regulated in pilocytic astrocytoma compared to glioblastoma samples.
Genes down-regulated in pilocytic astrocytoma compared to glioblastoma samples.
Genes up-regulated in U87MG cells (glioblastoma multiforme) after knockdown of PRKCI [Gene ID=5584] by RNAi.
Delayed early genes (DEG) which are coordinately down-regulated in multiple epithelial tumor types.
Genes up-regulated in post-GC, BCL6 [Gene ID=604] dependent B cell non-Hodgkin's lymphoma (B-NHL) vs MYC [Gene ID=4609] driven pre-GC lymphoma; GC = germinal center.
Genes down-regulated in post-GC, BCL6 [Gene ID=604] dependent B cell non-Hodgkin's lymphoma (B-NHL) vs MYC [Gene ID=4609] driven pre-GC lymphoma; GC = germinal center.
Set 'ES exp1': genes overexpressed in human embryonic stem cells according to 5 or more out of 20 profiling studies.
Set 'Set 'ES exp2': genes overexpressed in human embryonic stem cells according to a meta-analysis of 8 profiling studies.
Set 'Nanog targets': genes upregulated and identified by ChIP on chip as Nanog [Gene ID=79923] transcription factor targets in human embryonic stem cells.
Set 'Oct4 targets': genes upregulated and identified by ChIP on chip as OCT4 [Gene ID=5460] transcription factor targets in human embryonic stem cells.
Set 'Sox2 targets': genes upregulated and identified by ChIP on chip as SOX2 [Gene ID=6657] transcription factor targets in human embryonic stem cells.
Set 'NOS targets': genes upregulated and identified by ChIP on chip as targets of the transcription factors NANOG [Gene ID=79923], OCT4[Gene ID=5460], and Sox2 [Gene ID=6657] (NOS) in human embryonic stem cells.
Set 'Suz12 targets': genes identified by ChIP on chip as targets of the Polycomb protein SUZ12 [Gene ID=23512] in human embryonic stem cells.
Set 'Eed targets': genes identified by ChIP on chip as targets of the Polycomb protein EED [Gene ID=8726] in human embryonic stem cells.
Set 'H3K27 bound': genes posessing the trimethylated H3K27 (H3K27me3) mark in their promoters in human embryonic stem cells, as identified by ChIP on chip.
Set 'PRC2 targets': Polycomb Repression Complex 2 (PRC) targets; identified by ChIP on chip on human embryonic stem cells as genes that: posess the trimethylated H3K27 mark in their promoters and are bound by SUZ12 [Gene ID=23512] and EED [Gene ID=8726] Polycomb proteins.
Set 'Myc targets1': targets of c-Myc [Gene ID=4609] identified by ChIP on chip in cultured cell lines, focusing on E-box???containing genes; high affinity bound subset
Set 'Myc targets2': targets of c-Myc [Gene ID=4609] and Max [Gene ID=4149] identified by ChIP on chip in a Burkitt???s lymphoma cell line; overlap set.
Genes showing cell-cycle stage-specific expression [PMID=12058064].
Set 'Proliferation Cluster': genes defined in human breast tumor expression data.
Genes that correlated most highly with left ventricular mass (LVM) index.
Genes up-regulated in prefrontal cortex (PFC) of mice carrying a hemizygotic microdeletion in the 22q11.2 region.
Genes down-regulated in prefrontal cortex (PFC) of mice carrying a hemizygotic microdeletion in the 22q11.2 region.
Genes up-regulated in hyppocampus of mice carrying a hemizygotic microdeletion in the 22q11.2 region.
Genes down-regulated in hyppocampus of mice carrying a hemizygotic microdeletion in the 22q11.2 region.
Genes located outside the microdeletion region in 22q11 which were differentially expressed in the same manner both in hyppocampus and prefrontal cortex.
Ampliconic (multicopy) genes on X chromosome that are up-regulated in round spermatids compared to the single-copy X chromosome genes.
Single copy (non-ampliconic) genes on the X chromosome that are down-regulated in round spermatids compared to the multicopy X chromosome genes.
Set 'Core 9': 'embryonic stem cell' transcription regulators that are preferentially and coordinately overexpressed in the high-grade, ER-negative breast cancer tumors.
Breast cancer compendium: 100 transcription regulators showing most correlated expression with the 9 'embryonic stem cell' transcription factors that are preferentially and coordinately overexpressed in the high-grade, ER-negative breast cancer tumors.
Genes that are most strongly positively correlated with systolic blood pressure (SBP).
Genes that are most strongly negatively correlated with systolic blood pressure (SBP).
Up-regulated cis-regulated expression quantitative loci (cis-eQTL) in the heart that colocalize with previously mapped cardiac mass QTLs.
Down-regulated cis-regulated expression quantitative loci (cis-eQTL) in the heart that colocalize with previously mapped cardiac mass QTLs.
Genes whose expression peaked at 20 min after stimulation of HeLa cells with EGF [Gene ID=1950].
Genes whose expression peaked at 40 min after stimulation of HeLa cells with EGF [Gene ID=1950].
Genes whose expression peaked at 60 min after stimulation of HeLa cells with EGF [Gene ID=1950].
Genes whose expression peaked at 120 min after stimulation of HeLa cells with EGF [Gene ID=1950].
Genes whose expression peaked at 240 min after stimulation of HeLa cells with EGF [Gene ID=1950].
Genes whose expression peaked at 480 min after stimulation of HeLa cells with EGF [Gene ID=1950].
Genes whose expression peaked at 20 min after stimulation of MCF10A cells with EGF [Gene ID=1950].
Genes whose expression peaked at 40 min after stimulation of MCF10A cells with EGF [Gene ID=1950].
Genes whose expression peaked at 60 min after stimulation of MCF10A cells with EGF [Gene ID=1950].
Genes whose expression peaked at 120 min after stimulation of MCF10A cells with EGF [Gene ID=1950].
Genes whose expression peaked at 240 min after stimulation of MCF10A cells with EGF [Gene ID=1950].
Genes whose expression peaked at 480 min after stimulation of MCF10A cells with EGF [Gene ID=1950].
Genes whose expression peaked at 20 min after stimulation of MCF10A cells with serum.
Genes whose expression peaked at 40 min after stimulation of MCF10A cells with serum.
Genes whose expression peaked at 60 min after stimulation of MCF10A cells with serum.
Genes whose expression peaked at 120 min after stimulation of MCF10A cells with serum.
Genes whose expression peaked at 240 min after stimulation of MCF10A cells with serum.
Genes whose expression peaked at 480 min after stimulation of MCF10A cells with serum.
Experimentally validated direct targets of MIR192 [Gene ID=406967] microRNA; MIR192 caused cell cycle arrest in HCT116 cells (colon cancer).
Genes down-regulated in HCT116 cells (colon cancer) by expression of MIR192 or MIR215 [Gene ID=406967, 406997] at 24 h.
Genes whose expression positively correlated with that of SMARCA2 [Gene ID=6595] in prostate cancer samples.
Genes whose expression negatively correlated with that of SMARCA2 [Gene ID=6595] in prostate cancer samples.
Genes downregulated in MCF10A cells (breast cancer) co-cultured with cancer-associated fibroblasts (CAF).
Selected genes down-regulated in inflammatory monocytes infiltrating hepatocellular carcinoma (HCC).
Selected genes up-regulated in inflammatory monocytes infiltrating hepatocellular carcinoma (HCC).
Selected genes down-regulated in peripheral blood monocytes (PBMC) of patients with hepatocellular carcinoma (HCC) compared to those with chronic hepatitis.
Genes up-regulated in H1299 cells (lung cancer) upon knockdown of SMAD6 [Gene ID=4091] by RNAi.
Genes down-regulated in H1299 cells (lung cancer) upon knockdown of SMAD6 [Gene ID=4091] by RNAi.
Genes changed in prostate cancer: androgen independent vs androgen dependent samples.
Genes up-regulated in metastatic vs non-metastatic stromal cells originated from either bone or prostate tissues.
Genes down-regulated in metastatic vs non-metastatic stromal cells originated from either bone or prostate tissues.
Genes up-regulated in BxPC3 cells (pancreatic cancer) after treatment with TNF [Gene ID=7124] or IKI-1, an inhibitor of I?B kinase (IKK).
Genes down-regulated in BxPC3 cells (pancreatic cancer) after treatment with TNF [Gene ID=7124] or IKI-1, an inhibitor of I?B kinase (IKK).
Down-regulated genes in the B lymphocyte developmental signature, based on expression profiling of lymphomas from the Emu-myc transgenic mice: the Pre-BI stage.
Up-regulated genes in the B lymphocyte developmental signature, based on expression profiling of lymphomas from the Emu-myc transgenic mice: the  Large Pre-BII stage.
Down-regulated genes in the B lymphocyte developmental signature, based on expression profiling of lymphomas from the Emu-myc transgenic mice: the  Large Pre-BII stage.
Up-regulated genes in the B lymphocyte developmental signature, based on expression profiling of lymphomas from the Emu-myc transgenic mice: the Small Pre-BII stage.
Down-regulated genes in the B lymphocyte developmental signature, based on expression profiling of lymphomas from the Emu-myc transgenic mice: the Small Pre-BII stage.
Up-regulated genes in the B lymphocyte developmental signature based on expression profiling of lymphomas from the Emu-myc transgenic mice: the immature B stage.
Down-regulated genes in the B lymphocyte developmental signature based on expression profiling of lymphomas from the Emu-myc transgenic mice: the immature B stage.
Up-regulated genes in the B lymphocyte developmental signature, based on expression profiling of lymphomas from the Emu-myc transgenic mice: the  mature B
Down-regulated genes in the B lymphocyte developmental signature, based on expression profiling of lymphomas from the Emu-myc transgenic mice: the  mature B
Up-regulated genes in the B lymphocyte developmental signature, based on expression profiling of lymphomas from the Emu-myc transgenic mice: plasma cell.
Down-regulated genes in the B lymphocyte developmental signature, based on expression profiling of lymphomas from the Emu-myc transgenic mice: plasma cell.
Genes correlated with the early tumor onset in the Emu-myc transgenic mouse lymphoma model.
Genes correlated with the late tumor onset in the Emu-myc transgenic mouse lymphoma model.
Substrates of PRKDC [Gene ID=5591].
Proteins that regulate activity of PRKDC [Gene ID=5591].
Genes up-regulated in medulloblastoma tumors from animals with  inactivating mutations of one copy of PTCH1 or SUFU [Gene ID=5727, 51684] in conjunction with TP53 [Gene ID=7157] loss.
Genes down-regulated in medulloblastoma tumors from animals with  inactivating mutations of one copy of PTCH1 or SUFU [Gene ID=5727, 51684] in conjunction with TP53 [Gene ID=7157] loss.
Genes involved in DNA repair, compiled manually by the authors.
Genes involved in DNA replication, compiled manually by the authors.
Genes within amplicon 1q21 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 1q32 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 5p15 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 6p24-p22 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 7p22 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 7p15 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 7q21-q22 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 8p12-p11 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 8q12-q22 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 8q23-q24 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 10q22 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon  11q12-q14 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 12q13-q21 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon  12q24 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 14q22 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 15q26 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 16p13 identified in a study of 191 breast tumor samples.
Genes within amplicon 16q24 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 17p11 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 17q11-q21 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 17q21-q25 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 19p13 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 19q13.1 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 19q13.4 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 20p13 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 20q11 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 20q12-q13 identified in a copy number alterations study of 191 breast tumor samples.
Genes within amplicon 21q22 identified in a copy alterations study of 191 breast tumor samples.
Genes within amplicon 22q13 identified in a copy number alterations study of 191 breast tumor samples.
Genes both mutated and amplified in a panel of 191 breast tumor samples.
Genes that reduced viability of NCI-H1155 cells (non-small-cell lung cancer, NSCLC) in the presence of otherwise sublethal concentrations of paclitaxel [PubChem=4666], based on RNAi synthetic lethal screen.
Pre-mitotic cell cycle regulators (CDC) identified in an shRNA screen of the ubiquitin pathway components.
Genes down-regulated in hES cells (human embryonic stem cells) after treatment with the ALK [Gene ID=238] inhibitor SB-431542 [PubChem=16079008].
Genes up-regulated in hES cells (human embryonic stem cells) after treatment with the ALK [Gene ID=238] inhibitor SB-431542 [PubChem=4521392].
Genes down-regulated in hES cells (human embryonic stem cells) after treatment with the ALK [Gene ID=238] inhibitor SB-431542 [PubChem=4521392].
Adenocarcinoma metastatic program genes up-regulated in A549 and H2126 cells (lung cancer) lacking functional STK11 [Gene ID=6794] but down-regulated by the normal gene.
Genes down-regulated in BJAB cell line (B lymphocyte) after expression of the viral microRNA miR-K12-11 which functions as an ortholog of cellular MIR155 [Gene ID=406947].
High-grade amplification (copy number, CN???5) detected in primary neuroblastoma samples.
Genes up-regulated and displaying increased copy number in glioblastoma samples.
Genes down-regulated and displaying decreased copy number in glioblastoma samples.
The lung adenocarcinoma TSP (tumor sequencing project) genes that were found significantly mutated by at least one method.
The lung adenocarcinoma TSP (tumor sequencing project) genes with significantly higher frequencies of nonsense, splice site, and frame-shift mutations.
The lung adenocarcinoma TSP (tumor sequencing project) genes showing strong correlation between DNA copy number variation and gene expression.
Genes up-regulated in HMLE cells (immortalized nontransformed mammary epithelium) after E-cadhedrin (CDH1) [Gene ID=999] knockdown by RNAi.
Genes down-regulated in HMLE cells (immortalized nontransformed mammary epithelium) after E-cadhedrin (CDH1) [Gene ID=999] knockdown by RNAi.
Genes up-regulated in HMLE cells (mmortalized nontransformed mammary epithelial) by expression of a dominant-negative form of E-cadhedrin (CDH1) [Gene ID=999].
Genes down-regulated in HMLE cells (mmortalized nontransformed mammary epithelial) by expression of a dominant-negative form of E-cadhedrin (CDH1) [Gene ID=999].
Genes up-regulated in HMLE cells (immortalized nontransformed mammary epithelial) cells after loss of function of E-cadhedrin (CDH1) [Gene ID=999], which was achieved either by RNAi knockdown or by expression of a dominan-negative form of CDH1.
Genes down-regulated in HMLE cells (immortalized nontransformed mammary epithelial) cells after loss of function of E-cadhedrin (CDH1) [Gene ID=999], which was achieved either by RNAi knockdown or by expression of a dominan-negative form of CDH1.
Genes changed in HMLE cells (mmortalized nontransformed mammary epithelium) after RNAi knockdown of both CDH1 [Gene ID=999] and CTNNB1 [Gene ID=1499], compared to the knockdown of CDH1 alone.
Genes present but differentially expressed between Hep3B cells (hepatocellular carcinoma, HCC) with RNAi knockdown of SDHB [Gene ID=6390] and control cells.
Genes linked to the ECM maintenance and angiogenesis that were changed in HT1080 cells (fibrosarcoma) over-expressing MMP14 [Gene ID=4323] compared to those with knockdown of the gene by RNAi.
Genes whose expression most uniformly correlated with that of MMP14 [Gene ID=4323] both in HT1080 cells (fibrosarcoma) and in 190 human tumors.
Genes up-regulated in HT1080 cells (fibrosarcoma) over-expressing MMP14 [Gene ID=4323] compared to those with knockdown of the gene by RNAi.
Genes down-regulated in HT1080 cells (fibrosarcoma) over-expressing MMP14 [Gene ID=4323] compared to those with knockdown of the gene by RNAi.
Genes associated with metastasis of breast cancer in the lung compared to the non-lung metastasis.
Genes turned on in Hep3B cells (hepatocellular carcinoma, HCC) upon knockdown of SDHB [Gene ID=6390] by RNAi.
Genes turned off in Hep3B cells (hepatocellular carcinoma, HCC) upon knockdown of SDHB [Gene ID=6390] by RNAi.
Genes down-regulated in P14 nerves of transgenic mice having hypomorhic (reduced function) allele of EGR2 [Gene ID=1959].
Top 100 probe sets for core-binding factor (CBF) acute myeloid leukemia (AML): contains CBFB MYH11 [Gene ID=865, 4629] or AML1 ETO [Gene ID=861, 862] fusions.
Genes up-regulated in HC11 cells (mammary epithelium) by expression of constantly active CTNNB1 [Gene ID=1499].
Genes specifically down-regulated in pediadric acute lymphoblastic leukemia (ALL) patients by mercaptopurine [PubChem=667490].
Genes down-regulated in LNCaP cells (prostate cancer) in response to synthetic androgen R1881 [PubChem=13766].
Genes up-regulated in plasma cells compared with B lymphocytes.
Genes down-regulated in A549 cells (lung cancer) after RNAi knockdown of activated KRAS [Gene ID=3845].
Human orthologs of genes up-regulated in the crb ('crash and burn') zebrafish mutant that represents a loss-of-function mutation in BMYB [Gene ID=4605].
Top 100 probe sets for pediatric acute myeloid leukemia (AML) subtype t(15;17): has PML RARA fusion [Gene ID=5371, 5914].
Genes down-regulated in hepatocellular carcinoma (HCC) induced by ciprofibrate [PubChem=2763].
Genes down-regulated in the temporal cortex samples from patients with major depressive disorder.
Genes up-regulated by induction of E2F1 expression in Saos2 (osteosarcoma) cells.
Top 50 down-regulated markers for the diffused large B-cell lymphoma (DLBCL) that distinguished between cured and fatal/refractory clinical outcomes.
Genes up-regulated in Jurkat cells (T lymphocyte) by IFN1@, and IFNB1 [Gene ID=3438, 3456] but not by overexpression of a constitutively active form of IRF3 [Gene ID=3661].
Molecular timetable composed of 96 time-indicating genes (103 probes) in the central (suprachiasmatic nucleus (SCN)) clock.
Up-regulated genes highly correlated with acute lymphoblastic leukemia (ALL) vs acute myeloid leukemia (AML).
Genes known to modulate ROS or whose expression changes in response to ROS
Genes which comprise the top 1% of highly interconnected genes (major hubs) that account for most of gene interactions in the reconstructed regulatory networks from expression profiles in B lymphocytes.
Genes down-regulated in P493-6 cells (Burkitt's lymphoma) induced to express MYC [Gene ID=4609].
Top 63 probe sets for pediatric acute myeloid leukemia (AML) subtype inv(16); has a CBFB-MYH11 fusion [Gene ID=865, 4629].
Genes up-regulated during transition from L0 (non-tumor, not infected with HCV) to L1 (non-tumor, infected with HCV) in the development of hepatocellular carcinoma.
Genes down-regulated during transition from L1 (non-tumor, infected with HCV) to G1 (well differentiated tumor, infected with HCV) in the development of hepatocellular carcinoma.
Nearest neighbors of TAL1 [Gene ID=6886], based on the close agreement of their expression profiles with that of TAL1 in pediatric T cell acute lymphoblastic leukemia (T-ALL)
Genes up-regulated in BJAB cells (B-lymphoma) after leucine [PubChem=857] deprivation.
Genes down-regulated in hepatocellular carcinoma (HCC) tissue of MYC and TGFA [Gene ID=4609, 7039] double transgenic mice.
Genes down-regulated during transition from G1 (well differentiated tumor, infected with HCV) to G2 (moderately differentiated tumor, infected with HCV) in the development of hepatocellular carcinoma.
Up-regulated in CD8+ [Gene ID=925] T lymphocytes undergoing homeostatic proliferation (HP) versus the naive cells; these genes are not up-regulated versus effector or memory cell population.
The cyclin D1 signature: genes whose expression correlated with the levels of CCND1 [Gene ID=595].
Top 50 most up-regulated genes in human platelet cells.
Human orthologs of genes down-regulated in zebra fish after knockdown of BMYB [Gene ID=4605] by morpholino.
Genes down-regulated in hepatocellular carcinoma of ACOX1 [Gene ID=51] knockout mice.
Genes up-regulated in BJAB cells (B-lymphoma) after glucose [PubChem=206] deprivation.
Genes consistently up-regulated in HMEC cells (primary mammary epithelium) upon expression of TERT [Gene ID=7015] off a retroviral vector.
Genes up-regulated in hepatocellular carcinoma (HCC) induced by overexpression of MYC [Gene ID=4609].
Genes up-regulated by adenoviral expression of c-MYC [Gene ID=4609] in HUVEC cells (umbilical vein endothelium).
Genes down-regulated during transition from L0 (non-tumor, not infected with HCV) to L1 (non-tumor, infected with HCV) in the development of hepatocellular carcinoma.
Genes up-regulated in HT1080 cells (fibrosarcoma) by treatment with interferon alpha for 6 h.
Primary targets of TP53 (p53) [Gene ID=7157] in the H1299 (lung cancer) cell line.
Genes up-regulated in BJAB cells (B-lymphoma) after glutamine [PubChem=738] deprivation.
Genes up-regulated in MCF-7 cells (breast cancer) by estradiol (E2) [PubChem=5757].
Genes up-regulated in hepatocellular carcinoma (HCC) tissue of MYC and TGFA [Gene ID=4609, 7039] double transgenic mice.
Genes upreglated in peripheral blood lymphocytes (PBL) from patients with well functioning kidneys more than 1-year post transplant compared to those from normal living kidney donors.
HOXA9 [Gene ID=3205] targets up-regulated in hematopoietic stem cells.
Genes down-regulated in HT1080 (fibrosarcoma) cells by treatment with interferon beta for 6 h.
Genes up-regulated during transition from G2 (moderately differentiated tumor, infected with HCV) to G3 (poorly differentiated tumor, infected with HCV) in the development of hepatocellular carcinoma.
Genes down-regulated in AIDS-related primary effusion lymphoma (PEL) samples compared to other tumor subtypes and normal B lymphocytes.
Human orthologs of BMYB [Gene ID=4605] target genes in zebra fish, identified as commonly changed in the BMYB loss of function mutant crb ('crush and burn') and after knockdown of BMYB by morpholino.
Primary targets of TP53 (p53) [Gene ID=7157] in the H1299 (lung cancer) cell line.
Genes up-regulated by POU5F1 [Gene ID=5460] in bladder cancer cell lines.
Genes down-regulated by POU5F1 [Gene ID=5460] in bladder cancer cell lines.
Genes down-regulated in five primary endothelial cell types (lung, aortic, iliac, dermal, and colon) by TNF [Gene ID=7124].
