E-GEOD-48445
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-48445 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-48445-analysis-methods.tsv | Tabular | |||
| E-GEOD-48445-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-48445-configuration.xml | Xml | |||
| E-GEOD-48445-percentile-ranks.tsv | Tabular | |||
| E-GEOD-48445.condensed-sdrf.tsv | Tabular |
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Project description:Gene expression profiling of liver biopsies from 21 chronic hepatitis C patients undergoing antiviral therapy
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Project description:In this study we aimed to identify a baseline intrahepatic transcriptional signature associated with response in chronic hepatitis B patients treated with peginterferon-alfa-2a (peg-IFN) and adefovir. Liver gene expression values of patients with combined response (responders; n=9) and non-response (n=6) were compared for 21,462 annotated gene transcripts. We identified 182 genes which differed on average more than 1.5-fold, of which 53 were relatively upregulated in non-responders and 129 in responders. 15 liver biopsies of chronic hepatitis B patients were selected for RNA extraction and hybridization on Affymetrix microarrays. Expression values in 9 biopsies of patients with a combined response to therapy were compared with 6 biopsies of non-responders. Differentially expressed genes between responders and non-responders were determined using filtering on minimal average expression, fold change (1.5 fold) and p-values from 2-sided t-tests (0 permutations) in GenePattern. This dataset is part of the TransQST collection.
2014-12-19 | E-GEOD-54747 | biostudies-arrayexpress
Project description:Chronic liver disease is becoming a leading cause of illness and mortality in people living with human immunodeficiency virus (HIV) (PLWH) undergoing suppressive anti-retroviral therapy. Its main etiology has been reported to be coinfection with hepatitis B (HBV) and C (HCV) viruses. Accumulating evidence indicate chronic liver inflammation and fibrosis can potentially lead to the development of hepatocellular carcinoma (HCC). Therefore, monitoring of the disease progression in PLWH is required. The present study aimed to explore the plasma protein profiles of patients with HIV infection and those coinfected with HBV and HCV using shotgun proteomics.
2024-06-29 | PXD053504 | JPOST Repository
Project description:Liver gene expression profiles of interferon therapy in chronic hepatitis B Patients
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Project description:Hepatitis C virus (HCV) chronically infects 170 million people worldwide and is a leading cause of liver-related mortality due to hepatocellular carcinoma and cirrhosis1. Standard-of-care treatment is shifting from interferon-alpha (IFNM-NM-1)-based to IFNM-NM-1-free directly acting antiviral (DAA) regimens, which demonstrate improved efficacy and tolerability in clinical trials2,3. Virologic relapse after completion of DAA therapy is a common cause of treatment failure, although mechanisms are unclear2,3. We conducted a clinical trial using the DAA sofosbuvir with ribavirin (SOF/RBV)4, and report here detailed mRNA expression analysis of pre- and end-of-treatment (EOT) liver biopsies and blood samples. On-treatment viral clearance was accompanied by rapid down-regulation of interferon-stimulated genes (ISGs) in liver and blood. Analysis of paired liver biopsies from patients who achieved a sustained virologic response (SVR) revealed that viral clearance was accompanied by decreased expression of ISGs, IFNG, and IFNLs, but increased expression of IFNA2. Patients who achieved SVR had higher expression of a hepatic type-I interferon gene signature in unpaired EOT liver biopsies than patients who later relapsed. Together, these results support a model whereby restoration of type-I intrahepatic interferon signaling at the EOT is associated with sustained hepatic HCV suppression and prevention of relapse upon withdrawal of SOF/RBV. Sustained Virologic Response for Chronic Hepatitis C Patients Treated with Sofosbuvir and Ribavirin
2014-08-15 | E-GEOD-51699 | biostudies-arrayexpress
Project description:Hepatitis C virus (HCV) infection is a major cause of chronic liver disease worldwide. The current standard therapy for chronic hepatitis C (CHC) consists of a combination of pegylated IFN alpha (pegIFN-alpha) and ribavirin. It achieves a sustained viral clearance in only 50â??60% of patients. To learn more about molecular mechanisms underlying treatment failure, we investigated IFN-induced signaling in paired liver biopsies collected from CHC patients before and after administration of pegIFN-alpha. In patients with a rapid virological response to treatment, pegIFN-alpha induced a strong up-regulation of IFN-stimulated genes (ISGs). As shown previously, nonresponders had high expression levels of ISGs before therapy. Analysis of posttreatment biopsies of these patients revealed that pegIFN-alpha did not induce expression of ISGs above the pretreatment levels. In accordance with ISG expression data, phosphorylation, DNA binding, and nuclear localization of STAT1 indicated that the IFN signaling pathway in nonresponsive patients is preactivated and refractory to further stimulation. Some features characteristic of nonresponders were more accentuated in patients infected with HCV genotypes 1 and 4 compared with genotypes 2 and 3, providing a possible explanation for the poor response of the former group to therapy. Taken together with previous findings, our data support the concept that activation of the endogenous IFN system in CHC not only is ineffective in clearing the infection but also may impede the response to therapy, most likely by inducing a refractory state of the IFN signaling pathway. Experiment Overall Design: Total of 78 Samples (before and after interferon treatement) are analyzed using Affymetrix Human U133 Plus 2.0 Array.
