Molecular Signature of Hepatitis D Virus-Associated Hepatocellular Carcinoma
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA238512PRJNA384961PRJNA419216
ORGANISM(S): Homo sapiens
PROVIDER: GSE98383 | GEO | 2018/04/09
REPOSITORIES: GEO
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Project description:To investigate the role of viral and host factors in HDV-associated HCC we carried out an integrated clinicopathological and gene expression study of tissue specimens and laser microdissected hepatocytes obtained at the time of liver transplantation from livers with HDV-HCC, HDV-cirrhosis without HCC, HCV-HCC and HBV-HCC. References to GSM series of HDV and HBV livers, already deposited in GEO, are included in this series. Part of data of HCV livers are a re-analysis of GSE series GSE69715 and GSE78737, the re-analyzed GSM is indicated in the 'description' column and with a link at the bottom of the page.
2018-04-09 | GSE107170 | GEO
Project description:Background: The pathogenesis of hepatitis B virus (HBV)-caused hepatocellular carcinoma (HCC) is complex and not fully understood. In clinical, the effective prevention and treatment of HCC rely on the accurate diagnosis. We developed a biology network approach to investigate the potential mechanisms and biomarkers of each stages from HBV infection to HCC. Methods Global gene profiling of healthy individuals (HC), HBV carriers (HBVC), chronic hepatitis B patients (CHB), liver cirrhosis (LC) and HCC was analyzed by gene array. Differentially expressed genes (DEG) were found by RVM (Random variance model) corrective ANOVA and STC (Series Test of Cluster) analysis.
2019-10-28 | GSE114783 | GEO
Project description:Gene-expression profiles of hepatitis C-related, early-stage liver cirrhosis Background & Aims: Liver cirrhosis affects 1%M-bM-^HM-^R2% of population and is the major risk factor of hepatocellular carcinoma (HCC). Hepatitis C cirrhosis-related HCC is the most rapidly increasing cause of cancer death in the US. Non-invasive methods have been developed to identify patients with asymptomatic, early-stage cirrhosis, increasing the burden of HCC surveillance, but biomarkers are needed to identify patients with cirrhosis who are most in need of surveillance. We investigated whether a liver-derived 186-gene signature previously associated with outcomes of patients with HCC is prognostic for patients newly diagnosed with cirrhosis but without HCC. Methods: We performed gene expression profile analysis of formalin-fixed needle biopsies from the livers of 216 patients with hepatitis C-related early-stage (Child-Pugh class A) cirrhosis who were prospectively followed for a median of 10 years at an Italian center. We evaluated whether the 186-gene signature was associated with death, progression of cirrhosis, and development of HCC. Results: Fifty-five (25%), 101 (47%), and 60 (28%) patients were classified as having poor-, intermediate-, and good-prognosis signatures, respectively. In multivariable Cox regression modeling, the poor-prognosis signature was significantly associated with death (P=.004), progression to advanced cirrhosis (P<.001), and development of HCC (P=.009). The 10-year rates of survival were 63%, 74%, and 85% and the annual incidences of HCC were 5.8%, 2.2%, and 1.5% for patients with poor-, intermediate-, and good-prognosis signatures, respectively. Conclusions: A 186-gene signature used to predict outcomes of patients with HCC is also associated with outcomes of patients with hepatitis C-related early-stage cirrhosis. This signature might be used to identify patients with cirrhosis in most need of surveillance and strategies to prevent their development of HCC. 216 liver biopsy specimens
2013-01-22 | E-GEOD-15654 | biostudies-arrayexpress
Project description:The post-translational modification of lysine acetylation is related to hepatocellular carcinoma (HCC), and understanding this relationship requires detailed knowledge about the acetylated proteome in HCC tissue and about differences in protein acetylation between cirrhosis and liver cancer. Here we characterized the acetylome in three paired sets of cirrhotic tissue and hepatitis B-related HCC tissue. Combining affinity-based enrichment of acetylated peptides with highly sensitive mass spectrometry, we identified 1493 acetylation sites in 777 proteins and quantified 1040 acetylation sites in 587 proteins. We discovered that the histone acetyltransferases p300 and CBP were hyperacetylated in HCC and cirrhosis but not in normal liver tissue. We also identified several proteins acetylated at more than 10 lysines in HCC and cirrhosis. In addition, our results revealed that HCC was associated with up-regulation of acetylation at 353 sites in 237 proteins and down-regulation of acetylation at 209 sites in 122 proteins. We validated our results using western blotting and immunohistochemistry. Validation with an independent set of clinical samples confirmed our initial screening result that acetylation of lysine 120 in histone H2B type 1-C/E/F/G/I and lysine 18 in histone H3.3 was significantly associated with survival of HCC patients. Acetylation of lysine 77 in histone H4 was associated with survival as well as recurrence. Our study provides numerous new leads to examine the role of acetylation in HCC and its potential as a prognostic marker as well as therapeutic target.