Genes up-regulated in mature plasma cells compared with plasmablastic B lymphocytes.
Genes up-regulated in NCCIT cell line (embryonic teratocarcinoma) after stimulation with WNT3A [Gene ID=89780].
Genes down-regulated in BJAB cells (B-lymphoma) after leucine [PubChem=857] deprivation.
Genes down-regulated in HC11 cells (mammary epithelium) by expression of constantly active CTNNB1 [Gene ID=1499].
Genes specifically up-regulated in pediatric acute lymphoblastic leukemia (ALL) patients by mercaptopurine [PubChem=667490] and low-dose methotrexate (LDMTX) [PubChem=4112].
Genes up-regulated in hepatocellular carcinoma (HCC) cell lines  resistant to IFNA2 [Gene ID=3440].
Genes up-regulated during transition from G1 (well differentiated tumor, infected with HCV) to G2 (moderately differentiated tumor, infected with HCV) in the development of hepatocellular carcinoma.
Genes up-regulated in a breast cancer cell line resistant to tamoxifen [PubChem ID=5376] compared to the parental line sensitive to the drug.
Human orthologs of genes down-regulated in the crb ('crash and burn') zebrafish mutant that represents a loss-of-function mutation in BMYB [Gene ID=4605].
Genes up-regulated in primary hepatocytes and Hep3B (hepatocyte) cells in response to IFNA [Gene ID=3439].
Genes down-regulated in plasma cells compared with B lymphocytes.
Genes used to predict the response of patients with hepatocellular carcinoma (HCC) to combination chemotherapy with 5-fluorouracil (5-FU) [PubChem=3385] and IFN alpha (IFN1@) [Gene ID=3438].
Genes associated with clinical prognosis of pediatric AML (acute myeloid leukemia): good prognosis=no relapse > 3 years; poor prognosis=relapse < 1 year or no response to therapy.
Top 50 up-regulated markers for the diffused large B-cell lymphoma (DLBCL) that distinguished between cured and fatal/refractory clinical outcomes.
Genes differentially expressed in kidney biopsies from patients with acute transplant rejection compared to the biopsies from patients with well functioning kidneys more than 1-year post transplant.
Genes up-regulated in hepatocellular carcinoma of ACOX1 [Gene ID=51] knockout mice.
Genes down-regulated during transition from G2 (moderately differentiated tumor, infected with HCV) to G3 (poorly differentiated tumor, infected with HCV) in the development of hepatocellular carcinoma.
Genes specifically up-regulated in pediadric acute lymphoblastic leukemia (ALL) patients by mercaptopurine [PubChem=667490].
Molecular timetable composed of 162 time-indicating genes (182 probes) in the peripheral (liver) clock.
Protein profiles associated with survival in lung adenocarcinoma.
Top up-regulated marker genes for medulloblastoma classification: desmoplastic vs classic morphology.
Genes induced in the liver during hepatitis B (HBV) viral clearance in chimpanzees.
Human orthologs of genes up-regulated in zebra fish after knockdown of BMYB [Gene ID=4605] by morpholino.
Down-regulated genes highly correlated with acute lymphoblastic leukemia (ALL) vs acute myeloid leukemia (AML).
Genes that escape X inactivation.
Genes up-regulated in HT1080 (fibrosarcoma) cells by treatment with interferon beta for 6 h.
Genes down-regulated in response to both hypoxia and overexpression of an active form of HIF1A [Gene ID=3091].
Genes down-regulated in hepatocellular carcinoma (HCC) from MYC and E2F1 [Gene ID=4609, 1869] double transgenic mice.
Genes up-regulated in LNCaP cells (prostate cancer) in response to synthetic androgen R1881 [PubChem=13766].
Genes up-regulated by forced expression of APC [Gene ID=324] in the APC-deficient SW480  cell line (colon cancer).
Genes whose expression is significantly and negatively correlated with poor breast cancer clinical outcome (defined as developing distant metastases in less than 5 years).
Genes changed in INA-6 cells (multiple myeloma, MM) by re-addition of IL6 [Gene ID=3569] after its initial withdrawal for 12h.
Top down-regulated marker genes for medulloblastoma classification: desmoplastic vs classic morphology.
Genes down-regulated in MCF-7 cells (breast cancer) by estradiol (E2) [PubChem=5757].
Genes specifically down-regulated in pediatric acute lymphoblastic leukemia (ALL) patients by high-dose methotrexate (HDMTX) [PubChem=4112].
Genes essential to the development of megakaryocytes, as expressed in normal cells and essential thrombocythemic cells (ET).
Genes down-regulated in mature plasma cells compared with plasmablastic B lymphocytes.
Potential marker genes specifically up-regulated in the majority of hepatocellular carcinoma (HCC) tumors.
Top 100 probe sets for pediatric acute myeloid leukemia (AML) subtypes with chimeric MLL fusions [Gene ID=4297].
Genes up-regulated in Jurkat cells (T lymphocyte) by expression of a constitutively active form of IRF3 [Gene ID=3661].
Genes up-regulated in hepatocellular carcinoma (HCC) from MYC and E2F1 [Gene ID=4609, 1869] double transgenic mice.
Genes up-regulated in the temporal cortex samples from patients with major depressive disorder.
Genes up-regulated in P14 nerves of transgenic mice having hypomorhic (reduced function) allele of EGR2 [Gene ID=1959].
Genes identified by ChIP within the high-affinity group of MYC [Gene ID=4609] targets.
Genes upreglated in peripheral blood lymphocytes (PBL) from patients with well functioning kidneys more than 1-year post transplant compared to those from normal living kidney donors.
Top 100 probe sets for pediatric acute myeloid leukemia (AML) subtype FAB M7 (also known as acute megakaryoblastic leukemia, AMKL).
Genes involved in oxidative phosphorylation; based on literature and sequence annotation resources and converted to Affymetrix HG-U133A probe sets.
Genes diffierentially expressed in peripheral blood lymphocytes (PBL) from patients with acute transplant rejection compared to those from patients with well functioning kidneys more than 1-year post transplant.
Genes down-regulated in HT1080 (fibrosarcoma) cells by treatment with interferon gamma for 6 h.
Genes up-regulated in five primary endothelial cell types (lung, aortic, iliac, dermal, and colon) by IFNG [Gene ID=3458].
Genes up-regulated in five primary endothelial cell types (lung, aortic, iliac, dermal, and colon) by TNF [Gene ID=7124].
Top marker genes in medulloblastoma associated with good response to treatment (good outcome).
Genes up-regulated in P493-6 cells (Burkitt's lymphoma) induced to express MYC [Gene ID=4609].
Genes up-regulated in A549 cells (lung cancer) after RNAi knockdown of activated KRAS [Gene ID=3845].
Genes specifically up-regulated in pediatric acute lymphoblastic leukemia (ALL) patients by high-dose methotrexate (HDMTX) [PubChem=4112].
Genes up-regulated in mast cells (MC) after stimulation with a bacterial lipopolysaccharide (LPS).
Genes consistently down-regulated in HMEC cells (primary mammary epithelium) upon expression of TERT [Gene ID=7015] off a retroviral vector.
Top 50 down-regulated markers distinguishing diffuse large B-cell lymphoma (DLBCL) from follicular lymphoma (FL) samples.
Genes down-regulated in hepatocellular carcinoma (HCC) induced by diethylnitrosamine (DENA) [PubChem=5921].
Genes down-regulated in five primary endothelial cell types (lung, aortic, iliac, dermal, and colon) by IFNG [Gene ID=3458].
Genes specifically down-regulated in pediatric acute lymphoblastic leukemia (ALL) patients by mercaptopurine [PubChem=667490] and low-dose methotrexate (LDMTX) [PubChem=4112].
Genes down-regulated in hepatocellular carcinoma (HCC) induced by overexpression of MYC [Gene ID=4609].
Genes up-regulated in hepatocellular carcinoma (HCC) induced by ciprofibrate [PubChem=2763].
Genes up-regulated during transition from L1 (non-tumor, infected with HCV) to G1 (well differentiated tumor, infected with HCV) in the development of hepatocellular carcinoma.
Top marker genes in medulloblastoma associated with poor response to treatment (poor outcome).
Genes up-regulated in peripheral B lymphocytes after incubation with IL4 [Gene ID=3565] for 4 h.
Nearest neighbors of LYL1 [Gene ID=4066], based on the close agreement of their expression profiles with that of LYL1 in pediatric T cell acute lymphoblastic leukemia (T-ALL).
Genes down-regulated in BJAB cells (B-lymphoma) after glucose [PubChem=206] deprivation.
Genes whose expression is significantly and positively correlated with poor breast cancer clinical outcome (defined as developing distant metastases in less than 5 years).
Genes regulated by forced expression of MYC [Gene ID=4609] in 293T (transformed fetal renal cell).
Genes up-regulated in response to both hypoxia and overexpression of an active form of HIF1A [Gene ID=3091].
Genes whose promoters were bound by E2F1 [Gene ID=1869] and E2F4 [Gene ID=1874] in the primary fibroblasts WI-38, by ChIP on chip assay.
Genes down-regulated in hepatocellular carcinoma (HCC) cell lines  resistant to IFNA2 [Gene ID=3440].
HOXA9 [Gene ID=3205] targets down-regulated in hematopoietic stem cells.
Genes differentially expressed in kidney biopsies from patients with acute transplant rejection compared to the biopsies from patients with well functioning kidneys more than 1-year post transplant.
Genes up-regulated in hepatocellular carcinoma (HCC) with intra-hepatic metastasis compared to the non-metastatic tumors.
Top 50 up-regulated markers distinguishing diffuse large B-cell lymphoma (DLBCL) from follicular lymphoma (FL) samples.
Genes down-regulated in Jurkat cells (T lymphocyte) by expression of a constitutively active form of IRF3 [Gene ID=3661].
Genes used to construct a to develop a system for accurate prediction of early intrahepatic recurrence of hepatocellular carcinoma (HCC).
Genes down-regulated in primary hepatocytes and Hep3B (hepatocyte) cells in response to IFNA [Gene ID=3439].
Genes down-regulated in a breast cancer cell line resistant to tamoxifen [PubChem ID=5376] compared to the parental line sensitive to the drug.
Genes up-regulated in AIDS-related primary effusion lymphoma (PEL) samples compared to other tumor subtypes and normal B lymphocytes.
Genes up-regulated in adult T-cell leukemia (ATL) cells compared to T lymphocytes from healthy controls.
Genes down-regulated in BJUB cells (B-lymphoma) in response to  rapamycin [PubChem=6610346] treatment.
Genes regulated by forced expression of MYC [Gene ID=4609] in 293T (transformed fetal renal cell).
Genes down-regulated in hepatocellular carcinoma (HCC) induced by overexpression of E2F1 [Gene ID=1869].
Genes up-regulated in hepatocellular carcinoma (HCC) induced by diethylnitrosamine (DENA) [PubChem=5921].
Genes diffierentially expressed in kidney biopsies from patients with well functioning kidneys more than 1-year post transplant compared to the biopsies from normal living kidney donors.
Genes up-regulated in BJUB cells (B-lymphoma) in response to  rapamycin [PubChem=6610346] treatment.
Genes down-regulated in BJAB cells (B-lymphoma) after glutamine [PubChem=738] deprivation.
Genes diffierentially expressed in peripheral blood lymphocytes (PBL) from patients with acute transplant rejection compared to those from patients with well functioning kidneys more than 1-year post transplant.
Genes diffierentially expressed in kidney biopsies from patients with well functioning kidneys more than 1-year post transplant compared to the biopsies from normal living kidney donors.
'Memory genes' expressed uniquely in CD8+ [Gene ID=925] memory T lymphocytes (compared with effector or na??ve cells)
Genes up-regulated in hepatocellular carcinoma (HCC) induced by overexpression of E2F1 [Gene ID=1869].
Top 100 probe sets for pediatric acute myeloid leukemia (AML) subtype t(8;21) ; has AML1 ETO fusion [Gene ID=861, 862].
The 'stemnes' signature: genes up-regulated and common to 6 human embryonic stem cell lines tested.
Genes up-regulated in Hc cells (normal hepatocyte) by  TNF [Gene ID=7124].
Genes up-regulated in HT1080 (fibrosarcoma) cells by treatment with interferon gamma for 6 h.
Genes changed in the B cell chronic lymphocytic leukemia (B-CLL) with deletions in the 17p13 region.
Genes up-regulated in the uteri of ovariectomized mice 6 h after progesterone [PubChem=5994] injection: HOXA10 [Gene ID=3206] knockout vs wild type animals.
Top 30 increased eosinophil specific transcripts.
Selected genes changed in K562 (immortalized erythroleukemia) cells induced by hemin [PubChem=26945] treatment to express erythroid properties.
Top genes up-regulated in MM4 vs MM1 subgroup of multiple myeloma samples.
Genes up-regulated in hematopoietic stem cells (HSC) overexpressing a constitutively active form of STAT5 [Gene ID=6776] off retroviral vector.
Genes up-regulated in hematopoietic progenitor cells (HPC) of T lymphocyte and NK (natural killer) lineage.
Cluster 2: genes down-regulated by RB1 [Gene ID=5925], CDNK2A [Gene ID=1029], and one of the E2Fs (E2F1, E2F2, or E2F3 [Gene ID=1869, 1870, 1871]).
Genes changed in the B cell chronic lymphocytic leukemia (B-CLL) with mutations in the variable immunoglobulin veriable heavy chain (VH) genes.
Metastatic propensity markers of head and neck squamous cell carcinoma (HNSCC): up-regulated in metastatic vs non-metastatic tumors.
Genes changed in acute myeloid leukemia (AML) with respect to cellular localization of NPM1 [Gene ID=4869]: cytoplasmic vs. nucleolar.
Genes up-regulated in B-CLL (B-cell chronic lymphocytic leukemia) patients with mutated immunoglobulin variable heavy chain (VH) genes.
Genes up-regulated in HEL cells (erythroleukemia) upon expression of ELF4 [Gene ID=2000].
Genes up-regulated synergistically in NB4 cells (acute promyelocytic leukemia, APL) by tretinoin and NSC682994 [PubChem=5538, 388304].
Genes up-regulated by estradiol (E2) [PubChem=5757] in U2OS cells (osteosarcoma) expressing ESR1 or ESR2 [[Gene ID = 2099, 2100].
Genes down-regulated in normal bone marrow plasma cells (BMPC) compared to polyclonal plasmablasts (PPC) that also distinguished multiple myeloma (MM) samples by expression of levels of TACI [Gene ID=23495].
Genes in a cCDNA library from hematopoietic stem cells (HSC) after subtraction of lineage-specific markers.
Top 100 genes positively (UP) and negatively (DN)  associated with T-cell acute lymphoblastic leukemia MLL T-ALL) expressing MLL-ENL fusion [Gene ID=4297, 4298].
Genes down-regulated in lymph nodes from patients with mantle cell lymphoma (MCL) compared to the non-malignant hyperplastic lymph nodes.
Genes changed between developmental stages of Valpha14i  natural killer T lymphocyte cells (NKT).
Genes changed in the B cell chronic lymphocytic leukemia (B-CLL) with deletions in the 13q14 region.
Genes up-regulated in lymph nodes from patients with mantle cell lymphoma (MCL) compared to the non-malignant hyperplastic lymph nodes.
Liver selective genes
Top genes down-regulated in metastatic (T24T) vs non-metastatic (T24) bladder cancer cell lines.
'Spiked' genes: genes most highly up-regulated in multiple myeloma samples; were not differentially expressed as compared to the normal plasma cells.
Genes down-regulated in multiple myeloma (MM) compared to normal plasma cells from the patient's identical twin.
Integrin signaling signature in precursor B leukemia (PBL) cells:  fibronectin (FN1) [Gene ID=2335] vs control treatment with poly-L-lysine.
Genes changed in the B cell chronic lymphocytic leukemia (B-CLL) with deletions in the 11q23 region.
Myb-regulated genes in MCF7 (breast cancer) and lung epithelial cell lines overexpressing MYBL2, MYBL1 or MYB [Gene ID=4605, 4603, 4602].
Genes down-regulated in T lymphocytes overexpressing TERT [Gene ID=7015] off a retrovirus vector.
Genes down-regulated in Wilm's tumor samples compared to fetal  kidney.
Genes down-regulated in hematopoietic precursor cells conditionally expressing HOXA9 and MEIS1 [Gene ID=3205, 4211].
Genes down-regulated in H358 cells (lung cancer) by inducible expression of CEBPA [Gene ID=1050] off plasmid vector.
Top 100 genes positively (UP) and negatively (DN)  associated with T-cell acute lymphoblastic leukemia MLL T-ALL) expressing MLL-ENL fusion [Gene ID=4297, 4298].
Genes down-regulated in acute promyelocytic leukemia (APL) patients with mutated FLT3 [Gene ID=2322].
ES/PNET (Ewing sarcoma; primitive neuroectodermal tumors) markers up-regulated in neuroblastoma cell lines expressing ESWR1-FLI1 [Gene ID=2130, 2313] fusion protein.
Genes up-regulated in H358 cells (lung cancer) by inducible expression of CEBPA [Gene ID=1050] off plasmid vector.
Genes most significantly up-regulated in multiple myeloma samples, compared to normal bone marrow plasma cells.
Genes up-regulated during in vitro maturation of CD14+ [Gene ID=929] monocytes (day 0) into immature (day 7) and mature dendritic cells (day 14).
Genes down-regulated in KCL22 cells (chronic myelogenous leukemia, CML, with BCR-ABL1 [GeneID=613, 25] fusion) by expression of CEBPA [GeneID=1050].
Genes down-regulated during in vitro maturation of CD14+ [Gene ID=929] monocytes (day 0) into immature (day 7) and mature dendritic cells (day 14).
Genes up-regulated in hematopoietic progenitor cells (HPC) of B lymphocyte lineage CD34+CD45RA+CD10+ [Gene ID=947, 5788, 4311].
Genes up-regulated in primary keratinocytes by expression of constantly active NOTCH1 [Gene ID=4851].
Genes changed in the B cell chronic lymphocytic leukemia (B-CLL) with trisomy of chromosome 12.
Genes up-regulated in immunoglobulin light chain amyloidosis plasma cells (ALPC) compared to multiple myeloma (MM) cells.
Genes up-regulated in polymorphonuclear neutrophilic granulocytes (PMNs) attracted to skin wounds.
Genes changed in NIH 3T3 cells (embryonic fibroblast) by expression of one or more of C/EBP proteins: CEBPA, CEBPB, CEBPG,  and CEBPD [Gene ID=1050, 1051, 1054, 1052].
Genes up-regulated in acute myeloid leukemia (AML) patients with mutated NPM1 [Gene ID=4869].
Up-regulated genes in the signature of adipose stromal cells (ADSC) immortalized by forced expression of telomerase (TERT) [Gene ID=7015].
Gene changed by CD40 [Gene ID=958] signaling in Ramos cells (EBV negative Burkitt lymphoma).
Genes abnormally regulated in response to CD40L and IL4 [Gene ID=959, 3565] stimulation of B lymphocytes from patients with a hypomorphic mutation of IKBKG [Gene ID=8517].
Genes up-regulated in T lymphocytes overexpressing TERT [Gene ID=7015] off a retrovirus vector.
Genes up-regulated in Wilm's tumor samples compared to fetal  kidney.
Genes up-regulated in Ewing family tumors (EFT) compared with normal bone marrow samples.
Genes up-regulated in acute promyelocytic leukemia (APL) patients with mutated FLT3 [Gene ID=2322].
Genes down-regulated in polymorphonuclear neutrophilic granulocytes (PMNs) attracted to skin wounds.
Genes down-regulated in B-CLL (B-cell chronic lymphocytic leukemia) patients with mutated immunoglobulin variable heavy chain (VH) genes.
Cluster 1: genes up-regulated by RB1 [Gene ID=5925], CDNK2A [Gene ID=1029], and one of the E2Fs (E2F1, E2F2, or E2F3 [Gene ID=1869, 1870, 1871]).
Genes changed in acute myeloid leukemia (AML) with respect to cellular localization of NPM1 [Gene ID=4869]: cytoplasmic vs. nucleolar.
Down-regulated genes in the signature of adipose stromal cells (ADSC) immortalized by forced expression of telomerase (TERT) [Gene ID=7015].
Genes up-regulated in hematopoietic precursor cells conditionally expressing HOXA9 and MEIS1 [Gene ID=3205, 4211].
Genes down-regulated in the uteri of ovariectomized mice 6 h after progesterone [PubChem=5994] injection: HOXA10 [Gene ID=3206] knockout vs wild type animals.
Genes down-regulated in primary keratinocytes by expression of constantly active NOTCH1 [Gene ID=4851].
Genes distinguishing in multiple myeloma (MM) samples with higher expression of TACI [Gene ID=23495].
Differentially expressed genes between high vs low ZAP70 [Gene ID=7535] acute lymphoblastic leukemia (ALL) cases with no known molecular aberrations.
Genes directly down-regulated by CD44 [Gene ID=960] stimulation of B lymphocytes.
Genes significantly up-regulated in the blood mononuclear cells from patients with systemic lupus erythematosus compared to those from healthy persons.
Genes up-regulated in NB4 cells (acute promyelocytic leukemia, APL) by tretinoin [PubChem ID=5538] alone.
Genes down-regulated in immunoglobulin light chain amyloidosis plasma cells (ALPC) compared to multiple myeloma (MM) cells.
Hypoxia response genes in both astrocytes and HeLa cell line.
The v2LDG set: 50 most variable late differentiation genes (LDG) with similar expression patterns in bone marrow plasma cells (BPC) and multiple myeloma (MM) samples.
Genes up-regulated by expression of GAB2 [Gene ID=9846] in K562 cells (chronic myeloid leukemia (CML) cell line with p210 BCR-ABL [Gene ID=613, 25]).
Genes down-regulated in hematopoietic progenitor cells (HPC) of T lymphocyte and NK (natural killer) lineage.
Top 50 most-increased mast cell specific genes.
The 'Bullinger validation signature' [PMID=15084693] used to validate prediction of prognostic outcome of acute myeloid leukemia (AML) patients with a normal karyotype.
Metastatic propensity markers of head and neck squamous cell carcinoma (HNSCC): down-regulated in metastatic vs non-metastatic tumors.
Genes whose CpG islands are hyper-methylated in the NB4 cell line (APL, acute promyelocytic leukemia) compared to PBMC (normal peripheral peripheral blood mononuclear cells).