2008-06-19 | E-GEOD-11190 | biostudies-arrayexpress
Project description:Liver gene expression profiles of interferon therapy in chronic hepatitis B Patients (mRNA)
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Project description:Liver gene expression profiles of interferon therapy in chronic hepatitis B Patients (Exon)
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Project description:Approximately 50% of patients with chronic hepatitis C (CHC) have a sustained virologic response (SVR) to treatment with pegylated interferon (pegINF)-M-NM-1 and ribavirin. Non-response to treatment is associated with constitutively increased expression of IFN-stimulated genes (ISGs) in the liver. Treatment of patients with acute hepatitis C (AHC) is more effective, with SVR rates >90%. We investigated mechanisms of the different responses of patients with CHC and AHC to pegIFN-M-NM-1 therapy. We analyzed IFN signaling and ISG expression in liver samples from patients with acute hepatitis C (AHC), patients with chronic hepatitis (CHC), and individuals without hepatitis C (controls) using microarray, immunohistochemical, and protein analyses. Findings were compared with those from primary human hepatocytes stimulated with IFN-M-NM-1 or IFN-M-NM-3, as reference sets. Expression levels of 100s of genes, primarily those regulated by IFN-M-NM-3, were altered in liver samples from patients with AHC compared with controls. Expression of IFN-M-NM-3M-bM-^@M-^Sstimulated genes was induced in liver samples from patients with AHC, whereas expression of IFN-M-NM-1M-bM-^@M-^Sstimulated genes was induced in samples from patients with CHC. In an expression analysis of negative regulators of IFN-M-NM-1 signaling, we did not observe differences in expression of SOCS1 or SOCS3 between liver samples from patients with AHC and those with CHC. However, USP18 (another negative regulator of IFN-M-NM-1 signaling), was upregulated in liver samples of patients with CHC that did not respond to therapy, but not in AHC. In conclusion, differences in expression of ISGs might account for the greater response of patients with AHC, compared to those with CHC, to treatment with pegINF-M-NM-1 and ribavirin. Specifically, USP18 is upregulated in liver samples of patients with CHC that do not respond to therapy, but not in patients with AHC. (Interferon-M-NM-3 Stimulated Genes, but not USP18, are Expressed in Livers of Patients with Acute Hepatitis C; Dill MT, Makowska Z et al, Gastroenterology 2012 (in press)) Liver biopsy samples from 6 patients with acute hepatitis C virus infection were analyzed CHC data and controls previously submitted as GSE11190
2012-06-08 | E-GEOD-38597 | biostudies-arrayexpress
Project description:This dataset is part of the paper: Pegylated interferon-α regulates hepatic gene expression by transient activation of the Jak-STAT pathway; Dill MT et al; Journal of Clinical Investigation; in review Pegylated interferon-α (pegIFN-α) has replaced un-modified recombinant IFN-α for the treatment of chronic viral hepatitis because of its superior anti-viral efficacy that is generally attributed to improved pharmacokinetic properties. However, the pharmacodynamic effects of pegIFN-α in the liver have not been studied. We analyzed pegIFN-α induced signaling and gene regulation in paired liver biopsies obtained before treatment and during the first week after injection of pegIFN-α in 18 patients. Despite sustained high serum concentrations of pegIFN-α over the entire one-week dosing interval, IFN-α signaling through the Jak-STAT pathway occurs only during the first day. PegIFN-α induces hundreds of genes that can be classified into 4 clusters based on different temporal expression profiles. In all clusters, gene transcription is mainly driven by IFN stimulated gene factor 3 (ISGF3). IFN induced secondary transcription factors do not cause additional waves of gene expression. We could not confirm a role of un-phosphorylated STAT1 in prolonging IFN-α induced gene transcription. Collectively, our results reveal that the major effects of pegIFN-α in the liver are caused by an early and transient activation of ISGF3. Prolonging the serum half-life of IFN-α does not necessarily improve its pharmacodynamic properties. Paired liver biopsy samples were collected before and during the first week of pegylated interferon alpha treatment of 21 chronic hepatitis C patients. Total: 21 patients and 42 samples. This dataset is part of the TransQST collection.
2014-01-30 | E-GEOD-48445 | biostudies-arrayexpress