Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-41804
PROVIDER: PRJNA178219 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:IL28B genotype was shown to be associated with treatment outcome of antiviral thearpy for HCV infection. We tried to clarify the molecular feature that was asocciated with IL2B genotype by comparing Hepatic gene expression of HCV related Hepatocellular carcinoma and non-cancerous tissue with Il28B rs8099917 TT genotype and TG/GG genotype.
2013-05-02 | GSE41804 | GEO
Project description:IL28B genotype was shown to be associated with treatment outcome of antiviral thearpy for HCV infection. We tried to clarify the molecular feature that was associated with IL2B genotype by comparing Hepatic gene expression of HCV related Hepatocellular carcinoma and non-cancerous tissue with Il28B rs8099917 TT genotype and TG/GG genotype. We analyzed ten HCC patients were selected from each IL28B genotype, and their gene expression was determined using Affymetrix genechip analysis.
2013-05-02 | E-GEOD-41804 | biostudies-arrayexpress
Project description:Hepatic gene expression of HCV related Hepatocellular carcinoma and non-cancerous tissue with Il28B rs8099917 TT genotype and TG/GG genotype
2015-07-29 | E-GEOD-41804 | ExpressionAtlas
Project description:The hepatitis C virus (HCV) is one of the major risk factors for the development of hepatocellular carcinoma (HCC). Nevertheless, transgenic mice which express the whole HCV polyprotein (HCV-Tg) do not develop HCC. Whereas chronic HCV infection causes inflammation in patients, in HCV-Tg mice, the host immune reaction against viral proteins is lacking. We aimed to test the role of HCV proteins in HCC development on the background of chronic inflammation in vivo. We crossed the HCV-Tg mice which do not produce HCC with the Mdr2-knockout (Mdr2-KO) mice which develop inflammation-associated HCC, to generate Mdr2-KO/HCV-Tg mice. We studied the effect of the HCV transgene on tumor incidence, hepatocyte mitosis and apoptosis, and on gene expression in the liver of produced mice.
2009-03-22 | GSE12184 | GEO
Project description:The hepatitis C virus (HCV) is one of the major risk factors for the development of hepatocellular carcinoma (HCC). Nevertheless, transgenic mice which express the whole HCV polyprotein (HCV-Tg) do not develop HCC. Whereas chronic HCV infection causes inflammation in patients, in HCV-Tg mice, the host immune reaction against viral proteins is lacking. We aimed to test the role of HCV proteins in HCC development on the background of chronic inflammation in vivo. We crossed the HCV-Tg mice which do not produce HCC with the Mdr2-knockout (Mdr2-KO) mice which develop inflammation-associated HCC, to generate Mdr2-KO/HCV-Tg mice. We studied the effect of the HCV transgene on tumor incidence, hepatocyte mitosis and apoptosis, and on gene expression in the liver of produced mice.
2009-03-22 | GSE12183 | GEO
Project description:The hepatitis C virus (HCV) is one of the major risk factors for the development of hepatocellular carcinoma (HCC). Nevertheless, transgenic mice which express the whole HCV polyprotein (HCV-Tg) do not develop HCC. Whereas chronic HCV infection causes inflammation in patients, in HCV-Tg mice, the host immune reaction against viral proteins is lacking. We aimed to test the role of HCV proteins in HCC development on the background of chronic inflammation in vivo. We crossed the HCV-Tg mice which do not produce HCC with the Mdr2-knockout (Mdr2-KO) mice which develop inflammation-associated HCC, to generate Mdr2-KO/HCV-Tg mice. We studied the effect of the HCV transgene on tumor incidence, hepatocyte mitosis and apoptosis, and on gene expression in the liver of produced mice. This SuperSeries is composed of the SubSeries listed below.
2009-03-22 | GSE12185 | GEO
Project description:To identifythe the functional roles and the pathophysiological contributions of coding genes and noncoding RNAs in human hepatic carcinogenesis, we analysed the differenial expression of genes and noncoding RNAs in hepatocellular carcinoma tissues and the corresponding non-cancerous tissues. We used microarrays to detail the global programme of gene expression in human hepatocellular carcinomas and correponding non-cancerous tissues.
2017-09-14 | GSE84402 | GEO
Project description:Chronic hepatitis C virus (HCV) infection and cirrhosis are major risk factors for developing hepatocellular carcinoma (HCC). Genetic polymorphisms in the IFNL3/IFNL4 locus have been associated both with poor clearance of HCV and protection from liver fibrosis, an early stage of cirrhosis. Here, we aimed to address the genetic and functional relationships between IFNL3/IFNL4 polymorphisms, cirrhosis, and HCC risk. We evaluated associations between IFNL4 genotype (presence of rs368234815-dG or rs12979860-T alleles) with cirrhosis and HCC risk in patients with chronic HCV - 2,931 from Taiwan and 3,566 from Japan, and with gene expression and somatic mutations in 370 HCC tumors in The Cancer Genome Atlas (TCGA). Functional analyses were performed in primary human hepatocytes and hepatic stellate cells and a panel of hepatoma HepG2 cell lines with gene-edited IFNLR1 and inducible expression of IFN-λ3 or IFN-λ4. We detected associations between IFNL4 genotype and decreased risk of cirrhosis (OR=0.66, 95%CI=0.46-0.93, P=0.018, in Taiwan), but increased risk of HCC in patients without HCV clearance (OR=1.28, 95%CI=1.07-1.52, P=0.0058, in Japan). IFNL4 genotype was also associated with reduced cell proliferation and enrichment of CTNNB1 mutations in HCC tumors in TCGA. Reduced proliferation in hepatic cells was contributed by intracellular accumulation of IFN-λ4 leading to induction of ER stress and enhanced IRF1 signaling. The strong anti-proliferative effects of IFN-λ4 in hepatic cells could explain the association of IFNL3/IFNL4 polymorphisms with decreased cirrhosis. However, by sustaining persistent HCV infection, IFN-λ4 may contribute to the development of CTNNB1 mutations and increased risk of HCC in patients without viral clearance.
2021-09-15 | GSE145038 | GEO
Project description:A quantitative label-free proteome analysis was performed using plasma samples from 22 hepatitis-C virus (HCV)-induced liver cirrhosis patients, 16 HCV-positive hepatocellular carcinoma patients with underlying cirrhosis and 18 healthy controls. Plasma microparticles (PMPS) were isolated using ultracentrifugation and analyzed via label-free LC-MS/MS. A quantitative label-free proteome analysis was performed using plasma samples from 22 hepatitis-C virus (HCV)-induced liver cirrhosis patients, 16 HCV-positive hepatocellular carcinoma patients with underlying cirrhosis and 18 healthy controls. Plasma microparticles (PMPS) were isolated using ultracentrifugation and analyzed via label-free LC-MS/MS.
2020-03-12 | MSV000085094 | MassIVE
Project description:A quantitative label-free proteome analysis was performed using plasma samples from 22 hepatitis-C virus (HCV)-induced liver cirrhosis patients, 16 HCV-positive hepatocellular carcinoma patients with underlying cirrhosis and 18 healthy controls. Plasma microparticles (PMPS) were isolated using ultracentrifugation and analyzed via label-free LC-MS/MS. A quantitative label-free proteome analysis was performed using plasma samples from 22 hepatitis-C virus (HCV)-induced liver cirrhosis patients, 16 HCV-positive hepatocellular carcinoma patients with underlying cirrhosis and 18 healthy controls. Plasma microparticles (PMPS) were isolated using ultracentrifugation and analyzed via label-free LC-MS/MS.
2017-06-21 | PXD005777 | Pride