Genes down-regulated in NB4 cells (acute promyelocytic leukemia, APL) by tretinoin [PubChem ID=5538] alone.
Genes up-regulated in KCL22 cells (chronic myelogenous leukemia, CML, with BCR-ABL1 [GeneID=613, 25] fusion) by expression of CEBPA [GeneID=1050].
Genes differentially expressed in pediatric AML (acute myeloid leukemia) samples from patients with good survival (>3 years without relapse) compared to those with poor survival (relapsed within one year after treatment).
Genes up-regulated in pro-B lymphocytes after knockout of CREBBP [Gene ID=1387].
Genes down-regulated in acute myeloid leukemia (AML) patients with mutated NPM1 [Gene ID=4869].
Neuroblastoma markers down-regulated in neuroblastoma cell lines expressing ESWR1-FLI1 [Gene ID=2130, 2313] fusion protein.
Genes up-regulated by imatinib [PubChem ID=5291] during dendritic cell differentiation.
Genes specifically expressed in FAB subtypes M2, M4, M5 and M7 of pediatric AML (acute myeloid leukemia).
Genes distinguishing in multiple myeloma (MM) samples with lower expression of TACI [Gene ID=23495].
Genes down-regulated in pro-B lymphocytes after knockout of CREBBP [Gene ID=1387].
Genes temporally up-regulated by CD44 [Gene ID=960] stimulation of B lymphocytes.
Genes temporally down-regulated by CD44 [Gene ID=960] stimulation of B lymphocytes.
Genes up-regulated in multiple myeloma (MM) compared to normal plasma cells from the patient's identical twin.
Genes most significantly down-regulated in multiple myeloma samples, compared to normal bone marrow plasma cells.
Gene changed by CD40 [Gene ID=958] signaling in Ramos cells (EBV negative Burkitt lymphoma).
Genes changed in the B cell chronic lymphocytic leukemia (B-CLL) with deletions in the  6q21 region.
Genes changed in samples from B-CLL (B-cell chronic lymphocytic leukemia) using the immunoglobulin heavy chain VH3-21 gene.
Genes down-regulated synergistically in NB4 cells (acute promyelocytic leukemia, APL) by tretinoin and NSC682994 [PubChem=5538, 388304].
Genes whose CpG islands showed greatly increased histone H4 acetylation in NB4 cells (acute promyelocytic leukemia, APL) upon treatment with tretinoin [PubChem=5538].
Genes up-regulated in normal bone marrow plasma cells (BMPC) compared to polyclonal plasmablasts (PPC) that also distinguished multiple myeloma (MM) samples by expression of levels of TACI (TNFRSF13B) [Gene ID=23495].
Genes directly up-regulated by CD44 [Gene ID=960] stimulation of B lymphocytes.
Myeloid leukemia model in mice with germ-line MLL-AF9 fusion knock-in [Gene ID=4297, 4300]: genes changed in comparison among the leukemic, preleukemic and wild-type animals.
Genes changed in samples from B-CLL (B-cell chronic lymphocytic leukemia) using the immunoglobulin heavy chain VH3-21 gene.
Genes commonly up-regulated in human alveolar rhabdomyosarcoma (ARMS) and its mouse model overexpressing PAX3-FOXO1 [Gene ID=5077, 2308] fusion.
Genes commonly down-regulated in human alveolar rhabdomyosarcoma (ARMS) and its mouse model overexpressing PAX3-FOXO1 [Gene ID=5077, 2308] fusion.
Genes up-pregulated by dsRNA in GRE cells (glioma; no interferon system).
Genes down-regulated in gastric cancer cell lines resistant to 5-fluorouracil [PubChem=3385].
Genes up-regulated in gastric cancer cell lines resistant to 5-fluorouracil [PubChem=3385].
Genes differentialy expressed in gastric cancer cell lines: doxorubicin [PubChem=31703] resistant vs sensitive.
Genes differentialy expressed in gastric cancer cell lines: doxorubicin [PubChem=31703] resistant vs sensitive.
Upregulated by induction of exogenous BRCA1 in EcR-293 cells
Genes up-pregulated by dsRNA in GRE cells (glioma; no interferon system).
DNA replication genes up-regulated in a Rat-1a cell line (fibroblast) by expression of E2F1 [Gene ID=1869].
Upregulated by induction of exogenous BRCA1 in EcR-293 cells
Genes selected in supervised analyses to discriminate cells expressing c-Myc [Gene ID=4609] from control cells expressing GFP.
Genes selected in supervised analyses to discriminate cells expressing E2F3 [Gene ID=1871] from control cells expressing GFP.
Genes selected in supervised analyses to discriminate cells expressing activated HRAS [Gene ID=3265] oncogene from control cells expressing GFP.
Genes selected in supervised analyses to discriminate cells expressing c-Src (CSK) [Gene ID=1445] from control cells expressing GFP.
Genes selected in supervised analyses to discriminate cells expressing activated beta-catenin (CTNNB1) [Gene ID=1499] oncogene from control cells expressing GFP.
Genes up-regulated in A4573 cells (Ewing's sarcoma, ESFT) after knockdown of BMI1 [Gene ID=648] by RNAi.
Genes down-regulated in A4573 cells (Ewing's sarcoma, ESFT) after knockdown of BMI1 [Gene ID=648] by RNAi.
The 'amino acid deprivation response' (AADR): genes up-regulated in HL-60 cells (acute promyelocytic leukemia, APL) after amino acid deprivation or treatment with the aminopeptidase inhibitor tosedostat (CHR-2797) [PubChem=15547703].
Genes up-regulated in HL-60 cells (acute promyelocytic leukemia, APL) after treatment with the aminopeptidase inhibitor tosedostat (CHR-2797) [PubChem=15547703] for 6 h.
Genes down-regulated in HL-60 cells (acute promyelocytic leukemia, APL) after treatment with the aminopeptidase inhibitor tosedostat (CHR-2797) [PubChem=15547703] for 6 h.
Genes up-regulated in HL-60 cells (acute promyelocytic leukemia, APL) after treatment with the aminopeptidase inhibitor tosedostat (CHR-2797) [PubChem=15547703] for 24 h.
Genes down-regulated in HL-60 cells (acute promyelocytic leukemia, APL) after treatment with the aminopeptidase inhibitor tosedostat (CHR-2797) [PubChem=15547703] for 24 h.
Genes up-regulated in HEP3B cells (liver cancer) overexpressing ATF5 [Gene ID=22809] off a plasmid vector.
Genes down-regulated in HEP3B cells (liver cancer) overexpressing ATF5 [Gene ID=22809] off a plasmid vector.
Genes whose expression in a panel of lymphoblastoid cell lines was associated with cytotoxicity of the anti-cancer analogs of cytidine, gemcitabine and cytarabine [PubChem=596, 3461, 6253].
The 'cytidine analog pathway': genes involved in transport and metabolism of the anti-cancer analogs of cytidine: gemcitabine and cytarabine [PubChem=596, 3461, 6253].
Immune response genes up-regulated in zenograft tumors formed by SNU-601 cells (gastric cancer) made to express LRRC3B [Gene ID=116135].
Selected genes up-regulated during invasion of lymphatic vessels during metastasis.
Selected genes down-regulated during invasion of lymphatic vessels during metastasis.
The postradiation tumor escape signature: genes up-regulated in tumors from irradiated stroma vs those from non-irradiated stroma.
The postradiation tumor escape signature: genes down-regulated in tumors from irradiated stroma vs those from non-irradiated stroma.
Genes up-regulated in A549GARS cells (lung cancer) resistant to the geldanamycin and 17-AAG [PubChem=5476289, 6440175].
Genes down-regulated in A549GARS cells (lung cancer) resistant to the geldanamycin and 17-AAG [PubChem=5476289, 6440175].
The 'group 1 set' of genes associated with acquired endocrine therapy resistance in breast tumors expressing ESR1 and ERBB2 [Gene ID=2099, 2064].
The 'group 2 set' of genes associated with acquired endocrine therapy resistance in breast tumors expressing ESR1 and ERBB2 [Gene ID=2099, 2064].
The 'group 3 set' of genes associated with acquired endocrine therapy resistance in breast tumors expressing ESR1 and ERBB2 [Gene ID=2099, 2064].
The 'group 4 set' of genes associated with acquired endocrine therapy resistance in breast tumors expressing ESR1 but not ERBB2 [Gene ID=2099, 2064].
The 'group 5 set' of genes associated with acquired endocrine therapy resistance in breast tumors expressing ESR1 but not ERBB2 [Gene ID=2099, 2064].
Top genes up-regulated in colon epithelium biopsies from FAP (familial adenomatous polyposis) patients with mutated APC [Gene ID=324].
Top genes down-regulated in colon epithelium biopsies from FAP (familial adenomatous polyposis) patients with mutated APC [Gene ID=324].
Selected electrophile and drug detoxication genes down-regulated in A549 and H460 cells (lung cancer) upon knockdown of NFE2L2 [Gene ID=4780] by RNAi.
Antigen processing and presentation genes up-regulated in JY cells (B lymphocytes) treated with TSA [PubChem=5562].
Antigen processing and presentation genes down-regulated in JY cells (B lymphocytes) treated with trichostatin A (TSA) [PubChem=5562].
Genes methylated aberrantly in HCT116 and Colo320 (colon cancer) cells.
Genes un-methylated aberrantly in HCT116 and Colo320 (colon cancer) cells.
Common up-regulated transcripts in fibroblasts expressing either XP/CS or TDD mutant forms of ERCC3 [Gene ID=2071], after UVC irradiation.
Genes with promoters bound by FOXP3 [Gene ID=50943], dependent on it, and changed in hybridoma cells stimulated by PMA [PubChem=4792] and ionomycin [PubChem=3733].
Genes with promoters bound by FOXP3 [Gene ID=50943], dependent on it, and changed in hybridoma cells stimulated by PMA [PubChem=4792] and ionomycin [PubChem=3733].
Genes expressed in at least one prostate cancer cell line but not in normal prostate epithelial cells or stromal cells
Genes up-regulated SUM44/LCCTam cells (breast cancer) resistant to 4-hydroxytamoxifen [PubChem=63062] relative to the parental SUM44 cells sensitive to the drug.
Genes down-regulated SUM44/LCCTam cells (breast cancer) resistant to 4-hydroxytamoxifen [PubChem=63062] relative to the parental SUM44 cells sensitive to the drug.
Overconnected mutated transcription factors regulating genes within the breast cancer amplicome.
Genes up-regulated by estradiol [PubChem=5757] and up-regulated by ESRRA [Gene ID=2101] in MCF-7 cells (breast cancer).
Genes down-regulated by estradiol [PubChem=5757] and down-regulated by ESRRA [Gene ID=2101] in MCF-7 cells (breast cancer).
Genes up-regulated by ESRRA [Gene ID=2101] only.
Genes down-regulated by ESRRA [Gene ID=2101] only.
Genes up-regulated by bacterial lipopolysaccharide (LPS) in non-tolerizeable (NT class) macrophages, compared to the ???tolerizeable??? (T class) ones.
Genes down-regulated by bacterial lipopolysaccharide (LPS) in non-tolerizeable (NT class) macrophages, compared to the ???tolerizeable??? (T class) ones.
Genes specifically responding to 4NQO treatment of primary fibroblasts.
Genes specifically responding to gamma radiation.
UV only responding genes in primary fibroblasts from young donors.
Genes responding to 4NQO treatment and gamma irradiation.
4NQO treatment and UV irradiation responding genes.
Gamma and UV responding genes.
Human environmental etress response genes not changed in primary fibroblasts from old donors in response to 4NQO treatment.
Human environmental stress response genes not changed in primary fibroblasts from Wilmor syndrom (WS) patients in response to 4NQO treatment.
Human environmental stress response (H-ESR) genes not changed in primary fibroblasts from old donors in response to gamma radiation.
Human environmental stress response genes not changed in primary fibroblasts from Werner syndrom (WS) patients in response to gamma radiation.
Human environmental stress response genes not changed in primary fibroblasts from old donors in response to UV radiation.
Human environmental stress response genes not changed in primary fibroblasts from patients with Warner syndrom (WS) .
Genes changed after DNA damage in cell lines from young donors, and that had a GO annotation.
Genes changed after DNA damage in cell lines from young donors, and that had a GO annotation.
All common stress response genes (Human Environmental Stress Response, H-ESR).
Genes with high histone H3 trimethylation mark at K27 (H3K27me3) in PC3 cells (prostate cancer) by ChIP-chip assay on a 12K CpG array (high-CpG-density promoters, HCP).
Top 200 genes with high histone H3 trimethylation mark at K27 (H3K27me3) in PC3 cells (prostate cancer), by ChIP-chip assay on an 88K microarray (all promoters).
Genes with high levels of histone H3 monomethylation mark at K27 (H3K27me1) in SW48 cells (colon cancer) by ChIP-chip assay on a 12K CpG array (CpG promoters only, HCP=high-CpG-density promoters).
Genes with high histone H3 tri-methylation mark at K27 (H3K27me3) in SW48 cells (colon cancer), by ChIP-chip assay on a 12K CpG array (high-CpG-density promoters, HCP).
Genes up-regulated in PC3 cells (prostate cancer) after EZH2 [Gene ID=2146] knockdown by RNAi.
Genes down-regulated in tumor compared to non-tumor liver samples from patients with hepatocellular carcinoma (HCC).
Genes up-regulated in gastric cancer cell lines resistant to cisplatin [PubChem=2767].
Genes down-regulated in gastric cancer cell lines resistant to cisplatin [PubChem=2767].
Up-regulated genes in the 'Field Effect' signature of normal lung tissue adjacent to the tumor.
Genes classifying non-tumor lung tissues by age after incution of lung cancer by urethane injection [PubChem=5641]: early (24-26 weeks) vs late (46 weeks).
Genes classifying non-tumor lung tissues by age after incution of lung cancer by urethane injection [PubChem=5641]: early (24-26 weeks) vs late (46 weeks).
Genes up-regulated in at least one of three multiple myeloma (MM) cell lines treated with the DNA hypomethylating agent decitabine (5-aza-2'-deoxycytidine) [PubChem=451668].
Genes down-regulated in at least one of three multiple myeloma (MM) cell lines treated with the DNA hypomethylating agent decitabine (5-aza-2'-deoxycytidine) [PubChem=451668].
Genes up-regulated in at least one of three multiple myeloma (MM) cell lines by TSA [PubChem=5562].
Genes down-regulated in at least one of three multiple myeloma (MM) cell lines by TSA [PubChem=5562].
Genes up-regulated in multiple myeloma (MM) cell lines treated with both decitabine [PubChem=451668] TSA [PubChem=5562].
Genes down-regulated in multiple myeloma (MM) cell lines treated with both decitabine [PubChem=451668] TSA [PubChem=5562].
Genes changed in meningioma samples positive for PGR [Gene ID=5241] compared to those without the receptor.
Genes changed in meningioma samples positive for PGR [Gene ID=5241] compared to those without the receptor.
Genes that comprise the mitochondria gene module
Genes that comprise the proteasome gene module
Gene predicting resistance of the NCI-60 cell lines to gamma radiation.
Genes down-regulated across the entire panel of NCI-60 cell lines in response to gamma radiation.
Genes with basal expression distinguishing NCI-60 cell lines with poor survival after 8 Gy gamma irradiation.
Genes with basal expression distinguishing NCI-60 cell lines with poor survival after 2 Gy gamma irradiation.
Up-regulated genes distinguishing between M1 (pro-inflammatory) and M2 (anti-inflammatory) macrophage subtypes.
Down-regulated genes distinguishing between M1 (pro-inflammatory) and M2 (anti-inflammatory) macrophage subtypes.
Components of RNA post-transcriptional modification machinery up-regulated in MDA-MB-435 cells (breast cancer) whose metastatic potential has been reduced by expression of NME1 [Gene ID=4830].
Up-regulated genes displaying alternative splicing in MDA-MB-435 cells (breast cancer) whose metastatic potential has been reduced by expression of NME1 [Gene ID=4830].
Down-regulated genes displaying alternative splicing in MDA-MB-435 cells (breast cancer) whose metastatic potential has been reduced by expression of NME1 [Gene ID=4830].
Candidate genes in significant regions of chromosomal copy number gains in a panel of melanoma samples.
Candidate genes in significant regions of chromosomal copy number losses in a panel of melanoma samples.
Genes up-regulated in mice with skin specific knockout of RB1 [Gene ID=5925] by Cre-lox.
Genes down-regulated in mice with skin specific knockout of RB1 [Gene ID=5925] by Cre-lox.
Genes up-regulated in mice with skin specific knockout of TP53 [Gene ID=7157].
Genes down-regulated in mice with skin specific knockout of TP53 [Gene ID=7157].
Genes up-regulated in mice with skin specific double knockout of both RB1 and TP53 [Gene ID=5925, 7157] by Cre-lox.
Genes down-regulated in mice with skin specific double knockout of both RB1 and TP53 [Gene ID=5925, 7157] by Cre-lox.
Genes in the red cluster of protein kinases distinguishing between luminal A and basal breast cancer subtypes.
Genes in the green cluster of protein kinases distinguishing between luminal A and basal breast cancer subtypes.
Genes in the blue cluster of protein kinases distinguishing between luminal A and basal breast cancer subtypes.
Genes in the gray cluster of protein kinases distinguishing between luminal A and basal breast cancer subtypes.
Protein kinases distinguishing between basal and luminal A subtypes of breast cancer.
Genes up-regulated in breast cancer tumors (formed by MCF-7 xenografts) resistant to tamoxifen [PubChem=5376].
Genes down-regulated in breast cancer tumors (formed by MCF-7 xenografts) resistant to tamoxifen [PubChem=5376].
Genes rapidly up-regulated in breast cancer cell cultures by estradiol [PubChem=5757].
Genes up-regulated in prostate tumor vs normal tissue samples.
Genes down-regulated in prostate tumor vs normal tissue samples.
Genes up-regulated in prostate cancer samples from African-American patients compared to those from the European-American patients.
Genes down-regulated in prostate cancer samples from African-American patients compared to those from the European-American patients.
Genes up-regulated in MCF10A cells (breast cancer) grown at low (mesenchymal phenotype) compared to those grown at high (epithelial, basal-like phenotype) confluency.
Genes down-regulated in MCF10A cells (breast cancer) grown at low (mesenchymal phenotype) compared to those grown at high (epithelial, basal-like phenotype) confluency.
Genes up-regulated in chronic lymphocytic leukemia (CLL) samples bearing deletions in the 13q14 region.
Genes down-regulated in chronic lymphocytic leukemia (CLL) samples bearing deletions in the 13q14 region.
Genes up-regulated in both colorectal cancer cells and normal testis relative to normal colon epithelium.
Genes up-regulated by IL2 [Gene ID=3558] in cells derived from  CD4+ [Gene ID=920] cutaneous T-cell lymphoma (CTCL).
Genes down-regulated by IL2 [Gene ID=3558] in cells derived from  CD4+ [Gene ID=920] cutaneous T-cell lymphoma (CTCL).
Cluster 1: genes up-regulated in lung tissue samples from mice with oncogenic form of KRAS [Gene ID=3845] and inactivated PTEN [Gene ID=5728].
Cluster 2: genes down-regulated in lung tissue samples from mice with oncogenic form of KRAS [Gene ID=3845] and inactivated PTEN [Gene ID=5728].
Cluster 3: genes up-regulated in lung tissue samples from mice with tumor-bearing genotypes (activated KRAS [Gene ID=3845] alone or together with inactivated PTEN [Gene ID=5728]).
Cluster 4: genes down-regulated in lung tissue samples from mice with tumor-bearing genotypes (activated KRAS [Gene ID=3845] alone or together with inactivated PTEN [Gene ID=5728]).
Genes down-regulated in HT1080 cells (fibrosarcoma) by treatment with interferon alpha for 6 h.
Genes from chromosomal copy number gains in a panel of 51 primary colon carcinoma samples.
Genes from chromosomal copy number losses in a panel of 51 primary colon carcinoma samples.
Genes up-regulated in three-dimentional (3D) cultures of preinvasive (S3-C) vs invasive (T4-2) breast cancer cells.
Genes down-regulated in three-dimentional (3D) cultures of preinvasive (S3-C) vs invasive (T4-2) breast cancer cells.
Genes up-regulated in monolayer (2D) cultures of preinvasive (S3-C) vs invasive (T4-2) breast cancer cells.
Genes down-regulated in monolayer (2D) cultures of preinvasive (S3-C) vs invasive (T4-2) breast cancer cells.
Genes up-regulated in MCF-7 cells (breast cancer) after knockdown of YBX1 [Gene ID=4904] by RNAi.
Genes down-regulated in MCF-7 cells (breast cancer) after knockdown of YBX1 [Gene ID=4904] by RNAi.
Genes up-regulated in A549 cells (lung cancer) upon expression of ASCL1 [Gene ID=429] off a viral vector.
Genes down-regulated in A549 cells (lung cancer) upon expression of ASCL1 [Gene ID=429] off a viral vector.
Genes whose CpG islands became hypermethylated in breast progenitor cells pre-exposed to estradiol [PubChem=5757].
Genes up-regulated in SaOS-2 cells (osteosarcoma) upon knockdown of YY1 [Gene ID=7528] by RNAi.
Genes down-regulated in SaOS-2 cells (osteosarcoma) upon knockdown of YY1 [Gene ID=7528] by RNAi.
Inflammatory genes down-regulated in mammary carcinoma cells after stimulation with TGFB1 [Gene ID=7040] for 1 hr.
Genes whose promoters where bound by HOXC6 [Gene ID=3223] in LNCaP cells (prostate cancer), according to a ChIP-chip analysis.
'Cancer prone response profile' (CPRP): genes changed in response to estradiol [PubChem=5757]  in epithelial cell cultures from patients at high risk of breast cancer.
'Cancer prone response profile' (CPRP): genes changed in response to bisphenol A [PubChem=6623]  in epithelial cell cultures from patients at high risk of breast cancer.
'Cancer prone response profile' (CPRP): genes common to estradiol and bisphenol A [PubChem=5757, 6623]  response of epithelial cell cultures from patients at high risk of breast cancer.
Genes up-regulated in prostate cancer cell lines after treatment with 5-aza-2'-deoxycytidine (decitabine) [PubChem=451668].
