E-GEOD-19665
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA122481
PROVIDER: E-GEOD-19665 | ExpressionAtlas | 2015-07-31
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:We applied small RNA Solexa sequencing technology to identify microRNA expression in human liver samples from surgically removed liver tissues including three normal liver tissues (distal normal liver tissue of liver hemangioma), an hepatitis B virus (HBV)-infected liver, a severe chronic hepatitis B liver, two HBV-related hepatocellular carcinoma (HCC), an hepatitis C virus (HCV)-related HCC, and an HCC without HBV or HCV infection. All samples were collected with the informed consent of the patients and the experiments were approved by the ethics committee of Second Military Medical University, Shanghai, China. We investigated the miRNome in human normal liver and suggested some deregulated abundantly expressed microRNAs in HCC. center_name: National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, China. Examination of miRNome in human liver samples from surgically removed liver tissues including three normal liver tissues (distal normal liver tissue of liver hemangioma), an hepatitis B virus (HBV)-infected liver tissue, a severe chronic hepatitis B liver tissue, an HBV-related hepatocellular carcinoma (HCC) tissue and adjacent liver tissues of different regions,an HBV-related HCC tissue and adjacent liver tissue, an hepatitis C virus (HCV)-related HCC tissue and adjacent liver tissue, and an HCC without HBV or HCV infection and adjacent liver tissue. All 15 human liver tissue samples.
2010-04-10 | E-GEOD-21279 | biostudies-arrayexpress
Project description:We applied small RNA Solexa sequencing technology to identify microRNA expression in human liver samples from surgically removed liver tissues including three normal liver tissues (distal normal liver tissue of liver hemangioma), an hepatitis B virus (HBV)-infected liver, a severe chronic hepatitis B liver, two HBV-related hepatocellular carcinoma (HCC), an hepatitis C virus (HCV)-related HCC, and an HCC without HBV or HCV infection. All samples were collected with the informed consent of the patients and the experiments were approved by the ethics committee of Second Military Medical University, Shanghai, China. We investigated the miRNome in human normal liver and suggested some deregulated abundantly expressed microRNAs in HCC. center_name: National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, China.
2010-04-10 | GSE21279 | GEO
Project description:Infection with hepatitis B and C viruses (HBV and HCV) is a major cause of hepatocellular carcinoma (HCC). While troponin T (TNNT1) is essential for actin thin filament function, little is known about its role in HBV/HCV-associated HCC. Here, we found TNNT1 expression was significantly upregulated in HBV/HCV-infected hepatoma cells, HCC tissues, and mouse models. HBV/HCV-induced c-Myc acts as a transcription factor for TNNT1 induction. HBV/HCV-induced TNNT1 binds metastasis-associated protein 2 (MTA2) and activates the PI3K-AKT-mTOR-TNNT1 loop, causing lysosomal dysfunction and autophagy suppression. This leads to increased proliferation and epithelial-mesenchymal transition (EMT) of liver cancer cells marked by Vimentin and ZEB2. Four amino acid residues (R110A, E112A, R115A, and E119A) within the TNNT1 troponin domain are required for TNNT1-MTA2 binding and mediate TNNT1’s suppression of autophagy and promotion of proliferation/EMT. Importantly, liver-specific TNNT1 deficiency in mice attenuates HBV/HCV-induced c-Myc-driven HCC EMT properties in vivo. This study reveals for the first time that hepatitis virus-induced TNNT1 can induce EMT and hepatocellular carcinogenesis. TNNT1 may be a promising target for viral HCC therapy.
2023-11-21 | GSE233441 | GEO
Project description:Gene expression profiling of hepatocellular carcinoma (HCC) and background liver has been studied extensively; however, the relationship between the gene expression profiles of different lesions has not been assessed. We examined the expression profiles of 34 HCC specimens (17 hepatitis B virus [HBV]-related and 17 hepatitis C virus [HCV]-related) and 71 non-tumor liver specimens (36 chronic hepatitis B [CH-B] and 35 chronic hepatitis C [CH-C]) using an in-house cDNA microarray consisting of liver-predominant genes. Graphical Gaussian modeling (GGM) was applied to elucidate the interactions of gene clusters among the HCC and non-tumor lesions. Gene expression profiling of HCC and non-tumor lesions revealed the predisposing changes of gene expression in HCC. This approach has potential for the early diagnosis and possible prevention of HCC. We examined the expression profiles of 34 HCC specimens (17 hepatitis B virus [HBV]-related and 17 hepatitis C virus [HCV]-related) and 71 non-tumor liver specimens (36 chronic hepatitis B [CH-B] and 35 chronic hepatitis C [CH-C]) using an in-house cDNA microarray consisting of liver-predominant genes. Graphical Gaussian modeling (GGM) was applied to elucidate the interactions of gene clusters among the HCC and non-tumor lesions.