2021-09-08 | PXD014994 | Pride
Project description:Detection of HCC can improve the survival rate for patients with HCC. Thus, effective methods and biomarkers are required to improve the rate of early-HCC detection. We analyzed glycopeptides from AFP in the sera of patients with HCC and liver cirrhosis for the detection of HCC using LC-PRM with immunoprecipitation. Our results suggest that glycopeptide-based LC-PRM is a promising detection tool and that the relative percentage of fucosylated AFP is a clinically useful parameter for the detection of HCC.
2021-02-15 | MSV000086881 | MassIVE
Project description:BACKGROUND & AIMS: Cirrhosis affects 1% to 2% of the world population and is the major risk factor for hepatocellular carcinoma (HCC). Hepatitis C cirrhosis-related HCC is the most rapidly increasing cause of cancer death in the United States. Noninvasive methods have been developed to identify patients with asymptomatic early-stage cirrhosis, increasing the burden of HCC surveillance, but biomarkers are needed to identify patients with cirrhosis who are most in need of surveillance. We investigated whether a liver-derived 186-gene signature previously associated with outcomes of patients with HCC is prognostic for patients with newly diagnosed cirrhosis but without HCC. METHODS: We performed gene expression profile analysis of formalin-fixed needle biopsy specimens from the livers of 216 patients with hepatitis C-related early-stage (Child-Pugh class A) cirrhosis who were prospectively followed up for a median of 10 years at an Italian center. We evaluated whether the 186-gene signature was associated with death, progression of cirrhosis, and development of HCC. RESULTS: Fifty-five (25%), 101 (47%), and 60 (28%) patients were classified as having poor-, intermediate-, and good-prognosis signatures, respectively. In multivariable Cox regression modeling, the poor-prognosis signature was significantly associated with death (P = .004), progression to advanced cirrhosis (P < .001), and development of HCC (P = .009). The 10-year rates of survival were 63%, 74%, and 85% and the annual incidence of HCC was 5.8%, 2.2%, and 1.5% for patients with poor-, intermediate-, and good-prognosis signatures, respectively. CONCLUSIONS: A 186-gene signature used to predict outcomes of patients with HCC is also associated with outcomes of patients with hepatitis C-related early-stage cirrhosis. This signature might be used to identify patients with cirrhosis in most need of surveillance and strategies to prevent the development of HCC.
2013-01-22 | GSE15654 | GEO
Project description:Background: Several studies have investigated the association of miRNAs with hepatocellular carcinoma (HCC) but the data are not univocal. Methods: We performed a microarray study of miRNAs in hepatitis C virus (HCV)-associated HCC and other liver diseases and healthy conditions. Results and Conclusions: The simultaneous comparison of different liver diseases and normal livers allowed the identification of 18 miRNAs exclusively expressed in HCV-associated HCC, with sensitivity and specificity values of diagnostic-grade. A total number of 76 liver specimens obtained from 43 patients were analyzed: 26 liver specimens obtained from 10 patients with HCV-associated HCC, including 9 specimens from the tumor area (HCC) and 17 specimens from the surrounding non-tumorous tissue affected by cirrhosis (HCC-CIR); 18 specimens from 10 patients with HCV-associated cirrhosis without HCC (CIR); 13 specimens from 4 patients with HBV-associated acute liver failure (ALF); 12 specimens from 12 liver donors (LD); and 7 from normal liver of 7 subjects who underwent hepatic resection for liver angioma (NL).