Genes up-regulated during prostate cancer progression in mice heterozygotic for both NKX3.1 and PTEN [Gene ID=4824, 5728].
Genes down-regulated during prostate cancer progression in mice heterozygotic for both NKX3.1 and PTEN [Gene ID=4824, 5728].
Mouse orthologs of human prostate cancer tumor markers which were deregulated in mice heterozygotic for both NKX3.1 and PTEN [Gene ID=4824, 5728].
Genes up-regulated in mesenchymal stem cells (MSC) engineered to express EWS-FLI1 [Gene ID=2130, 2321] fusion protein.
Genes down-regulated in mesenchymal stem cells (MSC) engineered to express EWS-FLI1 [Gene ID=2130, 2321] fusion protein.
Genes down-regulated in A549 cells (lung cancer) after treatment with AZD0530 [PubChem=10302451], a SRC [Gene ID=6714] kinase inhibitor.
The metastasis gene signature: genes up-regulated during metastasis of NSCLC (non-small cell lung carcinoma) tumors to bone.
The metastasis gene signature: genes down-regulated during metastasis of NSCLC (non-small cell lung carcinoma) tumors to bone.
Genes down-regulated by flavopiridol [PubChem=5287969] in the HCT116 cells (colon cancer) depending on their TP53 [Gene ID=7157] status: wild-type vs loss of the gene's function (LOF).
Genes up-regulated in SCLC (small cell lung cancer) cells with acquired resistance to ABT-737 [PubChem=11228183], an inhibitor of the BCL2 [Gene ID=596] family proteins.
Genes down-regulated in SCLC (small cell lung cancer) cells with acquired resistance to ABT-737 [PubChem=11228183], an inhibitor of the BCL2 [Gene ID=596] family proteins.
Up-regulated genes in the cancer progenitor (stem) cells corresponding to side population (SP) MCF7 cells (breast cancer) positive for MUC1 [Gene ID=4582].
Down-regulated genes in the cancer progenitor (stem) cells corresponding to side population (SP) MCF7 cells (breast cancer) positive for MUC1 [Gene ID=4582].
Genes up-regulated in H358 cells (lung cancer) by inducible expression of FOXA2 [GeneID=3170] in a Tet-off system.
Genes down-regulated in H358 cells (lung cancer) by inducible expression of FOXA2 [GeneID=3170] in a Tet-off system.
Genes up-regulated in derivatives of MCF-7aro cells (breast cancer) that developed resistance to tamoxifen [PubChem=5376] or  inhibitors of aromatase (CYP19A1) [Gene ID=1588].
Genes down-regulated in derivatives of MCF-7aro cells (breast cancer) that developed resistance to tamoxifen [PubChem=5376] or  inhibitors of aromatase (CYP19A1) [Gene ID=1588].
Top genes up-regulated in mesenchyme stem cells (MSC) grown in a tumor conditioned medium, which leads to carcinoma-associated fibroblast phenotype.
Genes whose promoters were bound by HOXC6 [Gene ID=3223] in LNCaP cells (prostate cancer) and whose expression changed upon loss of function (LOF) of HOXC6.
Genes whose promoters were bound by HOXC6 [Gene ID=3223] in LNCaP cells (prostate cancer) and whose expression changed upon loss of function (LOF) of HOXC6.
Epigenetically silenced genes up-regulated in HCT116 cells (colon cancer) hypomorphic for DICER1 [Gene ID=23405].
Embryonic genes targeted by LET7A1 [Gene ID=406881] and which are up-regulated in many human cancers.
Genes whose promoters were bound by HOXC6 [Gene ID=3223] in LNCaP cells (prostate cancer) and which were up-regulated in comparison of tumor vs normal prostate tissue samples.
Genes whose promoters were bound by HOXC6 [Gene ID=3223] in LNCaP cells (prostate cancer) and which were down-regulated in comparison of tumor vs normal prostate tissue samples.
Genes commonly up-regulated in SK-N-BE cells (neuroblastoma) after RNAi knockdown of CCND1 and CDK4 [Gene ID=595, 1019].
Genes commonly down-regulated in SK-N-BE cells (neuroblastoma) after RNAi knockdown of CCND1 and CDK4 [Gene ID=595, 1019].
Genes up-regulated in normal tissue adjacent to liver tumor, compared to the normal liver samples.
Genes down-regulated in normal tissue adjacent to liver tumor, compared to the normal liver samples.
Genes up-regulated in hepatocellular carcinoma (HCC) compared to normal liver samples.
Genes down-regulated in hepatocellular carcinoma (HCC) compared to normal liver samples.
Genes up-regulated in liver tumor compared to the normal adjacent tissue.
Genes down-regulated in liver tumor compared to the normal adjacent tissue.
Genes whose promoters display higher levels of histone H3 trimethylation mark at K27 (H3K27me3) in hepatocellular carcinoma (HCC) compared to normal liver.
Genes whose promoters display lower levels of histone H3 trimethylation mark at K27 (H3K27me3) in hepatocellular carcinoma (HCC) compared to normal liver.
Genes whose promoters display higher histone H3 trimethylation mark at K9 (H3K9me3) in hepatocellular carcinoma (HCC) compared to normal liver.
Genes whose promoters display lower histone H3 trimethylation mark at K9 (H3K9me3) in hepatocellular carcinoma (HCC) compared to normal liver.
Genes whose DNA is hypo-methylated in hepatocellular carcinoma (HCC) compared to normal liver.
Genes whose DNA is hyper-methylated in hepatocellular carcinoma (HCC) compared to normal liver.
Genes up-regulated in the MM1S cells (multiple myeloma) after treatment with aplidin [PubChem=44152164], a marine-derived compound with potential anti-cancer properties.
Genes down-regulated in the MM1S cells (multiple myeloma) after treatment with aplidin [PubChem=44152164], a marine-derived compound with potential anti-cancer properties.
Genes whose DNA was methylated both in primary tumors and across a panel of cancer cell lines.
Genes up-regulated in HT29 cells (colon cancer) after knockdown of CD24 [Gene ID=100133941] by both RNAi and monoclonal antibodies.
Genes down-regulated in HT29 cells (colon cancer) after knockdown of CD24 [Gene ID=100133941] by both RNAi and monoclonal antibodies.
Genes up-regulated in brain relapse of breast cancer.
Genes down-regulated in brain relapse of breast cancer.
Genes up-regulated in bone relapse of breast cancer.
Genes down-regulated in bone relapse of breast cancer.
Genes up-regulated in lung relapse of breast cancer.
Genes down-regulated in lung relapse of breast cancer.
Genes up-regulated in liver relapse of breast cancer.
Genes down-regulated in liver relapse of breast cancer.
Genes up-regulated in pleura relapse of breast cancer.
Genes down-regulated in pleura relapse of breast cancer.
Genes up-regulated in the luminal B subtype of breast cancer.
Genes down-regulated in the luminal B subtype of breast cancer.
Genes up-regulated in the luminal A subtype of breast cancer.
Genes down-regulated in the luminal A subtype of breast cancer.
Genes up-regulated in the erbb2 subype of breast cancer samples, characterized by higher expression of ERBB2 [Gene ID=2064].
Genes down-regulated in the erbb2 subype of breast cancer samples, characterized by higher expression of ERBB2 [Gene ID=2064].
Genes up-regulated in the normal-like subtype of breast cancer.
Genes down-regulated in the normal-like subtype of breast cancer.
Genes up-regulated in basal subtype of breast cancer samles.
Genes down-regulated in basal subtype of breast cancer samles.
Genes up-regulated in response to nutlin-3a [PubChem=216345], an inhibitor of MDM2 [Gene ID=4193],  in skin fibroblast cultures after knockdown of TP53 [Gene ID=7157] by RNAi.
Genes down-regulated in response to nutlin-3a [PubChem=216345], an inhibitor of MDM2 [Gene ID=4193],  in skin fibroblast cultures after knockdown of TP53 [Gene ID=7157] by RNAi.
Genes up-regulated in HSA/c and KYSE140 cells (esophageal squamous cell carcinoma, ESCC) after knockdown of PTTG1 [Gene ID=9232] by RNAi.
Genes down-regulated in HSA/c and KYSE140 cells (esophageal squamous cell carcinoma, ESCC) after knockdown of PTTG1 [Gene ID=9232] by RNAi.
Selected genes implicated in metastasis and epithelial-to-mesenchymal transition (EMT) which were up-regulated in MDA-MB-231 cells (breast cancer) upon knockdown of SKI [Gene ID=6497] by RNAi.
Selected genes implicated in metastasis and epithelial-to-mesenchymal transition (EMT) which were down-regulated in MDA-MB-231 cells (breast cancer) upon knockdown of SKI [Gene ID=6497] by RNAi.
Top highly correlated genes positively associated with poor survival of patients with suboptimally debulked ovarian tumors.
Top highly correlated genes negatively associated with poor survival of patients with suboptimally debulked ovarian tumors.
Genes whose expression in optimally debulked ovarian tumors is associated with survival prognosis.
Genes whose expression in suboptimally debulked ovarian tumors is associated with survival prognosis.
Apoptosis genes up-regulated by TP53 [Gene ID=7157] in HCT116 cells (colon cancer) treated with thymoquinone [PubChem=10281].
Apoptosis genes down-regulated by TP53 [Gene ID=7157] in HCT116 cells (colon cancer) treated with thymoquinone [PubChem=10281].
Top 50 genes up-regulated in ovarian cancer progenitor cells (also known as side population, SP, cells) in response to interferon alpha (IFNA).
Genes silenced in HCT116 cells (colon cancer) by methylation of CpG islands in their promoters.
DNA methylation status of germline-specific genes with high-CpG-density promoters (HCP) in primary fibroblasts: UP=methylated, DN=unmethylated.
DNA methylation status of germline-specific genes with high-CpG-density promoters (HCP) in primary fibroblasts: UP=methylated, DN=unmethylated.
DNA methylation status of germline-specific genes with high-CpG-density promoters (HCP) in sperm: UP=methylated, DN=unmethylated.
DNA methylation status of germline-specific genes with high-CpG-density promoters (HCP) in sperm: UP=methylated, DN=unmethylated.
Genes up-regulated in hairy cell leukemia (HCL) compared with normal and other neoplastic B cell populations.
Genes down-regulated in hairy cell leukemia (HCL) compared with normal and other neoplastic B cell populations.
Genes down-regulated in HCT116 cells (colon cancer) upon expression of MIR34B or MIR34C [Gene ID=407041, 407042] microRNAs.
50 genes the most significantly down-regulated in comparison of tumor vs non-tumor liver tissue from patients with hepatocellular carcinoma (HCC).
Genes up-regulated in adipose tissue mesenchymal stem cells (ASC) vs bone marrow mesenchymal stem cells (rBMSC)
Genes down-regulated in adipose tissue mesenchymal stem cells (ASC) vs bone marrow mesenchymal stem cells (rBMSC)
Genes changed in cancer stem cells isolated from mammary tumors compared to the non-tumorigenic cells.
Genes changed in cancer stem cells isolated from mammary tumors compared to the non-tumorigenic cells.
Top genes down-regulated in mesenchyme stem cells (MSC) grown in a tumor conditioned medium, which leads to carcinoma-associated fibroblast phenotype.
Genes up-regulated in ZR-75-1 cells (breast cancer, amplified 8p11-12 region) upon knockdown of PPAPDC1B [Gene ID=84513] by RNAi.
Genes down-regulated in ZR-75-1 cells (breast cancer, amplified 8p11-12 region) upon knockdown of PPAPDC1B [Gene ID=84513] by RNAi.
Inflammatory cytokines, chemokines and their cognate receptors up-regulated in THP-1 cells (monocyte) after treatment with PSMD4 [Gene ID=5710].
Up-regulated genes in the expression signature of aneuploidy in uveal melanoma tumors: low vs high aneuploidy.
Down-regulated genes in the expression signature of aneuploidy in uveal melanoma tumors: low vs high aneuploidy.
Genes up-regulated in microdissected endothelial samples from ovarian cancer tumors with tumor-infiltrating lymphocytes (TIL) vs those without TILs.
Genes  down-regulated in microdissected endothelial samples from ovarian cancer tumors with tumor-infiltrating lymphocytes (TIL) vs those without TILs.
Genes changed in HBE cells (bronchial epithelium) after treatment with IL22 [Gene ID=50616] and IL17A [Gene ID=3605].
Genes up-regulated in MCF7-ADR cell line (breast cancer) resistant to docetaxel [PubChem=148124].
Atherosclerotic process genes whose coronary expression changed after darapladib [PubChem=9939609] treatment.
Potential targets of MIR15A and MIR16-1 [Gene ID=406948, 406950] microRNAs in prostate cancer.
Genes changed in blister cells from patients with adverse drug reactions (ADR).
Genes changed in blister cells from patients with adverse drug reactions (ADR).
Differentially expressed genes in a panel of xenografts representing 8 common pediatric tumors compared to the normal tissues.
Down-regulated genes in colon carcinoma tumors with lymph node metastases.
Up-regulated genes in colon carcinoma tumors compared to the matched normal mucosa samples.
Down-regulated genes in colon carcinoma tumors compared to the matched normal mucosa samples.
Up-regulated genes in both rectal and colon carcinoma compared to normal mucosa samples.
Down-regulated genes in both rectal and colon carcinoma compared to normal mucosa samples.
Genes up-regulated in rectal but down-regulated in colon carcinoma compared to normal mucosa samples.
Genes down-regulated in rectal but up-regulated in colon carcinoma compared to normal mucosa samples.
Genes down-regulated in freshly isolated CD31- [Gene ID=5175] (stromal stem cells from adipose tissue) versus the CD31+ (non-stem) counterparts.
Genes up-regulated in cultured stromal stem cells from adipose tissue, compared to the freshly isolated cells.
Genes down-regulated in cultured stromal stem cells from adipose tissue, compared to the freshly isolated cells.
Genes up-regulated in highly metastatic pancreatic cancer cells.
Top genes up-regulated in orthotopic tumors from highly metastatic pancreatic cancer cells.
Top genes up-regulated in subcutaneous tumors from highly metastatic pancreatic cancer cells.
Genes from 16q24 region up-regulated in retinoblastoma tumors with 16q24 LOH (loss of heterozygocity) compared to those without the LOH.
Up-regulated genes in pediatric adrenocortical tumors (ACT) compared to the normal tissue.
Down-regulated genes in pediatric adrenocortical tumors (ACT) compared to the normal tissue.
Up-regulated genes in pediatric adrenocortical carcinoma (ACC) compared to the adenoma (ACA) tumors.
Down-regulated genes in pediatric adrenocortical carcinoma (ACC) compared to the adenoma (ACA) tumors.
Genes involved in cell cycle regulation which were up-regulated in MCF-7 cells (breast cancer) by tretinoin (retinoic acid) [PubChem=5538].
Genes up-regulated in RKO cells (colon cancer) after treatment with the NR4A1 [Gene ID=3164] agonist, DIM-C-pPhOCH3.
Up-regulated genes in MDA-MB-435 cells (breast cancer) undergoing G2/M arrest after treatment with 2-methoxyestradiol (2ME2)[PubChem=1573].
Down-regulated genes in MDA-MB-435 cells (breast cancer) undergoing G2/M arrest after treatment with 2-methoxyestradiol (2ME2) [PubChem=1573].
Genes from the most frequent genomic gains and amplifications in a panel of patients with lymph node negative breast cancer (NNBC).
Genes from the most frequent genomic losses and homozygous deletions in a panel of patients with lymph node negative breast cancer (NNBC).
Genes up-regulated in pilocytic astrocytoma (PA) samples from patients with type 1 neurofibromatosis syndrom (NF1) compared to the PA tumors from non-NF1 patients.
Genes up-regulated in pilocytic astrocytoma (PA) from supratentorial regions compared to the infratentorial PA tumors.
Genes down-regulated in pilocytic astrocytoma (PA) from supratentorial regions compared to the infratentorial PA tumors.
Protein kinase genes most significantly up-regulated in ASPS (alveolar soft part sarcoma) tumors compared to four other types of primitive sarcomas.
Up-regulated genes common to all pretumorigenic cells with acquired drug resistance.
Down-regulated genes common to all pretumorigenic cells with acquired drug resistance.
Genes up-regulated in A549 cells (lung cancer) expressing MIRLET7A3 [Gene ID=406883] microRNA off a plasmid vector.
Genes down-regulated in A549 cells (lung cancer) expressing MIRLET7A3 [Gene ID=406883] microRNA off a plasmid vector.
Up-regulated genes in MM1.S cells (multiple myeloma) treated with adaphostin [PubChem=387042], a tyrosine kinase inhibitor with anticancer properties.
Down-regulated genes in MM1.S cells (multiple myeloma) treated with adaphostin [PubChem=387042], a tyrosine kinase inhibitor with anticancer properties.
Genes specifically up-regulated in tumor endothelium.
Genes specifically down-regulated in tumor endothelium.
Up-regulated genes of putative pathways stimulated in tumor endothelial cells by papillary serous ovarian epithelial tumor cells.
Differentially expressed genes 6 hr after tinduction of HoxA5 [Gene ID=3205] expression in a breast cancer cell line.
Differentially expressed genes 6 hr after tinduction of HoxA5 [Gene ID=3205] expression in a breast cancer cell line.
Differentially expressed genes 9 hr after tinduction of HoxA5 [Gene ID=3205] expression in a breast cancer cell line.
Differentially expressed genes 9 hr after tinduction of HoxA5 [Gene ID=3205] expression in a breast cancer cell line.
Genes up-regulated in neurons after NPAS4 [Gene ID=266743] knockdown by RNAi.
Genes down-regulated in neurons after NPAS4 [Gene ID=266743] knockdown by RNAi.
Genes up-regulated in Paneth cell (part of intestiinal epithelium) of mice with hypomorphic (reduced function) form of ATG16L1 [Gene ID=55054].
Genes down-regulated in Paneth cell (part of intestiinal epithelium) of mice with hypomorphic (reduced function) form of ATG16L1 [Gene ID=55054].
Genes up-regulated in pre B lymphocyte after induction of physiological DNA double-strand breaks (DSB) by RAG2 [Gene ID=5897]; the changes are independent of ATM [Gene ID=472] signaling.
Genes down-regulated in pre B lymphocyte after induction of physiological DNA double-strand breaks (DSB) by RAG2 [Gene ID=5897]; the changes are independent of ATM [Gene ID=472] signaling.
Genes up-regulated in pre B lymphocyte after induction of physiological DNA double-strand breaks (DSB) by RAG2 [Gene ID=5897]; the changes depend on ATM [Gene ID=472] but not NFKB signaling.
Genes down-regulated in pre B lymphocyte after induction of physiological DNA double-strand breaks (DSB) by RAG2 [Gene ID=5897]; the changes depend on ATM [Gene ID=472] but not NFKB signaling.
Supplementary Table 2. Genelist comparing microarray expression profiles of spermatogonial cells, haGSCs and hES (H1) cells. Examples of expression rates of different hES cell enriched and germ cell specific genes, surface markers for germ cell selection and signal transduction in all three cell types (spermatogonial cells = SC).
Genes enriched in pluripotent adult germline stem cells.
Genes up-regulated in a mouse model of heart disease whose expression reverted to normal by silencing of MIR21 [Gene ID=406991] microRNA.
Genes down-regulated in a mouse model of heart disease whose expression reverted to normal by silencing of MIR21 [Gene ID=406991] microRNA.
List of genes in the 19q13 amplicon region based on a copy number alterations study of a panel of 16 pancreatic cancer cell lines and 31 primary tumors.
Genes whose expression positively correlated with sensitivity of breast cancer cell lines to dasatinib [PubChem=3062316].
Genes whose expression negatively correlated with resistance of breast cancer cell lines to dasatinib [PubChem=3062316].
Genes whose DNA methylation differed between primary ALL cells (acute lymphoblastic leukemia) and normal peripheral blood samples.
Protein biosynthesis, transport or catabolism genes up-regulated in hyperploid multiple myeloma (MM) compared to the non-hyperploid MM samples.
Protein biosynthesis, transport or catabolism genes down-regulated in hyperploid multiple myeloma (MM) compared to the non-hyperploid MM samples.
Genes up-regulated in basal mammary epithelial cells compared to the luminal ones.
Genes down-regulated in basal mammary epithelial cells compared to the luminal ones.
Representative genes up-regulated in MiaPaCa2 cells (pancreatic cancer) under glucose-deprived conditions.
Selected genes up-regulated in response to the Ras inhibitor salirasib [PubChem=5469318] in a panel of cancer cell lines with constantly active HRAS [Gene ID=3265].
Selected genes down-regulated in response to the Ras inhibitor salirasib [PubChem=5469318] in a panel of cancer cell lines with constantly active HRAS [Gene ID=3265].
Genes regulated by hypoxia, based on literature searches.
EMT (epithelial-mesenchymal transition) genes up-regulated genes in melanoma tumous that developed metastatic disease compared to primary melanoma that did not.
EMT (epithelial-mesenchymal transition) genes down-regulated genes in melanoma tumous that developed metastatic disease compared to primary melanoma that did not.
Neural-related genes up-regulated in melanoma tumors that developed metastases compared to primary melanoma that did not.
Up-regulated genes in melanoma tumous that developed metastatic disease compared to primary melanoma that did not.
Down-regulated genes in melanoma tumors that developed metastatic disease compared to primary melanoma that did not.
Tumorigenesis markers of head and neck squamous cell carcinoma (HNSCC): up-regulated in the 'early' tumors vs normal samples.
Tumorigenesis markers of head and neck squamous cell carcinoma (HNSCC): down-regulated in the 'early' tumors vs normal samples.
Genes up-regulated in naive T lymphocytes lacking FURIN [Gene ID=5045]: Cre-Lox knockout of FURIN in CD4+ [Gene ID=920] cells.
Genes down-regulated in naive T lymphocytes lacking FURIN [Gene ID=5045]: Cre-Lox knockout of FURIN in CD4+ [Gene ID=920] cells.
Genes constituting the PluriNet protein-protein network shared by the pluripotent cells (embryonic stem cells, embryonical carcinomas and induced pluripotent cells).
Genes up-regulated in mouse stroma of pancreatic adenocarcinoma zenografts after treatment with HhAntag, a hedgehog (Hh) pathway inhibitor.
Genes down-regulated in mouse stroma of pancreatic adenocarcinoma zenografts after treatment with HhAntag, a hedgehog (Hh) pathway inhibitor.