2013-11-14 | E-GEOD-44074 | biostudies-arrayexpress
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:Chronic infections by hepatitis B virus (HBV) and hepatitis C virus (HCV) appear to be the most significant causes of hepatocellular carcinoma (HCC). Aberrant promoter methylation is known to be deeply involved in cancer, including HCC. In this study, we analyzed aberrant promoter methylation on genome-wide scale in 6 HCCs including 3 HBV-related and 3 HCV-related HCCs, 6 matched noncancerous liver tissues and 3 normal liver tissues by methylated DNA immunoprecipitation-on-chip analysis. Candidate genes with promoter methylation were detected more frequently in HCV-related HCC. Candidate genes methylated preferentially to HBV-related or HCV-related HCCs were detected and selected, and methylation levels of the selected genes were validated using 125 liver tissue samples, including 61 HCCs (28 HBV-related HCCs and 33 HCV-related HCCs) and matched 59 matched noncancerous livers, and 5 normal livers, by quantitative methylation analysis using MALDI-TOF mass spectrometry. Among analyzed genes, preferential methylation in HBV-related HCC was validated in 1 gene only. However, 15 genes were found methylated preferentially in HCV-related HCC, which was independent from age. Hierarchical clustering of HCC using these 15 genes stratified HCV-related HCC as a cluster of frequently methylated samples. The 15 genes included genes inhibitory to cancer-related signaling such as RAS/RAF/ERK and Wnt/b-catenin pathways. It was indicated that genes methylated preferentially in HCV-related HCC exist, and it was suggested that DNA methylation might play an important role in HCV-related HCC by silencing cancer-related pathway inhibitors. we analyzed aberrant promoter methylation in 6 HCC clinical samples (including 3 HBV-related HCCs and 3 HCV-related HCCs) and their matched noncancerous tissues on genome-wide scale by the method. Candidate regions of promoter methylation preferentially to HBV-related HCC and HCV-related HCC were selected, and the methylation levels of these genes were measured quantitatively using MALDI-TOF mass spectrometry. Expression levels of these 6 pairs of HCC and 4 more pairs of HCCs and surrounding noncancerous tissues were analyzed by expression array and are reported in this Series. <br><br>This experiment was reloaded in November 2010 after additional curation. this dataset is part of the TransQST collection.
2010-07-06 | E-GEOD-19665 | biostudies-arrayexpress
Project description:<p>Hepatocellular carcinoma (HCC) accounts for 85-90% of primary liver cancers. We have focused on three major HCC etiologies:hepatitis C virus (HCV), hepatitis B virus (HBV), and nonviral causes. The onset and progression of cancer is driven by extensive rearrangement and mutation of the genome. We combined our capability to capture and enrich exome DNA with the next generation sequencing capacity to allow us to detect and characterize the somatic mutation profile of patients with HCC. Patient samples were collected by the Liver Center, Division of Abdominal Transplantation in the Baylor College of Medicine Department of Surgery. Sequencing of HCC is one of the NHGRI Center Initiated Projects in progress in the Human Genome Sequencing Center at Baylor College of Medicine.</p>
| phs000509 | dbGaP
Project description:Chronic infections by hepatitis B virus (HBV) and hepatitis C virus (HCV) appear to be the most significant causes of hepatocellular carcinoma (HCC). Aberrant promoter methylation is known to be deeply involved in cancer, including HCC. In this study, we analyzed aberrant promoter methylation on genome-wide scale in 6 HCCs including 3 HBV-related and 3 HCV-related HCCs, 6 matched noncancerous liver tissues and 3 normal liver tissues by methylated DNA immunoprecipitation-on-chip analysis. Candidate genes with promoter methylation were detected more frequently in HCV-related HCC. Candidate genes methylated preferentially to HBV-related or HCV-related HCCs were detected and selected, and methylation levels of the selected genes were validated using 125 liver tissue samples, including 61 HCCs (28 HBV-related HCCs and 33 HCV-related HCCs) and matched 59 matched noncancerous livers, and 5 normal livers, by quantitative methylation analysis using MALDI-TOF mass spectrometry. Among analyzed genes, preferential methylation in HBV-related HCC was validated in 1 gene only. However, 15 genes were found methylated preferentially in HCV-related HCC, which was independent from age. Hierarchical clustering of HCC using these 15 genes stratified HCV-related HCC as a cluster of frequently methylated samples. The 15 genes included genes inhibitory to cancer-related signaling such as RAS/RAF/ERK and Wnt/b-catenin pathways. It was indicated that genes methylated preferentially in HCV-related HCC exist, and it was suggested that DNA methylation might play an important role in HCV-related HCC by silencing cancer-related pathway inhibitors.
2010-07-06 | GSE19665 | 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