2013-02-20 | E-GEOD-40744 | biostudies-arrayexpress
Project description:The aim of this study is to compare post-hepatitis C virus (HCV) and post-alcoholism cirrhosis gene expression profiling. By transcriptome analysis with a cDNA array virtually covering every transcript in liver, we compared transcript levels in alcoholic- , HCV-cirrhosis and control liver. A stringent selection identified a list of 70 transcripts which completely separated the 3 groups of patients (7 HCV-cirrhosis, 7 alcoholic cirrhosis and 8 control livers). In contrast, in an hepatocellular carcinoma (HCC) context, comparison of 10 HCV-cirrhosis, 10 alcoholic cirrhosis and the 8 control livers failed to identify such transcripts. We report that dysregulations at the transcriptional level do exist in HCC-free cirrhosis, are transiently observed prior to detectable HCC. Keywords: etiology-dependent and HCC-dependent analysis
2008-02-01 | GSE10356 | GEO
Project description:The molecular mechanisms whereby hepatitis B virus (HBV) induces hepatocellular carcinoma (HCC) remain elusive. We used genomic and molecular techniques to investigate host-virus interactions by mapping the entire liver of patients with HCC. We compared the gene signature of whole liver tissue (WLT) versus laser capture-microdissected (LCM) hepatocytes with intrahepatic expression of HBV. Gene expression profiling was performed on up to 17 WLT specimens obtained at various distances from the tumor center in individual livers of 11 patients with HCC and on selected LCM samples. HBV biomarkers were determined by real-time PCR and confocal immunofluorescence. Analysis of 5 areas of the liver showed a sharp change in gene expression between the immediate perilesional area and tumor periphery that correlated with a significant decrease in the intrahepatic expression of HBsAg. The tumor was characterized by a large preponderance of down-regulated genes, mostly involved in the metabolism of lipid and fatty acid, glucose, amino acids and drugs, with down-regulation of pathways involved in the activation of PXR/RXR and PPARa/RXRa nuclear receptors, comprising PGC1 and FOXO1, two key regulators of the hepatic metabolic functions and HBV transcription. These findings were confirmed by gene expression of microdissected hepatocytes. However, LCM of malignant hepatocytes also revealed up-regulation of unique genes associated with cancer and signaling pathways, including two novel HCC-associated cancer testis antigen (CTA) genes, NUF2 and TTK. HCC-associated with HBV is characterized by a metabolism switch-off and by a significant reduction in HBsAg. LCM proved to be a critical tool to validate gene signatures associated with HCC and to identify genes that may play a role in hepatocarcinogenesis opening new perspectives for the discovery of novel diagnostic markers and therapeutic targets. Samples were obtained at various distances from the tumor center in individual livers of 11 patients with HBV-associated HCC. Whole liver tissue samples were compared to LCM samples of malignant and non-malignant hepatocytes obtained from the same livers. This dataset is part of the TransQST collection.
2014-12-22 | E-GEOD-55092 | biostudies-arrayexpress
Project description:The molecular mechanisms whereby hepatitis B virus (HBV) induces hepatocellular carcinoma (HCC) remain elusive. We used genomic and molecular techniques to investigate host-virus interactions by mapping the entire liver of patients with HCC. We compared the gene signature of whole liver tissue (WLT) versus laser capture-microdissected (LCM) hepatocytes with intrahepatic expression of HBV. Gene expression profiling was performed on up to 17 WLT specimens obtained at various distances from the tumor center in individual livers of 11 patients with HCC and on selected LCM samples. HBV biomarkers were determined by real-time PCR and confocal immunofluorescence. Analysis of 5 areas of the liver showed a sharp change in gene expression between the immediate perilesional area and tumor periphery that correlated with a significant decrease in the intrahepatic expression of HBsAg. The tumor was characterized by a large preponderance of down-regulated genes, mostly involved in the metabolism of lipid and fatty acid, glucose, amino acids and drugs, with down-regulation of pathways involved in the activation of PXR/RXR and PPARa/RXRa nuclear receptors, comprising PGC1 and FOXO1, two key regulators of the hepatic metabolic functions and HBV transcription. These findings were confirmed by gene expression of microdissected hepatocytes. However, LCM of malignant hepatocytes also revealed up-regulation of unique genes associated with cancer and signaling pathways, including two novel HCC-associated cancer testis antigen (CTA) genes, NUF2 and TTK. HCC-associated with HBV is characterized by a metabolism switch-off and by a significant reduction in HBsAg. LCM proved to be a critical tool to validate gene signatures associated with HCC and to identify genes that may play a role in hepatocarcinogenesis opening new perspectives for the discovery of novel diagnostic markers and therapeutic targets.
2014-12-22 | GSE55092 | GEO