Genes required for both proliferation and CTNNB1 [Gene ID=1499] activity in DLD-1 cell (colon cancer with APC [Gene ID=324] deletions).
Genes required for CTNNB1 [Gene ID=1499] activity in DLD-1 cell (colon cancer with APC [Gene ID=324] deletions), based on shRNA screen.
Genes required for proliferation of DLD-1 cell (colon cancer with APC [Gene ID=324] deletions), based on shRNA screen.
Prmary innate immune response genes induced in 293T cells (embryonic kidney) by overexpression of STING (TMEM173) [Gene ID=340061].
Up-regulated genes in HepG2 cells (liver cancer) overexpressing an oncogenic variant of tumor suppressor TIP30 [Gene ID=10553] compared to its wild type form.
Down-regulated genes in HepG2 cells (liver cancer) overexpressing an oncogenic variant of tumor suppressor TIP30 [Gene ID=10553] compared to its wild type form.
Genes from common genomic gains observed in a meta analyis of copy number alterations across a panel of different cancer cell lines and tumor samples.
Genes from common genomic losses observed in a meta analyis of copy number alterations across a panel of different cancer cell lines and tumor samples.
Genes up-regulated in response to both single dose and fractionated radiation that were common to all three cell lines studied.
Up-regulated genes in medulloblastoma tumors from heterozygotic CXCR6 [Gene ID=10663] knockout mice compared to those from PTCH1 [Gene ID=5727] heterozygotic knockout mice.
Down-regulated genes in medulloblastoma tumors from heterozygotic CXCR6 [Gene ID=10663] knockout mice compared to those from PTCH1 [Gene ID=5727] heterozygotic knockout mice.
Genes up-regulated in cancer stem cells derived from glyoblastoma tumors: CD133+ [Gene ID=8842]  vs. CD133- cells.
Genes down-regulated in cancer stem cells derived from glyoblastoma tumors: CD133+ [Gene ID=8842]  vs. CD133- cells.
Angiogenic markers up-regulated in lymph endothelial cells upon infection with KSHV (Kaposi's sarcoma herpes virus).
Angiogenic markers down-regulated in lymph endothelial cells upon infection with KSHV (Kaposi's sarcoma herpes virus).
Genes up-regulated in multiple myeloma (MM) compared to monoclonal gammopathy of uncertain significance (MGUS).
Genes down-regulated in multiple myeloma (MM) compared to monoclonal gammopathy of uncertain significance (MGUS).
Genes from cluster 1: up-regulated in group C of tumors arising from overexpression of BCL2L1 and MYC [Gene ID=598, 4609] in plasma cells.
Genes from cluster 2: down-regulated in group C of tumors arising from overexpression of BCL2L1 and MYC [Gene ID=598, 4609] in plasma cells.
Genes from cluster 3: up-regulated in group D of tumors arising from overexpression of BCL2L1 and MYC [Gene ID=598, 4609] in plasma cells.
Genes from cluster 4: down-regulated in group D of tumors arising from overexpression of BCL2L1 and MYC [Gene ID=598, 4609] in plasma cells.
Genes up-regulated in group D of tumors arising from overexpression of BCL2L1 and MYC [Gene ID=598, 4609] in plasma cells.
Genes down-regulated in group D of tumors arising from overexpression of BCL2L1 and MYC [Gene ID=598, 4609] in plasma cells.
Genes up-regulated both in group C and D of tumors arising from overexpression of BCL2L1 and MYC [Gene ID=598, 4609] in plasma cells.
Genes down-regulated both in group C and D of tumors arising from overexpression of BCL2L1 and MYC [Gene ID=598, 4609] in plasma cells.
Genes up-regulated in group C of tumors arising from overexpression of BCL2L1 and MYC [Gene ID=598, 4609] in plasma cells.
Genes down-regulated in group C of tumors arising from overexpression of BCL2L1 and MYC [Gene ID=598, 4609] in plasma cells.
Genes silenced by DNA methylation in bladder cancer cell lines.
Genes up-regulated in HUVEC cells (umbilical vein endothelium) by fenretinide [PubChem=1744].
Genes down-regulated in HUVEC cells (umbilical vein endothelium) by fenretinide [PubChem=1744].
Genes down-regulated in  tumor-conditioned vs quiescent endothelial cells and up-regulated upon treatment with decitabine and TSA [PubChem=451668, 5562].
G1 to S phase regulators significantly changed in DanG cells (pancreatic cancer) treated with Ly294002 [PubChem=3973], a phosphoinositide 3-kinase (PI3K) inhibitor.
Integrin, VEGF, Wnt and TGF-?? signaling pathway genes up-regulated in PC-3 cells (prostate cancer) after knockdown of PDEF [Gene ID=25803] by RNAi.
Integrin, VEGF, Wnt and TGF-?? signaling pathway genes down-regulated in PC-3 cells (prostate cancer) after knockdown of PDEF [Gene ID=25803] by RNAi.
Up-regulated genes in Calu3 cells (non-small cell lung cancer, NSCLC) resistant to gemcitabine [PubChem=3461] compared to the parental line sensitive to the drug.
Down-regulated genes in Calu3 cells (non-small cell lung cancer, NSCLC) resistant to gemcitabine [PubChem=3461] compared to the parental line sensitive to the drug.
Up-regulated genes in Calu3 cells (non-small lung cancer cells, NSCLC) resitant to gemcitabine [PubChem=3461] in response to bexarotene [PubChem=82146].
Down-regulated genes in Calu3 cells (non-small lung cancer cells, NSCLC) resitant to gemcitabine [PubChem=3461] in response to bexarotene [PubChem=82146].
Genes up-regulated in B lymphocytes from patients with primary immunodefiency syndrom.
Genes down-regulated in B lymphocytes from patients with primary immunodefiency syndrom.
Up-regulated genes significantly associated with positive minimal residual disease (MRD) on day 46 after chemotherapy treatment of children with acute lymphoblastic leukemia (ALL).
Down-regulated genes significantly associated with positive minimal residual disease (MRD) on day 46 after chemotherapy treatment of children with acute lymphoblastic leukemia (ALL).
Up-regulated genes that distinguished smokers with and without lung cancer.
Down-regulated genes that distinguished smokers with and without lung cancer.
An assortment of osteoblast transcriptional regulators.
Genes whose expression most significantly correlated with cancer cell line sensitivity to the proapoptotic ligand APO2 [Gene ID=8797].
Up-regulated genes associated with sensitivity and resistance to gamma-secretase (GSI) in T-cell acute lymphoblastic leukemia (T-ALL) cell lines.
Down-regulated genes associated with sensitivity and resistance to gamma-secretase (GSI) in T-cell acute lymphoblastic leukemia (T-ALL) cell lines.
Chemokine genes up-regulated within 2 hr of c-Myc [Gene ID=4609] activation in a mouse model of Myc-induced pancreatic beta-cell tumorigenesis.
Genes up-regulated in hepatic stellar cells after stimulation with bacterial lipopolysacharide (LPS).
Genes down-regulated in hepatic stellar cells after stimulation with bacterial lipopolysacharide (LPS).
A biomarker of plasma signaling proteins that predicts clinical Alzheimer???s diagnosis.
Genes up-regulated by 2-methoxyestradiol (2ME2) [PubChem=1573] in the MM.1S cell line (multiple myeloma) sensitive to dexamethasone [PubChem=5743].
Genes down-regulated by 2-methoxyestradiol (2ME2) [PubChem=1573] in the MM.1S cell line (multiple myeloma) sensitive to dexamethasone [PubChem=5743].
Genes up-regulated in MCF-7 cells (breast cancer) by selective estrogen receptor modulators (SERM) 4-hydroxytamoxifen, raloxifene, or ICI 182780 but not by estradiol [PubChem=44959, 5035, 3478439, 5757].
Genes down-regulated in MCF-7 cells (breast cancer) by selective estrogen receptor modulators (SERM) 4-hydroxytamoxifen, raloxifene, or ICI 182780 but not by estradiol [PubChem=44959, 5035, 3478439, 5757].
Genes up-regulated at the peak of an antigen response of naive CD8+ [Gene ID=925, 926] T-cells.
Hepatic graft versus host disease (GVHD), day 7: up-regulated in allogeneic vs syngeneic bone marrow transplant.
Hepatic graft versus host disease (GVHD), day 7: down-regulated in allogeneic vs syngeneic bone marrow transplant.
Hepatic graft versus host disease (GVHD), day 35: genes up-regulated in allogeneic vs syngeneic bone marrow transplant.
Hepatic graft versus host disease (GVHD), day 35: genes down-regulated in allogeneic vs syngeneic bone marrow transplant.
Maturation of monocyte-derived dendritic cells (DC) in response to inflammatory stimuli: genes up-regulated only at 8 hr after the stimulation (cluster A).
Maturation of monocyte-derived dendritic cells (DC) in response to inflammatory stimuli: genes up-regulated both at 8 hr and 48 hr after the stimulation (cluster B).
Maturation of monocyte-derived dendritic cells (DC) in response to inflammatory stimuli: genes up-regulated only at 48 hr after the stimulation (cluster C).
Genes down-regulated during the course of maturation of monocyte-derived dendritic cells (DC) in response to inflammatory stimuli (cluster D).
Neutrophil-specific genes up-regulated in comparison of immature with mature neutrophils.
Neutrophil-specific genes down-regulated in comparison of immature with mature neutrophils.
Genes changed in neutrophils upon treatment with activated protein C (PROC) [Gene ID=5624] of pulmonary inflammation induced by bacterial lipopolysaccharide (LPS).
Genes changed in neutrophils after activated protein C (PROC) [Gene ID=5624] vs. placebo treatment of pulmonary inflammation induced by bacterial lipopolysaccharide (LPS).
Top 50 marker genes for glioblastoma multiforme (GBM), a class of high grade glioma.
Top 50 marker genes for anaplastic oligodendroglioma (AO), a class of high grade glioma.
Genes up-regulated in U937 cells (acute promyelocytic leukemia, APL) expressing RARA [Gene ID=5914] fused with either PML or PLZF [Gene ID=5371, 7704].
Genes down-regulated in U937 cells (acute promyelocytic leukemia, APL) expressing RARA [Gene ID=5914] fused with either PML or PLZF [Gene ID=5371, 7704].
Genes up-regulated in U937 cells (acute promyelocytic leukemia, APL) by tretinoin (all-trans retinoic acid, ATRA) [PubChem=5538].
Genes up-regulated by tretinoin (all-trans retinoic acid, ATRA) [PubChem=5538] in U937 cells (acute promyelocytic leukemia, APL) made sensitive to the drug by expression of the PML-RARA fusion [Gene ID = 5371, 5914].
Genes up-regulated by tretinoin (all-trans retinoic acid, ATRA) [PubChem=5538] in U937 cells (acute promyelocytic leukemia, APL) made resistant to the drug by expression of the PLZF-RARA fusion [Gene ID = 7704, 5914].
Interferon-inducible genes up-regulated in A549 cells (lung cancer) infected with a respiratory syncytial virus (RSV) that had its NS1 [Gene ID=1494468] gene knocked down by RNAi.
Genes up-regulated in brain endothelial cells from patients with Alzheimer disease.
Genes down-regulated in brain endothelial cells from patients with Alzheimer disease.
Genes up-regulated in DLD-1 cells (colon cancer) in response to hypoxia; might not be direct targets of HIF1A [Gene ID=3091].
Genes down-regulated in DLD-1 cells (colon cancer) in response to hypoxia; might not be direct targets of HIF1A [Gene ID=3091].
Genes predicting sensitivity to cytoxan [PubChem=2907].
Genes up-regulated in HL-60 cells (acute myeloid leukemia, AML) by expression of p210 BCR-ABL [Gene ID=613, 25] fusion protein.
Genes down-regulated in HL-60 cells (acute myeloid leukemia, AML) by expression of p210 BCR-ABL [Gene ID=613, 25] fusion protein.
Genes up-regulated in T98G cells (glioblastoma) by TNC [Gene ID=3371].
Genes down-regulated in T98G cells (glioblastoma) by TNC [Gene ID=3371].
Genes up-regulated in peripheral blood monocytes by CSF2RB (GM-CSF) [Gene ID=1437] and IL4 [Gene ID=3565].
Genes down-regulated in peripheral blood monocytes by CSF2RB (GM-CSF) [Gene ID=1437] and IL4 [Gene ID=3565].
Genes up-regulated in peripheral blood monocytes by HGF [Gene ID=3082].
Genes down-regulated in peripheral blood monocytes by HGF [Gene ID=3082].
Genes up-regulated in peripheral blood mononucleocytes by HGF [Gene ID=3082] compared to those regulated by CSF2RB (GM-CSF) [Gene ID=1437] and IL4 [Gene ID=3565].
Genes down-regulated in peripheral blood mononucleocytes by HGF [Gene ID=3082] compared to those regulated by CSF2RB (GM-CSF) [Gene ID=1437] and IL4 [Gene ID=3565].
Up-regulated genes in the canonical gene expression signature of the fibroblast core serum response (CSR) defined by the Stanford group.
Down-regulated genes in the canonical gene expression signature of the fibroblast core serum response (CSR) defined by the Stanford group.
Fibroblast serum response genes showing periodic expression during the cell cycle; excluded from the core serum response signature.
Up-regulated target genes shared by acute myeloid leukemia (AML) translocation products PML RARA [Gene ID=5371,   5914], AML1 ETO [Gene ID=861, 862], and PLZF RARA [Gene ID=5914, 7704].
Down-regulated target genes shared by acute myeloid leukemia (AML) translocation products PML RARA [Gene ID=5371,   5914], AML1 ETO [Gene ID=861, 862], and PLZF RARA [Gene ID=5914, 7704].
Top 100 probe sets associated with MLL fusions [Gene ID = 4297] irrespective of the lineage of the pediatric acute leukemia.
Up-regulated genes from the optimal set of 550 markers discriminating breast cancer samples by ESR1 [Gene ID=2099] expression: ER(+) vs ER(-) tumors.
Down-regulated genes from the optimal set of 550 markers discriminating breast cancer samples by ESR1 [Gene ID=2099] expression: ER(+) vs ER(-) tumors.
Up-regulated genes from the optimal set of 100 markers discriminating ER(-) breast cancer tumors by  BRCA1 [Gene ID=672] mutation status.
Down-regulated genes from the optimal set of 100 markers discriminating ER(-) breast cancer tumors by  BRCA1 [Gene ID=672] mutation status.
Genes changed more than 7-fold by expressing JAK2 [Gene ID=3717] in the JAK2 null cell line.
Up-regulated genes whose expression correlates with copy number gains in pancreatic adenocarcinoma cell lines and primary tumor specimens.
Down-regulated genes whose expression correlates with copy number losses in pancreatic adenocarcinoma cell lines and primary tumor specimens.
Genes up-regulated in the mouse lung cancer model with mutated KRAS [Gene ID=3845].
Genes down-regulated in the mouse lung cancer model with mutated KRAS [Gene ID=3845].
Genes that contributed maximally to the GSEA score of the up- and down-regulated gene sets from the KrasLA mouse model in two lung cancer expression data sets comparing mutant vs normal KRAS [Gene ID=3845].
Genes up-regulated in primary keratinocytes by expression of p50 (NFKB1) and p65 (RELA) [Gene ID=4790, 5970] components of NFKB.
Genes down-regulated in primary keratinocytes by expression of p50 (NFKB1) and p65 (RELA) [Gene ID=4790, 5970] components of NFKB.
Genes up-regulated in primary fibroblast cells by expression of p50 (NFKB1) and p65  (RELA) [Gene ID=4790, 5970] components of NFKB.
Genes up-regulated during differentiation from pre-BI to large pre-BII lymphocyte.
Genes down-regulated during differentiation from pre-BI to large pre-BII lymphocyte.
Genes up-regulated during differentiation from large pre-BII to small pre-BII lymphocyte.
Genes down-regulated during differentiation from large pre-BII to small pre-BII lymphocyte.
Genes up-regulated during differentiation from small pre-BII to immature B lymphocyte.
Genes down-regulated during differentiation from small pre-BII to immature B lymphocyte.
Genes up-regulated during differentiation of immature to mature B lymphocyte.
Genes down-regulated during differentiation of immature to mature B lymphocyte.
Genes up-regulated in bone marrow hematopoietic stem cells (HSC, CD34+ [Gene ID=947]) from patients with low risk of myelodysplastic syndrome (MDS) compared with healthy controls.
Genes down-regulated in bone marrow hematopoietic stem cells (HSC, CD34+ [Gene ID=947]) from patients with low risk of myelodysplastic syndrome (MDS) compared with healthy controls.
Genes up-regulated in bone marrow hematopoietic stem cells (HSC, CD34+ [Gene ID=947]) from patients with high risk of myelodysplastic syndrome (MDS) compared with healthy controls.
Genes down-regulated in bone marrow hematopoietic stem cells (HSC, CD34+ [Gene ID=947]) from patients with high risk of myelodysplastic syndrome (MDS) compared with healthy controls.
Genes up-regulated in bone marrow hematopoietic stem cells (HSC, CD34+ [Gene ID=947]) from patients with high risk of myelodysplastic syndrom (MDS) compared to the low risk patients.
Genes down-regulated in bone marrow hematopoietic stem cells (HSC, CD34+ [Gene ID=947]) from patients with high risk of myelodysplastic syndrom (MDS) compared to the low risk patients.
Genes up-regulated at early stages of progenitor T lymphocyte maturation compared to the late stages.
Genes down-regulated at early stages of progenitor T lymphocyte maturation compared to the late stages.
Genes enriched in the intrathymic T progenitor (ITTP) cells compared to all other T lymphocyte differentiation stages.
Genes enriched in the double polar (DP) thymocyte compared to all other T lymphocyte differentiation stages.
Genes enriched in the single positive 4 (SP4) thymocytes compared to all other T lymphocyte differentiation stages.
Candidate genes specific for recent thymic emigrants (RTEs).
Genes enriched in the naive circulating T lymphocytes compared to the earlier differentiation stages.
Genes enriched at every T lymphocyte differentiation stage compared to the early passage fetal thymic stromal cultures (TSC).
'Wilm's tumor signature': genes highly expressed in Wilm's tumor samples compared to normal fetal kidney and a heterologous tumor, Burkit lymphoma.
Genes in the stroma-derived prognostic predictor of breast cancer disease outcome.
Cluster 6 of method A: up-regulation of these genes in patients with non???small cell lung cancer (NSCLC) predicts poor survival outcome.
Cluster 4 of method A: up-regulation of these genes in patients with non-small cell lung cancer (NSCLC) predicts good survival outcome.
Genes for which mutations result in atrial septation defects, a major class of congenital heart disease.
Cluster 5 of method A: up-regulation of these genes in patients with non-small cell lung cancer (NSCLC) predicts good survival outcome.
Genes for which mutations result in developmental defects in ventricular septation and atrioventricular cushion formation, a major class of congenital heart disease.
Genes for which mutations result in developmental defects in the great vessels formation and valvulogenesis, a major class of congenital heart disease.
Genes up-regulated in HEK293 cells (embryo kidney) after knockdown of TUT1 [Gene ID=64852] by RNAi.
Genes down-regulated in HEK293 cells (embryo kidney) after knockdown of TUT1 [Gene ID=64852] by RNAi.
Genes up-regulated in MDA-MB-231 cells (breast cancer) after knockdown of SATB1 [Gene ID=6304] by RNAi.
Genes down-regulated in MDA-MB-231 cells (breast cancer) after knockdown of SATB1 [Gene ID=6304] by RNAi.
Cluster 12 of method A: up-regulation of these genes in patients with non-small cell lung cancer (NSCLC) predicts good survival outcome.
Up-regulated 'cooperation response genes': responded synergystically to the combination of mutant TP53 [Gene ID=7157] and HRAS [Gene ID=3265] in YAMC cells (colon).
Down-regulated 'cooperation response genes': responded synergystically to the combination of mutant TP53 [Gene ID=7157] and HRAS [Gene ID=3265] in YAMC cells (colon).
Genes up-regulated in transgenic mice expressing human MYC [Gene ID=4609] in prostate.
Genes down-regulated in transgenic mice expressing human MYC [Gene ID=4609] in prostate.
Direct targets of IRF4 [Gene ID=3662] that constitute a multiple myeloma program.
IRF4 [Gene ID=3662] target genes up-regulated in primary myeloma vs. mature B lymphocytes.
IRF4 [Gene ID=3662] target genes up-regulated in plasma cells compared to mature B lymphocytes.
IRF4 [Gene ID=3662] target genes induced after activation of primary B lymphocytes by anti-IgM crosslinking.
IRF4 [Gene ID=3662] target genes up-regulated in plasmacytoid dendritic cells compared to monocytes.
Housekeeping genes identified as expressed across 19 normal tissues.
Putative metastasis genes: up-regulated in metastatic cell lines LM2 (lung) and BoM2 (bone) relative to the parental MDA-MB-231 line (breast adenocarcinoma).
Cohesin targets identified by ChIP-chip which were up-regulated after knockdown of CTCF [Gene ID=10664] and RAD21 [Gene ID=5885] by RNAi.
Nearest neighbors of HOX11 [Gene ID=3195], based on the close agreement of their expression profiles with that of HOX11 in pediatric T cell acute lymphoblastic leukemia (T-ALL).
Genes specifically up-regulated in pediatric acute lymphoblastic leukemia (ALL) patients by mercaptopurine [PubChem=667490] and high dose methotrexate (HDMTX) [PubChem=4112].
Genes specifically down-regulated in pediatric acute lymphoblastic leukemia (ALL) patients by mercaptopurine [PubChem=667490] and high dose methotrexate (HDMTX) [PubChem=4112].
B lymphocyte early differentiation genes (EDG): top genes up-regulated in tonsil B lymphocytes (TBC) compared to the tonsil plasma cells (TPC).
B lymphocyte early differentiation genes (EDG): top genes down-regulated in tonsil B lymphocytes (TBC) compared to the tonsil plasma cells (TPC).
Transcripts significantly enriched in pseudopodia of NIH/3T3 cells (fibroblast) in response to both chemotactic (lysophosphatidic acid, LPA [PubChem=3988]) and haptotactic (fibronectin, FN1 [Gene ID=2335) migratory stimuli.
Transcripts enriched in pseudopodia of NIH/3T3 cells (fibroblast) in response to the chemotactic migration stimulus by lysophosphatidic acid (LPA) [PubChem=3988].
