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MicroRNA expression profiling predicts clinical outcome of chronic hepatitis C by interferon administration

ABSTRACT: We attempt to catalog the microRNA (miRNA) expression profile according to the response of combination therapy in order to predict the outcome of drug-response before administration and clarify the relationship between aberrant expression of miRNAs and chronic liver disease.

ORGANISM(S): Homo sapiens

PROVIDER: GSE16922 | GEO | 2010/12/30

SECONDARY ACCESSION(S): PRJNA117633

REPOSITORIES: GEO

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MicroRNA expression profiling predicts clinical outcome of chronic hepatitis C by interferon administration

Project description:We attempt to catalog the microRNA (miRNA) expression profile according to the response of combination therapy in order to predict the outcome of drug-response before administration and clarify the relationship between aberrant expression of miRNAs and chronic liver disease. We quantified expression profile of 474 mature miRNAs by microarray in the liver biopsy specimen from 99 CH patients without history of anti-viral therapy.

2010-12-30 | E-GEOD-16922 | biostudies-arrayexpress

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Interferon signaling related gene expression and clinical outcome of chronic hepatitis C

Project description:Chronic hepatitis C (CH) frequently developed liver cirrhosis and hepatocellular carcinoma without suitable treatment. However, peginterferon(IFN) and ribavirin therapy (combination therapy), which is present standard therapy, is imperfect effect because of several side effect. We attempt to catalog IFN related gene expression profile according to the response of combination therapy in to predict the outcome of drug-response before administration and establish the adequate treatment according to the individual clinical information. Chip1 [GPL9960-related Samples]: We quantified expression profile of 200 IFN related genes by microarray in the liver biopsy specimen from 88 CH patients without history of anti-viral therapy, 10 fatty liver patients without HCV infection were also enrolled. Chip2 [GPL9962-related Samples]: We quantified expression profile of 37 IFN related genes by microarray in the liver biopsy specimen from 88 CH patients without history of anti-viral therapy, 10 fatty liver patients without HCV infection were also enrolled.

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Interferon signaling and treatment outcome in chronic hepatitis C

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 50–60% 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. Keywords: Comparison of human patient biopses before and after interferon treatment

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NS5A sequence heterogeneity of hepatitis C virus genotype 4a predicts clinical outcome of pegylated-interferon-ribavirin therapy in Egyptian patients.

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Host methylation predicts SARS-CoV-2 infection and clinical outcome

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Distinct SOX signature determines neuroblastoma origin and predicts clinical outcome

Project description:Multimodality treatment of high-risk neuroblastoma can be effective, but up to 50% of children experience recurrent disease with fatal outcome. Extensive genetic intratumoral heterogeneity and diverse clinical outcomes pose therapeutic challenges in treating children affected by this aggressive disease. Several hypotheses have been proposed to explain the heterogeneity of neuroblastoma, including a possible origin from multipotent neural crest stem cells (NCSCs). Utilizing an in vivo mouse genetics approach, we demonstrate that lineage-restricted sympathoadrenal (SA) progenitors and not NCSCs are the cellular origin of neuroblastoma. Human neuroblastoma tissue is composed of two spatially juxtaposed cell types, neuroblasts and Schwann cells, both cell types derive from neural crest (NC) lineage. This composition mimics the architecture of sympathetic ganglions (SG) as well as of adrenal medulla at the late stage of neural crest (NC) development. Similarly to SG, SOX10 is restricted to Schwannian cells and is not present in tumorigenic neuroblasts. Transcriptional landscape of Sox genes can serve as paradigmatic model for stage identification along NC lineage development. While early multipotent NCSCs are characterized by the expression of Sox9/Sox10 transcription factors (TF), committed SA progenitor identity is defined by the presence of Sox4/Sox11 TFs. Molecularly, we show that the core transcriptional network that orchestrate neuroblastoma maintenance is highly reminiscent of the SA progenitors. Taken together, the data presented here show that neuroblastoma cells functionally resemble the committed SA progenitors, while lacking specific stem cell program.

2020-01-01 | GSE133014 | GEO

Interferon signaling and treatment outcome in chronic hepatitis C.

Project description: Not available

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