This SuperSeries is composed of the SubSeries listed below.
PCB congener specific oxidative stress response by microarray analysis using human liver cell line.
Age
View SamplesExposure to Polychlorobiphenyls (PCBs) is known to cause serious health effects in human but the gene expression profiles leading to development of differnet diseases is not fully understood. The knowledge of global gene expression will help us to devlop early diagnostic biomarkers for PCB induced health effects.
PCB congener specific oxidative stress response by microarray analysis using human liver cell line.
Age
View SamplesExposure to Polychlorobiphenyls (PCBs) is known to cause serious health effects in human but the gene expression profiles leading to development of different diseases is not fully understood. The knowledge of global gene expression will help us to develop early diagnostic biomarkers for PCB induced health effects.
PCB congener specific oxidative stress response by microarray analysis using human liver cell line.
Age
View Samples49 human patient mRNA profiles was generated using HG-U133 Plus 2.0 microarrays. Procesed in Affymetrix Expression console using Plier normalization method and later processed in Partek Genomics Suite. The clustering figure was generated using HCE clustering software.
Asynchronous remodeling is a driver of failed regeneration in Duchenne muscular dystrophy.
Sex, Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Specimen part, Cell line
View SamplesWe performed whole genome expression analysis using BCR/ABL expressing Kit+ cells derived from wild type and ROSACreERT2c-Fosfl/flDusp1-/- bone marrow cells. Wild type kit+ cells were treated with DFC+BCI and DFC+BC+Im to mimic the genetic loss of c-Fos and Dusp1. Overall design: The experiment was designed to test whether chemical inhibition by FOS and Dusp1 Inhibitor mimics the genetic deletion of cFOS and Dusp1 in mouse primary cells transduced with BCR-ABL. This data is part of the super series Mechanism of Oncogene addiction GSE75058.
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Specimen part, Cell line, Subject
View SamplesThe Baf3 are dependent on IL-3 for grwoth however transformation by BCR -ABL oncogene causes BAf3 cells independent of IL-3. The BAf3 cells expressing BCR-ABL are dependent on continuous expression of BCR_ABL for growth. Inhibitionof BCR-ABL by its inhibitor Imatinib cause these cells to undergo apoptosis. When these cells are grown with IL-3 these cells do not respond to Imatinib mediated grwoth arrest.
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Cell line
View SamplesK562 cells when grown with erythropeitin do not respond to Imatinib. Here we are comparing the gene expression profile from imatinib resistant and sensitive cells.
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Cell line
View SamplesBAF3 cells harboring constitutively expressing BCR-ABL were grown with or without IL-3 supplement and treated with Imatinib and live cells from the IL-3 and without IL-3 were sorted by FACS.
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Cell line
View SamplesHepatocellular carcinoma (HCC) is the second most common cause of cancer related death. NAFLD affects a large proportion of the US population. Its incidence and prevalence are increasing to epidemic proportions around the world and is known to increase the risk of HCC. We studied how intrahepatic lipids affect adaptive immunity and HCC development in different murine models of NASH and HCC. Linoleic acid, a fatty acid found in NAFLD caused a selective loss of hepatic CD4+ but not CD8+ T cells leading to accelerated hepatocarcinogenesis. CD4+ T cells were more dependent on oxidative phosphorylation for energy source than CD8+ T cells, and disruption of oxidative phosphorylation by linoleic acid caused more severe damage in CD4+ T cells leading to selective loss of these cells. In vivo blockade of ROS using n-acetylcysteine reversed the NASH-induced hepatic CD4+ T cell decrease and delayed NASH-promoted HCC. Our results provide a new link between lipid metabolism and impaired anti-tumor surveillance.
NAFLD causes selective CD4(+) T lymphocyte loss and promotes hepatocarcinogenesis.
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