Transcripts depleted in pseudopodia of NIH/3T3 cells (fibroblast) in response to the chemotactic migration stimulus by lysophosphatidic acid (LPA) [PubChem=3988].
Transcripts enriched in pseudopodia of NIH/3T3 cells (fibroblast) in response to haptotactic migratory stimulus by fibronectin, FN1 [Gene ID=2335].
Transcripts depleted from pseudopodia of NIH/3T3 cells (fibroblast) in response to haptotactic migratory stimulus by fibronectin, FN1 [Gene ID=2335].
Selected genes up-regulated in prostate tumors developed by transgenic mice overexpressing VAV3 [Gene ID=10451] in prostate epithelium.
Selected genes up-regulated in prostate tumors developed by transgenic mice overexpressing VAV3 [Gene ID=10451] in prostate epithelium.
Genes up-regulated in the ANBL-6 cell line (multiple myeloma, MM) after withdrawal of IL6 [Gene ID=3569].
Genes down-regulated in the ANBL-6 cell line (multiple myeloma, MM) after withdrawal of IL6 [Gene ID=3569].
Genes up-regulated in ANBL-6 cell line (multiple myeloma, MM) co-cultured with bone marrow stromal cells compared to those grown in the presence of IL6 [Gene ID=3569].
Genes down-regulated in ANBL-6 cell line (multiple myeloma, MM) co-cultured with bone marrow stromal cells compared to those grown in the presence of IL6 [Gene ID=3569].
Genes up-regulated in ANBL-6 cell line (multiple myeloma, MM)  expressing a constantly active form of NRAS [Gene ID=4893] off a plasmid vector compared to those grown in the presence of IL6 [Gene ID=3569].
Genes down-regulated in ANBL-6 cell line (multiple myeloma, MM)  expressing a constantly active form of NRAS [Gene ID=4893] off a plasmid vector compared to those grown in the presence of IL6 [Gene ID=3569].
Genes up-regulated in ANBL-6 cell line (multiple myeloma, MM) expressing an activated form of NRAS [Gene ID=4893] off a plasmid vector compared to those co-cultured with bone marrow stromal cells.
Genes down-regulated in ANBL-6 cell line (multiple myeloma, MM) expressing an activated form of NRAS [Gene ID=4893] off a plasmid vector compared to those co-cultured with bone marrow stromal cells.
B lymphocyte late differentiation genes (LDG): top genes up-regulated in plasma cells from tonsils (TPC) compared to those from bone marrow (BPC).
B lymphocyte late differentiation genes (LDG): top genes down-regulated in plasma cells from tonsils (TPC) compared to those from bone marrow (BPC).
The vEDG set: most variable early differentiation genes (EDG) with similar expression patterns in tonsil B lymphocytes (TBC) and multiple myeloma (MM) cells compared to the plasma cells from tonsil (TPC) and bone marrow (BPC).
The vEDG set: most variable early differentiation genes (EDG) with similar expression patterns in tonsil B lymphocytes (TBC) and multiple myeloma (MM) cells compared to the plasma cells from tonsil (TPC) and bone marrow (BPC).
The v1LDG set: most variable late differentiation genes (LDG) with similar expression patterns in tonsil plasma cells (TPC) and multiple myeloma (MM) samples.
The v1LDG set: most variable late differentiation genes (LDG) with similar expression patterns in tonsil plasma cells (TPC) and multiple myeloma (MM) samples.
Genes up-regulated by 3 h of euglycemic hyperinsulinemic clamp in the vastus lateralis muscle of healthy lean subjects.
Genes down-regulated by 3 h of euglycemic hyperinsulinemic clamp in the vastus lateralis muscle of healthy lean subjects.
Top 40 genes from cluster 1 of acute myeloid leukemia (AML) expression profile; 57% of the samples are FAB M1 subtype,  43% have 11q23 abnormalities, and 36% have up-regulated EVI1 [Gene ID=2122] expression.
Top 40 genes from cluster 2 of acute myeloid leukemia (AML) expression profile; 71% of the samples are FAB M4 or M5 subtypes, and 82% bear internal tundem duplications in FLT3 [Gene ID=2322].
Top 40 genes from cluster 3 of acute myeloid leukemia (AML) expression profile; 84% of the samples are FAB M1 or M2 subtypes, 52% bear intern tandem duplication in FLT3 [Gene ID=2322].
Top 40 genes from cluster 4 of acute myeloid leukemia (AML) expression profile; 87% of the samples are FAB M1 subtype, 53% bear mutations in CEBPA [Gene ID=1050].
Top 40 genes from cluster 5 of acute myeloid leukemia (AML) expression profile; 96% of the samples are FAB M4 or M5 subtype.
Top 40 genes from cluster 6 of acute myeloid leukemia (AML) expression profile; all samples are FAB M1 or M2 subtypes and all samples have internal tundem duplication of FLT3 [Gene ID=2322].
Top 40 genes from cluster 7 of acute myeloid leukemia (AML) expression profile; 61% of the samples are FAB M1 or M2 subtype.
Top 40 genes from cluster 8 of aculte myeloid leukemia (AML) expression profile; 69% of the samples are FAB M2 subtype.
Top 40 genes from cluster 9 of acute myeloid leukemia (AML) expression profile; 87% of the samples are FAB M4 or M5 subtype, all have inv(16) inversion producing the CBFB-MYH11 fusion [Gene ID=865, 4629]; indicate good survival.
Top 40 genes from cluster 10 of acute myeloid leukemia (AML) expression profile; 41% of the samples are FAB M1 subtype, 45% have up-regulated EVI1 [Gene ID=2122] expression; indicate poor survival.
Top 40 genes from cluster 11 of acute myeloid leukemia (AML) expression profile; 67% of the samples are FAB M4 or M5.
Top 40 genes from cluster 12 of acute myeloid leukemia (AML) expression profile; 89% of the samples are FAB M3 subtype, 95% bear the t(15;17) translocation, all have the PML-RARA fusion [Gene ID=5371,5914]; indicate good survival.
Top 40 genes from cluster 13 of acute myeloid leukemia (AML) expression profile; 91% of the samples are FAB M2 subtype, all bear the t(8;21) translocation producing the AML1-ETO fusion [Gene ID=861, 862]; indicate good survival.
Top 40 genes from cluster 15 of acute myeloid leukemia (AML) expression profile; 88% of the samples are FAB M1 or M2 subtype, 63% have mutations in CEBPA [Gene ID=1050].
Top 40 genes from cluster 16 of acute myeloid leukemia (AML) expression profile; 81% of the samples are FAB M5 subtype, 45% have 11q23 abnormalities.
Genes that best predicted acute myeloid leukemia (AML) with the t(8;21) translocation producing the AML1-ETO fusion [Gene ID=861, 862].
Genes that best predicted acute myeloid leukemia (AML) with the 11q23 rearrangements.
Genes that best predicted acute myeloid leukemia (AML) with the up-regulated expression of EVI1 [Gene ID=2122].
Genes that best predicted acute myeloid leukemia (AML) with mutations in CEBPA [Gene ID=1050].
Genes that best predicted acute myeloid leukemia (AML) with internal tandem duplications (IDT) in FLT3 [Gene ID=2322].
Genes up-regulated in peripheral blood mononuclear cells (PBMC) from sickle cell disease patients compared to those from healthy subjects.
Genes down-regulated in peripheral blood mononuclear cells (PBMC) from sickle cell disease patients compared to those from healthy subjects.
Genes up-regulated in atypical ductal hyperplastic tissues from patients with (ADHC) breast cancer vs those without the cancer (ADH).
Genes down-regulated in atypical ductal hyperplastic tissues from patients with (ADHC) breast cancer vs those without the cancer (ADH).
The lung adenocarcinoma TSP (tumor sequencing project) genes bearing recurrent somatic mutations.
The lung adenocarcinoma TSP (tumor sequencing project) genes mutations in which show positive correlation with the  higher overall mutation rate.
Genes significantly mutated in 91 glioblastoma samples.
Up-regulated genes in hepatocellular carcinoma (HCC) subclass G1, defined by unsupervised clustering
Down-regulated genes in hepatocellular carcinoma (HCC) subclass G1, defined by unsupervised clustering
Genes in hepatocellular carcinoma (HCC) subclass G2, defined by unsupervised clustering.
Up-regulated genes in hepatocellular carcinoma (HCC) subclass G3, defined by unsupervised clustering.
Down-regulated genes in hepatocellular carcinoma (HCC) subclass G3, defined by unsupervised clustering.
Up-regulated genes in hepatocellular carcinoma (HCC) subclass G5, defined by unsupervised clustering.
Down-regulated genes in hepatocellular carcinoma (HCC) subclass G5, defined by unsupervised clustering.
Up-regulated genes in hepatocellular carcinoma (HCC) subclass G6, defined by unsupervised clustering.
Down-regulated genes in hepatocellular carcinoma (HCC) subclass G6, defined by unsupervised clustering.
Up-regulated genes in hepatocellular carcinoma (HCC) subclass G12, defined by unsupervised clustering
Down-regulated genes in hepatocellular carcinoma (HCC) subclass G12, defined by unsupervised clustering
Up-regulated genes in hepatocellular carcinoma (HCC) subclass G23, defined by unsupervised clustering.
Down-regulated genes in hepatocellular carcinoma (HCC) subclass G23, defined by unsupervised clustering.
Up-regulated genes in hepatocellular carcinoma (HCC) subclass G56, defined by unsupervised clustering.
Down-regulated genes in hepatocellular carcinoma (HCC) subclass G56, defined by unsupervised clustering.
Up-regulated genes in hepatocellular  carcinoma (HCC) subclass G123, defined by unsupervised clustering.
Down-regulated genes in hepatocellular  carcinoma (HCC) subclass G123, defined by unsupervised clustering.
Top 200 marker genes up-regulated in the 'CTNNB1' subclass of hepatocellular carcinoma (HCC); characterized by activated CTNNB1 [Gene ID=1499].
Top 200 marker genes down-regulated in the 'CTNNB1' subclass of hepatocellular carcinoma (HCC); characterized by activated CTNNB1 [Gene ID=1499].
Top 200 marker genes up-regulated in the 'proliferation' subclass of hepatocellular carcinoma (HCC); characterized by increased proliferation, high levels of serum AFP [Gene ID=174], and chromosomal instability.
Top 200 marker genes down-regulated in the 'proliferation' subclass of hepatocellular carcinoma (HCC); characterized by increased proliferation, high levels of serum AFP [Gene ID=174], and chromosomal instability.
All marker genes up-regulated in the 'interferon' subclass of hepatocellular carcinoma (HCC).
All marker genes down-regulated in the 'interferon' subclass of hepatocellular carcinoma (HCC).
Marker genes up-regulated in the 'chromosome 7 polysomy' subclass of hepatocellular carcinoma (HCC); characterized by polysomy of chromosome 7 and by a lack of gains of chromosome 8q.
Marker genes down-regulated in the 'chromosome 7 polysomy' subclass of hepatocellular carcinoma (HCC); characterized by polysomy of chromosome 7 and by a lack of gains of chromosome 8q.
Marker genes up-regulated in the 'unannotated' subclass of hepatocellular carcinoma (HCC) samples.
Marker genes down-regulated in the 'unannotated' subclass of hepatocellular carcinoma (HCC) samples.
'Late-TGFB1 signature': genes overexpressed in primary hepatocytes at a late phase of TGFB1 [Gene ID=7040] treatment; is associated with a more invasive phenotype.
'Early-TGFB1 signature': genes overexpressed in primary hepatocytes at an early phase of TGFB1 [Gene ID=7040] treatment; is associated with a less invasive phenotype.
Genes whose expression correlated with higher risk of late recurrence of hepatocellular carcinoma (HCC).
Genes whose expression correlated with lower risk of late recurrence of hepatocellular carcinoma (HCC).
Survival signature genes defined in adjacent liver tissue: genes correlated with poor survival of hepatocellular carcinoma (HCC) patients.
Survival signature genes defined in adjacent liver tissue: genes correlated with good survival of hepatocellular carcinoma (HCC) patients.
Selected up-regulated MET [Gene ID=4233] target genes from a classifier of hepatocellular carcinoma (HCC) cases; associated with poor survival.
Selected down-regulated MET [Gene ID=4233] target genes from a classifier of hepatocellular carcinoma (HCC) cases; associated with poor survival.
Up-regulated genes distinguishing hepatocellular carcinoma (HCC) samples positive for EPCAM [Gene ID=4072] from the negative ones.
Down-regulated genes distinguishing hepatocellular carcinoma (HCC) samples positive for EPCAM [Gene ID=4072] from the negative ones.
Genes up-regulated in hepatocellular carcinoma (HCC) cells with hepatic stem cell properties.
Genes down-regulated in hepatocellular carcinoma (HCC) cells with hepatic stem cell properties.
Genes up-regulated in tumor-adjacent liver tissue, which is asociated with intrahepatic metastasis of hepatocellular carcinoma
Genes down-regulated in tumor-adjacent liver tissue, which is asociated with intrahepatic metastasis of hepatocellular carcinoma
Fig.5, Supplementary Fig.2 Genes overexpressed in human hepatocellular carcinoma with hepatoblast property
Genes up-regulated in samples from patients with recurrent hepatocellular carcinoma (HCC).
Genes down-regulated in samples from patients with recurrent hepatocellular carcinoma (HCC).
Genes positively correlated with recurrence free survival in patients with hepatitis B-related (HBV) hepatocellular carcinoma (HCC).
Genes negatively correlated with recurrence free survival in patients with hepatitis B-related (HBV) hepatocellular carcinoma (HCC).
Genes whose expression most strongly and consistently associated with the long term survival of patients with high grade glioma tumors.
Up-regulated genes predicting poor survival of patients with thyroid carcinoma.
Down-regulated genes predicting poor survival of patients with thyroid carcinoma.
Genes specifically expressed in samples from patients with pediatric AML (acute myeloid leukemia ) bearing t(8;21) translocation.
Genes specifically expressed in samples from patients with pediatric acute myeloid leukemia (AML) bearing inv(16) translocation.
Genes specifically expressed in samples from patients with pediatric acute myeloid leukemia (AML) bearing t(9;11) translocation.
Genes specifically expressed in samples from patients with pediatric acute myeloid leukemia (AML) bearing 11q23 rearrangements.
Genes up-regulated in hepatocellular carcinoma (HCC) samples from patients with early recurrence (within 2 years after surgery) after resection.
Genes down-regulated in hepatocellular carcinoma (HCC) samples from patients with early recurrence (within 2 years after surgery) after resection.
Genes whose over-expression is associated with the risk of death in multiple cancer types
Genes up-regulated in hepatocellular carcinoma (HCC) with early recurrence.
Genes down-regulated in hepatocellular carcinoma (HCC) with early recurrence.
Genes up-regulated in both the patients in the multicentric hepatocellular carcinoma (HCC) group and those with multicentric recurrence.
Genes up-regulated by FOXP3 [Gene ID=50943] in both ex vivo and hybridoma cells.
Genes down-regulated by FOXP3 [Gene ID=50943] in both ex vivo and hybridoma cells.
Genes up-regulated in prostate cancer samples bearing the fusion of TMPRSS2 with ERG [Gene ID=7113, 2078].
Genes down-regulated in prostate cancer samples bearing the fusion of TMPRSS2 with ERG [Gene ID=7113, 2078].
Proteins with reduced expression in mulignant glioma cell line (A172) which bears loss of heterozygosity (LOH) in the 1p region.
Genes defining a 25-signal proteomic signature associated with a high risk of cancer recurrence and poor survival of NSCLC (non-small cell lung cancer) patients.
Genes up-regulated in multiple drug resistant neuroblastoma cell lines.
The 'CLASS-11' set of pro- and anti-inflammatory cytokines whose expression identifies stage I lung adenocarcinoma patients with poor prognosis.
Genes from the 254-gene classifier which were down-regulated in melanoma patients with a reported distant metastasis within 4 years.
Genes up-regulated in CL1-5 cells (lung cancer) overexpressing DNAJB4 [Gene ID=11080] off a plasmid vector.
Genes down-regulated in CL1-5 cells (lung cancer) overexpressing DNAJB4 [Gene ID=11080] off a plasmid vector.
Down-regulated genes associated with poor survival prognosis of patients with metastatic neuroblastoma that lack MYCN [Gene ID=4613] amplification.
Genes affected by epigenetic aberrations in prostate cancer.
Interferon cluster genes up-regulated in skin tumors treated with imiquimod [PubChem=57469].
Genes up-regulated in follicular thyroid adenoma (FTA) compared to other thyroid tumors.
Genes down-regulated in follicular thyroid adenoma (FTA) compared to other thyroid tumors.
Genes up-regulated in thyroid tumors of uncertain malignancy (T-UM) compared to other thyroid tumors.
Genes down-regulated in thyroid tumors of uncertain malignancy (T-UM) compared to other thyroid tumors.
Genes up-regulated in papillary thyroid carcinoma (PTC) compared to other thyroid tumors.
Genes down-regulated in papillary thyroid carcinoma (PTC) compared to other thyroid tumors.
Genes changed in LSK cells (bone marrow) as a function of a QTL for the size of hematopoietic stem cell (HSC) population: comparison of reciprocal congenic strains D.B. Chr3 (DB), B.D. Chr3 (BD) and the parental strains B6 and D2.
DNA methylation status of germline-specific genes with low-CpG-density promoters (LCP) in primary fibroblasts: UP=methylated, DN=unmethylated.
DNA methylation status of germline-specific genes with low-CpG-density promoters (LCP) in primary fibroblasts: UP=methylated, DN=unmethylated.
Germline-specific genes with intermediate-CpG-density promoters (ICP) that are methylated in primary fibroblasts.
DNA methylation status of germline-specific genes with intermediate-CpG-density promoters (ICP) in sperm: UP=methylated, DN=unmethylated.
DNA methylation status of germline-specific genes with intermediate-CpG-density promoters (ICP) in sperm: UP=methylated, DN=unmethylated.
DNA methylation status of germline-specific genes with low-CpG-density promoters (LCP) in sperm: UP=methylated, DN=unmethylated.
DNA methylation status of germline-specific genes with low-CpG-density promoters (LCP) in sperm: UP=methylated, DN=unmethylated.
The XPRSS-Int network genes up-regulated in breast tumors from patients with germline mutations in BRCA1 [Gene ID=672] compared to those with the wild type allele.
The XPRSS-Int network genes up-regulated in breast tumors from patients with germline mutations in BRCA1 [Gene ID=672] compared to those with the wild type allele.
Genes responsive to estradiol [PubChem=5757] both in normal and cancer ovarian cell lines.
Genes regulated by ESR1 [Gene ID=2099] in MCF-7 cells (breast cancer).
Genes regulated by ESRRA [Gene ID=2101] in MCF-7 cells (breast cancer).
Genes up-regulated by estradiol [PubChem=5757] and not modulated by ESRRA [Gene ID=2101] in MCF-7 cells (breast cancer).
Selected genes up-regulated in peripheral blood monocytes (PBMC) of patients with hepatocellular carcinoma (HCC) compared to those with chronic hepatitis.
Top 20 genes expressed higher in epithelioid than in sarcomatoid mesothelioma samples.
Top genes associated with favorable overall survival of mesothelioma patients after surgery.
Top genes associated with unfavorable overall survival of mesothelioma patients after surgery.
Top genes associated with favorable survival after surgery of patients with epithelioid mesothelioma.
Top genes associated with unfavorable survival after surgery of patients with epithelioid mesothelioma.
Genes whose expression pattern in adult male germ cell tumors (GCT) correlates with POU5F1 [Gene ID=5460].
Top 25 most highly expressed genes in embryonic carcinoma relative to seminoma tumors.
Top 25 most highly expressed genes in seminoma relative to embryonic carcinoma tumors.
Genes up-regulated in H1975 cells (non-small cell lung cancer, NSCLC) resistant to gefitinib [PubChem=123631] after treatment with EGFR inhibitor CL-387785 [PubChem=2776] for 24h.
Genes down-regulated in H1975 cells (non-small cell lung cancer, NSCLC) resistant to gefitinib [PubChem=123631] after treatment with EGFR inhibitor CL-387785 [PubChem=2776] for 24h.
Genes identified by method 2 as coordinately down-regulated late in HMEC cells (mammary epithelium) during acinar development in vitro.
Top up-regulated genes from principal component 1 (PCA1) which captures variation between normal plasma cells and tumors arising from aberrant expression of BCL2L1 and MYC [Gene ID=598, 4609].
Top down-regulated genes from principal component 1 (PCA1) which captures variation between normal plasma cells and tumors arising from aberrant expression of BCL2L1 and MYC [Gene ID=598, 4609].
Top up-regulated genes from principal component 3 (PCA3) which captures variation among different plasma cell tumors arising from overexpression of BCL2L1 and MYC [Gene ID=598, 4609].
Top down-regulated genes from principal component 3 which captures variation among different plasma cell tumors arising from overexpression of BCL2L1 and MYC [Gene ID=598, 4609].
Genes from 'subtype S1' signature of hepatocellular carcinoma (HCC): aberrant activation of the WNT signaling pathway.
Genes from 'subtype S2' signature of hepatocellular carcinoma (HCC): proliferation, MYC and AKT1 [Gene ID=4609, 207] activation.
Genes from 'subtype S3' signature of hepatocellular carcinoma (HCC): hepatocyte differentiation.
Up-regulated genes in head and neck cancer compared to cervical carcinoma samples.
Down-regulated genes in head and neck cancer compared to cervical carcinoma samples.
Genes up-regulated in hepatoblastoma samples compared to normal liver tissue.
Genes down-regulated in hepatoblastoma samples compared to normal liver tissue.
Genes up-regulated in robust Cluster 2 (rC2) of hepatoblastoma samples compared to those in the robust Cluster 1 (rC1).
Genes down-regulated in robust Cluster 2 (rC2) of hepatoblastoma samples compared to those in the robust Cluster 1 (rC1).
Genes up-regulated at early fetal liver stage (embryonic days  E11.5 - E12.5) compared to the late fetal liver stage (embryonic days E14.5 - E16.5).
Genes down-regulated at early fetal liver stage (embryonic days  E11.5 - E12.5) compared to the late fetal liver stage (embryonic days E14.5 - E16.5).
Genes whose expression classifies hepatoblastoma tumors as belonging to either rC1 or rC2 subtypes and whose expression predicts poor survival.
Genes exclusively up-regulated in B lymphocytes from CLL (chronic lymphocytic leukemia) patients but with a similiar expression pattern in the normal cells and in the cells from WM (Waldenstroem's macroblobulinemia) patients.
Genes exclusively down-regulated in B lymphocytes from CLL (chronic lymphocytic leukemia) patients but with a similiar expression pattern in the normal cells and in the cells from WM (Waldenstroem's macroblobulinemia) patients.
Genes exclusively up-regulated in B lymphocytes from WM (Waldenstroem's macroblobulinemia) patients but with a similiar expression pattern in the normal cells and in the cells from CLL (chronic lymphocytic leukemia) patients.
Genes exclusively down-regulated in B lymphocytes from WM (Waldenstroem's macroblobulinemia) patients but with a similiar expression pattern in the normal cells and in the cells from CLL (chronic lymphocytic leukemia) patients.
Genes exclusively up-regulated in plasma cells from MM (multiple myeloma) patients but with a similiar expression pattern in the normal cells and in the cells from WM (Waldenstroem's macroblobulinemia) patients.
Genes exclusively down-regulated in plasma cells from MM (multiple myeloma) patients but with a similiar expression pattern in the normal cells and in the cells from WM (Waldenstroem's macroblobulinemia) patients.
Genes exclusively up-regulated in B lymphocytes from WM (Waldenstroem's macroglobulinemia) but with a similar expression profile in MM (macroglobulinemia) and normal cells.
Genes from the 254-gene classifier which were up-regulated in melanoma patients with a reported distant metastasis within 4 years.
Genes showing similar expression profiles in all subtypes of cutaneous T cell lymphoma (CTCL).
Differentially expressed genes relevant to pathogenesis of cutaneous T cell lymphoma (CTCL).
Genes up-regulated in HUVEC cells (primary endothelium) after stimulation with leukotriene LTD4 [PubChem=3908] or thrombin (F2) [Gene ID=2147] for 1 h.
The optimal set of 70 prognostic markers predicting poor breast cancer clinical outcome (defined as developing metastases with 5 years).
Genes down-regulated in T cell acute lymphocytic leukemia (T-ALL) patients refractory to chemotherapy treatment.
Genes whose expression predicted relapse in less than 2 years after chemotherapy for adult patients with T-ALL (T cell lymphoblastic leukemia).
Genes whose expression is coregulated with that of IL3RA [Gene ID=3563] in hematopoietic stem cells (HSC).
Top 50 down-regulated genes in cluster CD-1 of multiple myeloma samples with the characteristic expression spike of CCND1 [Gene ID=595].
Top 50 down-regulated genes in cluster CD-2 of multiple myeloma samples with the charachteristic expression spike of CCND3 [Gene ID=896].
Top 50 down-regulated genes in cluster LB of multiple myeloma samples belonging to the low bone disease group.
Top 50 down-regulated genes in cluster HP of multiple myeloma samples characterized by a hyperploid signature.
Top 50 down-regulated genes in cluster MF of multiple myeloma samples with characteristic expression spike of MAF family transcription factors.
Top 50 down-regulated genes in cluster MS of multiple myeloma samples with characteristic expression spike of WHSC1 [Gene ID=7468].
Top 50 down-regulated genes in cluster PR of multiple myeloma samples characterized by increased expression of proliferation and cell cycle genes.
Genes up-regulated by MYC [Gene ID=4609], according to the MYC Target Gene Database.
Genes down-regulated by MYC [Gene ID=4609], according to the MYC Target Gene Database.
Genes up-regulated by MYC [Gene ID=4609] and whose promoters are bound by MYC, according to MYC Target Gene Database.
Genes up-regulated by MYC [Gene ID=4609] and whose promoters are bound by MYC, according to MYC Target Gene Database.
Genes whose promoters are bound by MYC [Gene ID=4609], according to MYC Target Gene Database.
Genes up-regulated in HeLa cells (cervical carcinoma) 12 h after infection with adenovirus Ad12.
Genes down-regulated in HeLa cells (cervical carcinoma) 12 h after infection with adenovirus Ad12.
Genes up-regulated in HeLa cells (cervical carcinoma) 24 h after infection with adenovirus Ad12.
Genes down-regulated in HeLa cells (cervical carcinoma) 24 h after infection with adenovirus Ad12.
Genes up-regulated in HeLa cells (cervical carcinoma) 32 h after infection with adenovirus Ad12.
Genes down-regulated in HeLa cells (cervical carcinoma) 32 h after infection with adenovirus Ad12.
Genes up-regulated in HeLa cells (cervical carcinoma) 48 h after infection with adenovirus Ad12.
Genes down-regulated in HeLa cells (cervical carcinoma) 48 h after infection with adenovirus Ad12.
Genes modulated in HeLa cells (cervical carcinoma) by TNF [Gene ID=7124] via NFKB pathway.
Genes modulated in HeLa cells (cervical carcinoma) by TNF [Gene ID=7124] not via NFKB pathway.
The 'core ESC-like gene module': genes coordinately up-regulated in a compendium of mouse embryonic stem cells (ESC) which are shared with the human ESC-like module.
Top 100 probe sets contrubuting to the positive side of the 1st principal component; predominantly associated with spindle cell and pleomorphic sarcoma samples.
Top 100 probe sets contrubuting to the negative side of the 1st principal component; predominantly associated with synovial sarcoma and myxoid/round cell liposarcoma samples.
Top 100 probe sets contrubuting to the positive side of the 2nd principal component; associated with adipocytic differentiation.
Top 100 probe sets contrubuting to the negative side of the 2nd principal component; associated with adipocytic differentiation.
Genes up-regulated in metastatic tumors from the whole panel of patients with prostate cancer.
Genes down-regulated in metastatic tumors from the whole panel of patients with prostate cancer.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 0.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 1.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 3.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 4.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 5.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 6.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 7.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 8.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 9.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 11.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 11.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 12.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 13.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 14.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 15.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 16.
Genes co-regulated in uterus during a time course response to progesterone [PubChem=5994]: SOM cluster 17.
Genes whose reduced expression in nasopharyngeal carinoma (NPC) correlated most with the increased expression of EBNA1 [Gene ID=3783774], a latent gene of Epstein-Barr virus (EBV).
Genes involved in pyruvate metabolism; based on literature and sequence annotation resources and converted to Affymetrix HG-U133A probe sets.
Genes involved in free fatty acid oxidation; based on literature and sequence annotation resources and coverted to Affymetrix HG-U133A probe sets.
Genes involved in gluconeogenesis; based on literature and sequence annotation resources and converted to Affymetrix HG-U133A probe sets.
Genes involved in glycogen metabolism; based on literature and sequence annotation resources and converted to Affymetrix HG-U133A probe sets.
Genes involved in glycolysis; based on literature and sequence annotation resources and converted to Affymetrix HG-U133A probe sets.
Genes up-regulated in fibroblasts from old individuals, compared to those from young donors.
Cluster 6: ECM related genes up-regulated in dermal fibroblasts later than 30 min after TGFB1 [Gene ID=7040] addition; slowly increased up to 120 min time point, then reached a plateau.
Gene expression signature of vascular invasion of hepatocellular carcinoma (HCC).
Genes up-regulated in primary keratinocytes at 1 h after UVB irradiation.
Genes down-regulated in primary keratinocytes at 1 h after UVB irradiation.
Top genes associated with chemosensitivity to 5-fluorouracil [PubChem=3385] across 85 tumor xenografts.
Top genes associated with chemosensitivity to cisplatin [PubChem=2767] across 85 tumor xenografts.
Top genes associated with chemosensitivity to nimustine [PubChem=39214] across 85 tumor xenografts.
Top genes associated with chemosensitivity to doxorubicin [PubChem=31703] across 85 tumor xenografts.
Top genes associated with chemosensitivity to mitomycin [PubChem=5746] across 85 tumor xenografts.
Top genes associated with chemosensitivity to methotrexate [PubChem=4112] across 85 tumor xenografts.
Cluster G5: genes up-regulated in NHEK cells (normal keratinocyte) at 3 h and 24 h time points after UV-B irradiation.
Cluster G24: genes induced in NHEK (normal keratinocyte) but not in SCC12B2 cells (squamous cell carcinoma) by UV-B radiation.
A cluster of genes specifically up-regulated in gastrointestinal stromal tumors (GIST).
Top 20 negative significant genes associated with CNN1 [Gene ID=1264] negative leiomyosarcoma tumors.
Top 20 positive significant genes associated with synovial sarcoma tumors.
Top 20 negative significant genes associated with synovial sarcoma tumors.
Top 20 negative significant genes associated with schwannoma tumors.
Genes up-regulated in normal fibroblasts in response to IL6 [Gene ID=3569].
Genes down-regulated in normal fibroblasts in response to IL6 [Gene ID=3569].
Genes down-regulated in A172 cells (glioma, does not express MGMT [Gene ID=4255]) by carmustine [PubChem=2578] at 24 h.
Genes up-regulated in T98G cells (glioma, express MGMT [Gene ID=4255]) by carmustine [PubChem=2578] at 24 h.
Genes up-regulated in 786-0 cells (renal carcinoma, RCC) by the loss of VHL [Gene ID=7428] and in response to hypoxia.
Genes downstream of both CDKN1A and TP53 [Gene ID=1026, 7157] in 2774qw1 cells (ovarian cancer).
Genes downstream of CDKN1A [Gene ID=1026] in a TP53 [Gene ID=7157] independent pathway in 2774qw1 cells (ovarian cancer).
Genes up-regulated in primary granulosa cells after stimulation with LH or FSH gonadotrophic hormones for 24 h.
Genes down-regulated in primary granulosa cells after stimulation with LH or FSH gonadotrophic hormones for 24 h.
Genes up-regulated in primary granulosa cells in response to forskolin [PubChem=47936].
Genes down-regulated in primary granulosa cells in response to forskolin [PubChem=47936].
Genes up-regulated in primary fibroblast cell culture at 30 min time point after infection with HCMV (AD169 strain).
Genes down-regulated in primary fibroblast cell culture at 30 min time point after infection with HCMV (AD169 strain).
Genes up-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 1 h time point that were not up-regulated at the previous time point, 30 min.
Genes down-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 1 h time point that were not down-regulated at the previous time point, 30 min.
Genes up-regulated in primary fibroblast cell culture point after infection with HCMV (AD169 strain) at 2 h time point that were not up-regulated at the previous time point, 1 h.
Genes down-regulated in primary fibroblast cell culture point after infection with HCMV (AD169 strain) at 2 h time point that were not down-regulated at the previous time point, 1 h.
Genes up-regulated in primary fibroblast cell culture point after infection with HCMV (AD169 strain) at 4 h time point that were not up-regulated at the previous time point, 2 h.
Genes down-regulated in primary fibroblast cell culture point after infection with HCMV (AD169 strain) at 4 h time point that were not down-regulated at the previous time point, 2 h.
Genes in this set correspond to the most abuntant transcripts that are also specific to platelets.
Genes down-regulated in CD-1 compared to CD-2 cluster of multiple myeloma samples.
Genes up-regulated in CD-1 compared to CD-2 cluster of multiple myeloma samples.
Top 50 up-regulated genes in cluster PR of multiple myeloma samples characterized by increased expression of proliferation and cell cycle genes.
Genes commonly up-regulated in CD-1 and CD-2 clusters of multiple myeloma samples and which were higher expressed in the CD-1 group.
Genes commonly down-regulated in CD-1 and CD-2 clusters of multiple myeloma samples and which were higher expressed in the CD-1 group.
Top 50 up-regulated genes in cluster LB of multiple myeloma samples belonging to the low bone disease group.
Top 50 up-regulated genes in cluster MS of multiple myeloma samples with characteristic expression spike of WHSC1 [Gene ID=7468].
Top 50 up-regulated genes in cluster HP of multiple myeloma samples characterized by a hyperploid signature.
Top 50 up-regulated genes in cluster CD-1 of multiple myeloma samples with the characteristic expression spike of CCND1 [Gene ID=595].
Top 50 up-regulated genes in cluster CD-2 of multiple myeloma samples with the characteristic expression spike of CCND3 [Gene ID=896].
Top 50 up-regulated genes in cluster MF of multiple myeloma samples with characteristic expression spike of MAF family transcription factors.
Genes up-regulated in MCF-7 cells (breast cancer) in response to growth medium from L3T3-L1 cells (differentiated to pre-adipocytes).
Genes down-regulated in primary adipocytes compared to preadipocytes.
Genes up-regulated in primary adipocytes compared to preadipocytes.
Downregulated in the vastus lateralis muscle of aged vs young adult rhesus monkeys
Upregulated in the vastus lateralis muscle of aged vs young adult rhesus monkeys
Genes down-regulated in postmortem brain frontal cortex samples from old subjects compared to those from the young ones.
Genes up-regulated in postmortem brain frontal cortex samples from old subjects compared to those from the young ones.
Genes whose expression decreases with age in normal kidney.
Genes whose expression decreases with age in normal kidney, excluding those with higher expression in blood.
Genes whose expression increases with age in normal kidney, excluding those with higher expression in blood.
Genes whose expression increases with age in normal kidney.
Genes down-regulated in brain from patients with Alzheimer's disease.
Genes up-regulated in brain from patients with Alzheimer's disease.
Genes down-regulated in patients at the incipient stage of Alzheimer's disease.
Genes up-regulated in patients at the incipient stage of Alzheimer's disease.
Genes up-regulated in the atria of healthy hearts, compared to venticles.
Genes down-regulated in BT549 cells (breast cancer) by expression of SMARCE1 [Gene ID=6605] off a retroviral vector.
Genes up-regulated in BT549 cells (breast cancer) by expression of SMARCE1 [Gene ID=6605] off a retroviral vector.
Genes down-regulated in T98G cells (glioma, express MGMT [Gene ID=4255]) by carmustine [PubChem=2578] at 24 h.
Genes down-regulated in T98G cells (glioma, express MGMT [Gene ID=4255]) by carmustine [PubChem=2578] at 48 h.
Genes up-regulated in T98G cells (glioma, express MGMT [Gene ID=4255]) by carmustine [PubChem=2578] at 48 h.
Genes up-regulated in A172 cells (glioma, does not express MGMT [Gene ID=4255]) by carmustine [PubChem=2578] at 24 h.
Genes down-regulated in A172 cells (glioma, does not express MGMT [Gene ID=4255]) by carmustine [PubChem=2578] at 48 h.
Genes up-regulated in A172 cells (glioma, does not express MGMT [Gene ID=4255]) by carmustine [PubChem=2578] at 48 h.
Down-regulated genes distinguishing between two groups of non-BRCA1/BRCA2 [Gene ID=672, 675] breast tumors (BRACx): group A vs group B.
Up-regulated genes distinguishing between two groups of non-BRCA1/BRCA2 [Gene ID=672, 675] breast tumors (BRACx): group A vs group B.
Genes down-regulated in SW480 cells (colon cancer with mutated p53 [Gene ID=7157]) upon expression of BRCA1 [Gene ID=672] off an adenovirus vector.
Genes up-regulated in SW480 cells (colon cancer with mutated p53 [Gene ID=7157]) upon expression of BRCA1 [Gene ID=672] off an adenovirus vector.
Up-regulated genes distinguishing between breast cancer tumors with mutated BRCA1 [Gene ID=672] from those with mutated BRCA2 [Gene ID=675].
Up-regulated genes distinguishing between breast cancer tumors with mutated BRCA1 [Gene ID=672] from those with mutated BRCA2 [Gene ID=675].
Genes distinguishing between sporadic breast cancer tumors and hereditary breast cancer tumors that have mutated BRCA1 and BRCA2 [Gene ID=672, 675].
Genes differentially expressed in hereditary breast cancer tumors with mutated BRCA1 [Gene ID=672] compared to those with mutated BRCA2 [Gene ID=675].
Genes down-regulated in ALAB cells (breast cancer) upon reintroduction of SMARCA4 [Gene ID=6597] expressed off adenoviral vector.
Genes up-regulated in ALAB cells (breast cancer) upon reintroduction of SMARCA4 [Gene ID=6597] expressed off adenoviral vector.
Genes up-regulated in HT-29 cells (colon cancer) by the combination of trichostatin A (TSA) and sodium butyrate [PubChem=5562, 5222465].
Downregulated in the vastus lateralis muscle of middle aged rhesus monkeys subjected to caloric restriction since young adulthood vs age matched controls
Upregulated in the vastus lateralis muscle of middle aged rhesus monkeys subjected to caloric restriction since young adulthood vs age matched controls
Genes commonly up-regulated in cancer relative to normal tissue, according to the meta-analysis of the OncoMine gene expression database.
Genes commonly up-regulated in undifferentiated cancer relative to well-differentiated cancer, based on the meta-analysis of the OncoMine gene expression database.
Genes down-regulated in HL-60 cells (promyeloid leukemia) by cantharidin [PubChem=6708701].
Genes up-regulated in HL-60 cells (promyeloid leukemia) by cantharidin [PubChem=6708701].
Genes down-regulated in pulpal tissue extracted from carious teeth.
Genes up-regulated in pulpal tissue extracted from carious teeth.
Genes down-regulated in NCI-H2170 cells (lung cancer) upon induction of resistance to cisplatin [PubChem ID=2767].
Genes up-regulated in NCI-H2170 cells (lung cancer) upon induction of resistance to cisplatin [PubChem ID=2767].
Genes down-regulated in fibroblasts with defective XPC [Gene ID=7508] in response to cisplatin [PubChem=2767].
Genes up-regulated in fibroblasts with defective XPC [Gene ID=7508] in response to cisplatin [PubChem=2767].
Down-regulated at 24 h following infection of primary human foreskin fibroblasts with CMV
Up-regulated at 24 h following infection of primary human foreskin fibroblasts with CMV
Down-regulated at 8 h following infection of primary human foreskin fibroblasts with CMV
Up-regulated at 8 h following infection of primary human foreskin fibroblasts with CMV
Down-regulated at any timepoint following infection of primary human foreskin fibroblasts with CMV
Up-regulated at any timepoint following infection of primary human foreskin fibroblasts with CMV
Genes down-regulated in primary fibroblast cell culture point after infection with HCMV (AD169 strain) at 6 h time point that were not down-regulated at the previous time point, 4 h.
Genes up-regulated in primary fibroblast cell culture point after infection with HCMV (AD169 strain) at 6 h time point that were not up-regulated at the previous time point, 4 h.
Genes down-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 10 h time point that were not down-regulated at the previous time point, 8 h.
Genes up-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 10 h time point that were not up-regulated at the previous time point, 8 h.
Genes down-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 12 h time point that were not down-regulated at the previous time point, 10 h.
Genes up-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 12 h time point that were not up-regulated at the previous time point, 10 h.
Genes down-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 14 h time point that were not down-regulated at the previous time point, 12 h.
Genes up-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 14 h time point that were not up-regulated at the previous time point, 12 h.
Genes down-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 16 h time point that were not down-regulated at the previous time point, 14 h.
Genes up-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 16 h time point that were not up-regulated at the previous time point, 14 h.
Genes down-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 18 h time point that were not down-regulated at the previous time point, 16 h.
Genes up-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 18 h time point that were not up-regulated at the previous time point, 16 h.
Genes down-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 20 h time point that were not down-regulated at the previous time point, 18 h.
Genes up-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 20 h time point that were not up-regulated at the previous time point, 18 h.
Genes down-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 24 h time point that were not down-regulated at the previous time point, 20 h.
Genes up-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 24 h time point that were not up-regulated at the previous time point, 20 h.
Genes down-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 48 h time point that were not down-regulated at the previous time point, 24 h.
Genes up-regulated in primary fibroblast cell culture after infection with HCMV (AD169 strain) at 48 h time point that were not up-regulated at the previous time point, 24 h.
Genes down-regulated in primary fibroblast cell culture point after infection with HCMV (AD169 strain) at 8 h time point that were not down-regulated at the previous time point, 6 h.
Genes up-regulated in primary fibroblast cell culture point after infection with HCMV (AD169 strain) at 8 h time point that were not up-regulated at the previous time point, 6 h.
Cellular genes up-regulated in forskin fibroblasts by expression of CMV EI86 protein off an adenovirus vector.
Genes down-regulated in the nucleus accumbens (a major reward center in the brain) 8 weeks after induction of CREB1 [Gene ID=1385] expression in a transgenic Tet-Off system.
Genes up-regulated in the nucleus accumbens (a major reward center in the brain) 8 weeks after induction of CREB1 [Gene ID=1385] expression in a transgenic Tet-Off system.
Genes up-regulated in T24 cells (bladder carcinoma) after treatment with decitabine (5-aza-2'-deoxycytidine) [PubChem=451668].
Genes down-regulated in LD419 cells (fibroblast) after treatment with decitabine (5-aza-2'-deoxycytidine) [PubChem=451668].
Genes up-regulated in LD419 cells (fibroblast) after treatment with decitabine (5-aza-2'-deoxycytidine) [PubChem=451668].
50 most interesting genes up-regulated in the pancreatic cancer cell lines (AsPC1, Hs766T, MiaPaCa2, Panc1) but not in the non-neoplastic cells (HPDE) by decitabine (5-aza-2'-deoxycytidine) [PubChem=451668].
Genes up-regulated in the pancreatic cancer cell lines (AsPC1, Hs766T, MiaPaCa2, Panc1) but not in the non-neoplastic cells (HPDE) by decitabine (5-aza-2'-deoxycytidine) [PubChem=451668].
Genes up-regulated in the nucleus accumbens (a major reward center in brain) 2 weeks after induction of deltaFosB, a FOSB [Gene ID=2354] splice variant.
Genes up-regulated in the nucleus accumbens (a major reward center in brain) 8 weeks after induction of deltaFosB, a FOSB [Gene ID=2354] splice variant.
Top 50  down-regulated genes in glomeruli from kidneys with diabetic nephropathy (type 2 diabetes mellitus).
Top 50 up-regulated genes in glomeruli from kidneys with diabetic nephropathy (type 2 diabetes mellitus).
Genes up-regulated in HDMEC cells (microvascular endothelium): proliferating vs quiescent cells.
Genes down-regulated by trabectedin [PubChem=3199] and its synthetic analog phthalascidin Pt 650 in HCT116 cells (colon cancer).
Genes down-regulated in HeLa cells (cervical carcinoma) by trabectedin [PubChem=3199].
Genes up-regulated in HeLa cells (cervical carcinoma) by trabectedin [PubChem=3199].
Genes down-regulated in chondrosarcoma and ovarian carcinoma cell lines which developed resistance to trabectedin [PubChem=3199].
Genes up-regulated in chondrosarcoma and ovarian carcinoma cell lines which developed resistance to trabectedin [PubChem=3199].
Genes down-regulated in at least 8 of 11 sarcoma cell lines by trabectedin [PubChem=3199].
Genes up-regulated in at least 8 of 11 sarcoma cell lines by trabectedin [PubChem=3199].
Down-regulated in ovarian epithelial cells (MCV152) 72 hours following FSH treatment, compared to untreated
Genes up-regulated in MCV152 cells (ovarian cancer) treated with follicle stimulating hormone (FSH).
Genes down-regulated in MFCF-7 cells (breast cancer) upon stable autocrine expression of HG1 [Gene ID=2688].
Genes up-regulated in MFCF-7 cells (breast cancer) upon stable autocrine expression of HG1 [Gene ID=2688].
Genes down-regulated in MFCF-7 cells (breast cancer) by exogenous HG1 [Gene ID=2688].
Genes up-regulated in MFCF-7 cells (breast cancer) by exogenous HG1 [Gene ID=2688].
Genes down-regulated in bones at 24 h after injection of GH1 [Gene ID=2688] to mice without detectable endogenous growth hormone.
Genes down-regulated by expression of HBV X protein (HBVgp3) [Gene ID=944566] in SK-Hep-1 cells (hepatocellular carcinoma).
Genes up-regulated by expression of HBV X protein (HBVgp3) [Gene ID=944566] in SK-Hep-1 cells (hepatocellular carcinoma).
Genes down-regulated by expression of HBV X protein (HBVgp3) [Gene ID=944566] both in SK-Hep-1 cells (hepatocellular carcinoma) and normal primary hepatocytes.
Genes up-regulated by expression of HBV X protein (HBVgp3) [Gene ID=944566] both in SK-Hep-1 cells (hepatocellular carcinoma) and normal primary hepatocytes.
Genes down-regulated by expression of HBV X protein (HBVgp3) [Gene ID=944566] in primary hepatocytes.
Genes up-regulated by expression of HBV X protein (HBVgp3) [Gene ID=944566] in primary hepatocytes.
Cluster 5: genes up-regulated in SW260 cells (colon cancer) by curcumin and sulindac [PubChem=969516, 5352].
Genes down-regulated in atria of failing hearts (DCM and ICM) compared to healthy controls.
Genes up-regulated in atria of failing hearts (DCM and ICM) compared to healthy controls.
Genes down-regulated in the ventricles of failing hearts (DCM and ICM) compared to the healthy controls.
Genes up-regulated in HSC (hematopoietic stem cells) compared to HPC (hematopoietic progenitor cells).
Genes down-regulated in fibroblasts from patients with Hutchinson-Gilford progeria (premature aging), compared to those from normal young individuals.
Genes that are transcriptionally regulated by HIF1A [Gene ID=3091].
Genes highly expressed in the neonatal hippocampus (clusters 4 and 8).
Genes up-regulated in hyppocampus at late postnatal stages (clusters 11 and 15).
Genes highly expressed in prenatal hippocampus (cluster 1).
Genes down-regulated in normal keratinocytes immortalized by infection with the high risk HPV31 (human papilloma virus) strain.
Genes up-regulated in normal keratinocytes immortalized by infection with the high risk HPV31 (human papilloma virus) strain.
Genes in the expression cluster 'Early Progenitors Shared': up-regulated in hematopoietic progenitors from adult bone marrow and from fetal liver.
Genes in the expression cluster 'HSC and Progenitors Shared': up-regulated in hematopoietic stem cells (HSC) and progenitors from adult bone marrow and fetal liver.
Genes in the expression cluster 'HSC Shared': up-regulated in hematopoietic stem cells (HSC) from adult bone marrow and fetal liver.
Genes in the expression cluster 'Intermediate Progenitors Shared': up-regulated in hematopoietic intemediate progenitor cells from adult bone marrow and fetal liver.
Genes in the expression cluster 'Late Progenitors Shared': up-regulated in hematopoietic late progenitor cells from adult bone marrow and fetal liver.
Genes in the expression cluster 'LT-HSC Shared': up-regulated in long term hematopoietic stem cells (LT-HSC) from adult bone marrow and fetal liver.
Genes in the expression cluster 'MBC Fetal': up-regulated in mature blood cell populations from fetal liver.
Genes in the expression cluster 'MBC Shared': up-regulated in mature blood cell populations from adult bone marrow and fetal liver.
Genes in the expression cluster 'ST-HSC Shared': up-regulated in short term hematopoietic stem cells (ST-HSC) from adult bone marrow and fetal liver.
Genes up-regulated specifically in human kidney tissue.
Genes up-regulated specifically in human liver tissue.
Genes up-regulated specifically in human pancreas.
Genes up-regulated specifically in human placenta.
Genes up-regulated specifically in human salivary gland tissue.
Genes up-regulated specifically in human testis tissue.
Genes up-regulated specifically in human thymus.
Genes identi???ed as hypermethylated in SW48 cells (colon cancer).
Genes up-regulated in RPTEC cells (normal kidney) by hypoxia.
Genes up-regulated in 786-0 cells  (renal carcinoma, RCC) by hypoxia and in the absensce of VHL [Gene ID=7428].
Genes up-regulated in HK-2 cells kidney tubular epithelium) under hypoxia and down-regulated on re-oxygenation.
Genes known to be induced by hypoxia
Down-regulated in B lymphocytes from patients with ICF syndrom caused by mutations in DNMT3B [Gene ID=1789] compared to normals.
Up-regulated in B lymphocytes from patients with ICF syndrom caused by mutations in DNMT3B [Gene ID=1789] compared to normals.
Genes down-regulated in huT78R cells (cutaneous T-cell lymphoma, CTCL) resistant to IFNA2 [Gene ID=3440] compared to the IFN2A sensitive parental cell line.
Genes up-regulated in primary fibroblast culture after treatment with interferon alpha for 6 h.
Genes down-regulated in T98 cells (glioma) 48 h after treatment with interferon beta.
Genes up-regulated in T98 cells (glioma) 48 h after treatment with interferon beta.
Genes down-regulated in C2AS12 cells (myoblast) by IGF1 [Gene ID=3479] vs PDGFB [Gene ID=5155].
Genes up-regulated in C2AS12 cells (myoblast) by IGF1 [Gene ID=3479] vs PDGFB [Gene ID=5155].
Genes down-regulated in corneal fibroblasts after treatment with IL1A [Gene ID=3552].
Genes up-regulated in corneal fibroblasts after treatment with IL1A [Gene ID=3552].
Genes down-regulated in hypertrophic scar fibroblasts in response to IL6 [Gene ID=3569].
Genes up-regulated in hypertrophic scar fibroblasts in response to IL6 [Gene ID=3569].
Genes prefentially expressed in human inner ear tissue (cochlea and vestibule), at least 10-fold higher from a mixture of 29 other tissues.
Down-regulated in brown preadipocytes with IRS1 [Gene ID=3667] knockout vs wild type controls; the knockouts have severe defects in adipocyte differentiation.
Up-regulated in brown preadipocytes with IRS1 [Gene ID=3667] knockout vs wild type controls; the knockouts have severe defects in adipocyte differentiation.
Genes showing decreasing expression in brown preadipocytes with increasing ability of the cells to differentiate.
Genes showing increasing expression in brown preadipocytes with decreasing ability of the cells to differentiate.
Genes up-regulated at 3 months of age in lungs from LIPA [Gene ID=3988] knockout mice, which display pulmonary pathology.
Genes up-regulated at 6 months of age in lungs from LIPA [Gene ID=3988] knockout mice, which display pulmonary pathology.
Down-regulated genesin the left ventricle myocardium of patients with heart failure following implantation of LVAD (left ventricular assist device).
Up-regulated genesin the left ventricle myocardium of patients with heart failure following implantation of LVAD (left ventricular assist device).
Down-regulated genes in metastatic vs primary solid tumors.
Up-regulated genes in metastatic vs primary solid tumors.
Genes down-regulated in fibroblasts from middle-age individuals, compared to those from the young donors.
Genes up-regulated in fibroblasts from middle-age individuals, compared to those from the young donors.
Up-regulated at 4 hours following treatment of mouse lymphocytes (TK 3.7.2C) with a high dose of methyl methanesulfonate (MMS)
Down-regulated in GHOST(3)CXCR4 cells (osteosarcoma) upon ectopic expression of ILF3 [Gene ID=3609].
Up-regulated in GHOST(3)CXCR4 cells (osteosarcoma) upon ectopic expression of ILF3 [Gene ID=3609].
Genes down-regulated in HPL1D cells (lung epithelium) upon exposure to nickel acetate [PubChem=9756].
Genes down-regulated in D-341 MED (OBR) cells (medulloblastoma) resistant to both carmustine and O6-BG [PubChem=2578, 4578].
Genes up-regulated in D-341 MED (OBR) cells (medulloblastoma) resistant to both carmustine and O6-BG [PubChem=2578, 4578].
Genes up-regulated in fibroblasts from old individuals, compared to those from young donors.
Genes down-regulated in MCF7 cells (breast cancer) after treatment with the oxydants: hydrogen peroxyde, menadione, and t-butyl hydroperoxyde [PubChem=784, 4055, 6410].
Genes up-regulated in MCF7 cells (breast cancer) after treatment with the oxydants: hydrogen peroxyde, menadione, and t-butyl hydroperoxyde [PubChem=784, 4055, 6410].
Oxidative stress genes down-regulated in ARPE-19 cells (retinal pigmented epithelium) in response to HNE, tBH and H2O2 [PubChem=5283344, 6410, 784].
Oxidative stress genes down-regulated in ARPE-19 cells (retinal pigmented epithelium) in response to HNE and H2O2 [PubChem=5283344, 784].
Oxidative stress genes down-regulated in ARPE-19 cells (retinal pigmented epithelium) in response to tert-butyl hydroperoxide (tBH) and H2O2 [PubChem=6410, 784].
Oxidative stress genes down-regulated in ARPE-19 cells (retinal pigmented epithelium) in response to HNE and tBH [PubChem=5283344, 6410].
Genes whose promoters contain TP53 [Gene ID=7157] response elements.
Up-regulated in human fetal pituitary tissue, compared to adult pituitary tissue
Genes most strongly down-regulated in kidney glomeruli isolated from TCF21 [Gene ID=6943] knockout mice.
Genes most strongly up-regulated in kidney glomeruli isolated from TCF21 [Gene ID=6943] knockout mice.
Genes down-regulated in NIH-3T3 cells (fibroblast) after knockdown of PRMT5 [Gene ID=10419] by RNAi.
Genes up-regulated in NIH-3T3 cells (fibroblast) after knockdown of PRMT5 [Gene ID=10419] by RNAi.
Genes up-regulated in gastric cancer patients refractory to chemotherapy treatment with 5-fluorouracil and cisplatin [PubChem=3385, 2767] compared to the sensitive state.
Genes down-regulated in HEK293 cells (embryonic kidney) at 6 h, 12 h or 24 h after infection with reovirus strain T3A (known as a strong inducer of apoptosis).
Genes up-regulated in HEK293 cells (embryonic kidney) at 6 h, 12 h or 24 h after infection with reovirus strain T3A (known as a strong inducer of apoptosis).
Genes down-regulated in primary fibroblasts from Rett syndrom patients who carry mutations inactivating MECP2 [Gene ID=4204].
Genes up-regulated in primary fibroblasts from Rett syndrom patients who carry mutations inactivating MECP2 [Gene ID=4204].
Genes up-regulated in A549 cells (lung carcinoma) upon infection with RSV (respiratory syncytial virus) and down-regulated by further treatment with ribavirin [PubChem=5064].
Genes up-regulated in A549 cells (lung carcinoma) upon infection with RSV (respiratory syncytial virus) and up-regulated by further treatment with ribavirin [PubChem=5064].
Top 20 genes whose up-regulation correlated with gastrointestinal stromal tumors (GIST) compared to synovial sarcoma.
Top 20 positive significant genes associated with malignant fibrous histiocytoma tumors.
Top 20 positive significant genes associated with CNN1 [Gene ID=1264] negative leiomyosarcoma tumors.
Top 20 negative significant genes associated with liposarcomas, versus other soft-tissue tumors.
Top 20 positive significant genes associated with liposarcomas, versus other soft-tissue tumors.
Top 20 positive significant genes associated with schwannoma tumors.
Top 20 genes whose up-regulation correlated with gastrointestinal stromal tumors (GIST) and synovial sarcoma compared to other tumors.
Genes depleted in embryonic, neural and hematopoietic stem cells.
Genes enriched in embryonic, neural and hematopoietic stem cells.
Cluster 1: ECM related genes up-regulated in dermal fibroblasts within 30 min after TGFB1 [Gene ID=7040] addition, and which kept increasing with time.
Cluster 2: ECM related genes up-regulated in dermal fibroblasts within 30 min after TGFB1 [Gene ID=7040] addition; reached a plateau after that.
Cluster 3: ECM related genes up-regulated in dermal fibroblasts within 30 min after TGFB1 [Gene ID=7040] addition; returned rapidly to basal level after that.
Cluster 4: ECM related genes up-regulated in dermal fibroblasts later than 30 min after TGFB1 [Gene ID=7040] addition; kept increasing with time.
Cluster 5: ECM related genes up-regulated in dermal fibroblasts later than 30 min after TGFB1 [Gene ID=7040] addition; decreased slowly after the peak at 120 min time point.
ECM related genes up-regulated early (within 30 min) in dermal fibroblasts after addition of TGFB1 [Gene ID=7040].
ECM related genes up-regulated later than 30 min following addition of TGFB1 [Gene ID=7040] in dermal fibroblasts.
50 genes up-regulated in the pancreatic cancer cell lines (AsPC1, Hs766T, MiaPaCa2, Panc1) but not in the non-neoplastic cells (HPDE) by the combination of decitabine  and TSA [PubChem=451668, 5562].
Down-regulated in CD4+ [Gene ID=920] T lymphocytes after 4 h treatment with 100 nM TSA [PubChem=5562].
Up-regulated in CD4+ [Gene ID=920] T lymphocytes after 4 h treatment with 100 nM TSA [PubChem=5562].
Cancer related genes down-regulated in any of four hepatoma cell lines following 24 h treatment with TSA [PubChem=5562].
Cancer related genes up-regulated in any of four hepatoma cell lines following 24 h treatment with TSA [PubChem=5562].
Genes up-regulated in more than one of several human hepatoma cell lines by TSA [PubChem=5562].
50 most interesting genes up-regulated in pancreatic cancer cell lines (AsPC1, Hs766T, MiaPaCa2, Panc1) but not in the non-neoplastic cells (HPDE) by TSA [PubChem=5562].
Cluster G1: genes most highly up-regulated in NHEK cells (normal keratinocyte) between 6 h and 12 h after UV-B irradiation.
Cluster G2: genes increasingly up-regulated in NHEK cells (normal keratinocyte) and reaching maximum levels at 12 h and 24 h after UV-B irradiation.
Cluster G3: genes increasingly up-regulated in NHEK cells (normal keratinocyte) after 6 h time point upon UV-B irradiation.
Cluster G4: genes increasingly up-regulated in NHEK cells (normal keratinocyte) after 12 h time point after UV-B irradiation.
Cluster G6: genes increasingly down-regulated in NHEK cells (normal keratinocyte) after UV-B irradiation.
Genes down-regulated in NHEK cells (normal keratinocytes) by UV-B irradiation.
Genes up-regulated in NHEK cells (normal keratinocytes) by UV-B irradiation.
Genes down-regulated in primary tissue culture of epidermal kerationcytes after UVB irradiation.
Genes up-regulated in primary tissue culture of epidermal kerationcytes after UVB irradiation.
Cluster 0: genes changed in primary keratinocytes by UVB irradiation.
Cluster 1: genes changed in primary keratinocytes by UVB irradiation.
Cluster 2: genes changed in primary keratinocytes by UVB irradiation.
Cluster 3: genes changed in primary keratinocytes by UVB irradiation.
Cluster 4: genes changed in primary keratinocytes by UVB irradiation.
Cluster 5: genes changed in primary keratinocytes by UVB irradiation.
Cluster 6: genes changed in primary keratinocytes by UVB irradiation.
Cluster 7: genes changed in primary keratinocytes by UVB irradiation.
Cluster 8: genes changed in primary keratinocytes by UVB irradiation.
Genes down-regulated in primary keratinocytes at 24 h after UVB irradiation.
Genes down-regulated in primary keratinocytes at 6 h after UVB irradiation.
Genes up-regulated in primary keratinocytes at 6 h after UVB irradiation.
Genes down-regulated in SCC12B2 cells (squamous cell carcinoma) by UV-B irradiation.
Genes up-regulated in SCC12B2 cells (squamous cell carcinoma) by UV-B irradiation.
Selected genes down-regulated in WS1 (fibroblast) in response to irradiation with high dose UV-C.
Selected genes up-regulated in WS1 (fibroblast) in response to irradiation with high dose UV-C.
Cluster d1: genes down-regulated in WS1 cells (fibroblast) at 6 h after irradiation with high dose UV-C.
Cluster d2: genes down-regulated consistently in WS1 cells (fibroblast) between 6 h and 24 h after irradiation with high dose UV-C.
Cluster d3: genes progressively down-regulated in WS1 cells (fibroblast) through 12 h irradiation with high dose UV-C.
Cluster d4: genes progressively down-regulated in WS1 cells (fibroblast) through 12 h after irradiation with high dose UV-C.
Cluster d5: genes progressively down-regulated in WS1 cells (fibroblast) through 18 h after irradiation with high dose UV-C.
Cluster d6: genes progressively down-regulated in WS1 cells (fibroblast) through 18 h after irradiation with high dose UV-C.
Cluster d7: genes progressively down-regulated in WS1 cells (fibroblast) through 18 h after irradiation with high dose UV-C.
Cluster d8: genes progressively down-regulated in WS1 cells (fibroblast) through 18 h after irradiation with high dose UV-C.
Cluster d9: genes progressively down-regulated in WS1 cells (fibroblast) through 24 h after irradiation with high dose UV-C.
Selected genes down-regulated in WS1 (fibroblast) in response to irradiation with low dose UV-C.
Selected genes up-regulated in WS1 (fibroblast) in response to irradiation with low dose UV-C.
Genes up-regulated in HUVEC cells (endothelium) at 2 h after VEGFA [Gene ID=7422] stimulation.
Genes up-regulated in HUVEC cells (endothelium) at 30 min after VEGFA [Gene ID=7422] stimulation.
Genes most profoundly induced in HUVEC cells (endothelium) by VEGFA [Gene ID=7422].
Genes up-regulated in the ventricles of healthy hearts, compared to atria.
Genes up-regulated in 786-0 cells (renal carcinoma, RCC) upon expression of VHL [Gene ID=7428] off a retroviral vector under normoxia (normal oxygen) condition.
Top genes down-regulated in liver tissue from mice with knockout of ZMPSTE24 [Gene ID=10269].
Top genes up-regulated in liver tissue from mice with knockout of ZMPSTE24 [Gene ID=10269].
Mitochondrial genes; based on literature and sequence annotation resources and converted to Affymetrix HG-U133A probe sets.
Mitochondrial genes
Genes up-regulated in differentiating C2C12 cells (myoblasts) upon expression of PPARGC1A [Gene ID=10891] off an adenoviral vector.
Reactive oxidative species (ROS) genes; based on literature and sequence annotation resources and converted to Affymetrix HG-U133A probe sets.
Tricarboxylic acid related genes; based on literature and sequence annotation resources and converted to Affymetrix HG-U133A probe sets.
Down-regulated genes in lung tissue of smokers with chronic obstructive pulmonary disease (COPD) vs smokers without disease (GOLD-2 vs GOLD-0).
Up-regulated genes in lung tissue of smokers with chronic obstructive pulmonary disease (COPD) vs smokers without disease (GOLD-2 vs GOLD-0).
The 50 most down-regulated genes in primary invasive breast dutcal carcinoma (IDC) or lymph node metastases,  compared to normal mammary epithelium.
The 50 most up-regulated genes in primary invasive breast dutcal carcinoma (IDC) or lymph node metastases,  compared to normal mammary epithelium.
Genes highly expressed in hepatocellular carcinoma with poor survival.
Genes highly expressed in hepatocellular carcinoma with good survival.
Genes that physically map to the hematopoietic stem cell (HSC) proliferation QTL (quantitative trait locus) Scp2.
Genes whose expression is coregulated with that of FLI1 [Gene ID=2313] in hematopoietic stem cells (HSC).
Genes whose expression is coregulated with that of FGF3 [Gene ID=2248] in hematopoietic stem cells (HSC).
Genes whose expression is coregulated with that of RUNX1 [Gene ID=861] in hematopoietic stem cells (HSC).
Genes trans-regulated by the same QTL (quantitative trait loci) in brain and hematopoietic stem cells (HSC).
Genes associated with the same cis-regulatory QTL (quantitative trait loci) in both brain and hematopoietic stem cells (HSC).
Transcripts in hematopoietic stem cells (HSC) which are trans-regulated (i.e., modulated by a QTL (quantitative trait locus) not in a close proximity to the gene).
Transcripts in hematopoietic stem cells (HSC) which are cis-regulated (i.e., modulated by a QTL (quantitative trait locus) in close proximity to the gene).
Cis-regulatory QTLs (quantitative trait loci) found at the D6Mit150 region.
Best trans-regulated quantitative trait loci (QTLs) in the mouse genome which modulate transcription in brain tissue.
Neurologically relevant genes modulated in brain tissue by a trans-regulatory QTL (quantitative trait locus) near D6Mit150 marker.
Neurologically relevant transcripts with highest abundance fold range in brain tissue among mouse strains.
Neurologically relevant transcripts with highest variance accounted for by mouse strain (genotype) differences.
Best cis-regulated quantitative trait loci (QTLs) in the mouse genome which modulate transcription in brain tissue.
Genes up-regulated in RD-EF cells (rhabdomyosarcoma) engineered to express EWSR1-FLI1 fusion [Gene ID=2130, 2313] and which are also highly expressed in Ewing's famliy tumors.
Genes up-regulated in B cell lymphoma tumors expressing an activated form of MYC [Gene ID=4609].
Genes down-regulated in B cell lymphoma tumors expressing an activated form of MYC [Gene ID=4609].