DNA methylation data from hepatoma
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE59405 | GEO | 2014/07/15
SECONDARY ACCESSION(S): PRJNA255253
REPOSITORIES: GEO
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Project description:A large fraction of HCC in Peru arises in younger, non-cirrhotic patients. Global DNA methylation analysis of the HCC and non-tumor liver (NTL) tissues demostrate a profound overhaul of the developmental DNA methylation programme culminating in an global hyper-methylated pattern in HCC. We used microarrays to compare global DNA methylation between tumor and non-tumor liver tissues and identified CpGs and ontologies that are distinctively differentially methylated between subsets.
2021-01-31 | GSE136380 | GEO
Project description:A large fraction of HCC in Peru arises in younger, non-cirrhotic patients. Global DNA methylation analysis of the HCC and non-tumor liver (NTL) tissues demostrate a profound overhaul of the developmental DNA methylation programme culminating in an global hyper-methylated pattern in HCC. We used microarrays to compare global DNA methylation between tumor and non-tumor liver tissues and identified CpGs and ontologies that are distinctively differentially methylated between subsets.
2021-01-31 | GSE136319 | GEO
Project description:Transarterial chemoembolization or systemic chemotherapy with doxorubicin has been the treatment of choice for unresectable hepatocellular carcinoma (HCC) conferring the best survival benefit. However, HCC is notorious for its predisposition to develop therapeutic tolerance. Thus, Affymetrix microarray analysis was performed on doxorubicin-resistant hepatoma cells to identify the drug resistance-related genes. The RNA isolated from primary hepatoma cells and their doxorubicin-resistant counterparts, then subjected to Affymetrix microarray analysis to identify the differential expression profiles of drug resistance-related genes.
2019-01-17 | GSE125180 | GEO
Project description:We evaluate the epigenetic mechanisms of racial disparity in HCC through an integrated analysis of DNA methylation, miRNA, and combined regulation of gene expression. Specifically, we acquired DNA methylation, mRNA-seq, and miRNA-seq data through the analysis of tumor and adjacent normal liver tissues from African Americans (AA) and European Americans (EA) with HCC. Results: Using mixed ANOVA, we identified cytosine-phosphate-guanine (CpG) sites, mRNAs, and miRNAs that are statistically significantly altered in HCC vs. adjacent normal in a race-specific manner. Through integrative analysis, we identified significantly differentially expressed genes in HCC with disparate epigenetic regulation, associated with changes in miRNA expression for AA and DNA methylation for EA.
2021-09-29 | GSE176273 | GEO
Project description:Genome wide DNA methylation profiling of primary HCC tumors and their non-tumor tissue counterparts. The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,000 CpGs in 20 paired tumor and non-tumor tissues which were obtained from HCC patients who underwent surgery.
2015-09-15 | GSE73003 | GEO
Project description:Emerging evidences indicate that microRNAs (miRNAs) are often deregulated and have fundamental roles in hepatocellular carcinoma (HCC). However, the mechanism underlying miRNA dysregulation in HCC is still elusive. In this report, we used an integrated analysis strategy combining methylated DNA immunoprecipitation chip (MeDIP-chip) and miRNA expression microarray data to study the correlation between aberrant methylation and dysregulation of miRNA in HCC. In all, we showed that global miRNA methylation profiles were significantly different between cancerous and normal hepatocytes, and abnormal methylation was an important mechanism governing miRNA expression in HCC.
2015-08-05 | GSE49554 | GEO
Project description:Alcohol is a major risk factor for hepatocellular carcinoma (HCC) although the mechanisms underlying the alcohol-related liver carcinogenesis are still poorly understood. Alcohol is known to increase hepatocarcinogenesis possibly by inducing aberrant DNA methylation through the reduced provision of methyl groups within the hepatic one-carbon metabolism. Whether the epigenetically-regulated pathways in alcohol-associated HCC can be reversible or modifiable by nutritional factors is unknown. The aim of the present study was to investigate the genome wide promoter DNA methylation profiles along with array-based, gene expression profiles in non-viral, alcohol-associated HCC. From eight HCC patients the methylation status and transcriptional levels of all annotated genes were compared by analyzing HCC tissue and the cancer-free surrounding liver tissue, following curative surgery. After merging both the DNA methylation and gene expression data, we identified 159 hypermethylated-repressed, 30 hypomethylated-induced, 49 hypermethylated-induced and 56 hypomethylated-repressed genes. A number of potentially novel candidate tumor-suppressor genes (FAM107A, IGFALS, MT1G, MT1H, RNF180) demonstrated promoter hypermethylation and transcriptional repression in alcohol-associated HCC. Notably, promoter DNA methylation appeared as the regulatory mechanism for the transcriptional repression of genes controlling the retinol metabolic pathway (ADH1A, ADH1B, ADH6, CYP3A43, CYP4A22, RDH16) and SHMT1, a key gene within one-carbon metabolism. A genome-wide DNA methylation approach linked up with array-based gene expression profiles allowed identifying a number of novel, epigenetically-regulated candidate tumor-suppressor genes in alcohol-associated hepatocarcinogenesis. Retinol metabolism genes and SHMT1 are also epigenetically-regulated through promoter DNA methylation in alcohol-associated hepatocarcinogenesis.
2015-05-05 | GSE59260 | GEO
Project description:Genome-wide DNA methylation profiling was performed in peripheral leukocytes to identify biomarkers that could track hepatitis B progression to hepatocellular carcinoma (HCC). Samples included 48 HBsAg carriers who developed HCC and 48 HBsAg carriers who did not during follow-up.
2019-03-04 | GSE78904 | GEO
Project description:Introduction: Hepatocellular carcinoma (HCC) is one of the most aggressive solid tumors and oncogenic pathways (e.g Akt, IGF signaling) are often activated in high proliferating HCC. Among several genetic alterations, epigenetic changes seem to be involved in the development and progression of HCC. DNA hypermethylation of promoter regions is almost always associated with transcriptional silencing and can lead to inactivation of tumor suppressor genes (TSG) in cancer cells. Aim: (1) To identify genes differently methylated in a subclass of HCC associated with proliferation and, (2) To correlate methylation changes with activation of molecular pathways. Methods: gDNA of 20 HCC, 8 cirrhotic and 8 normal liver samples was extracted and the methylation status was detected by the Illumina HumanMethylation27 BeadChip and immunohistochemistry of p-AKT, pIGF IR, p-S6 was analyzed. Results: Unsupervised clustering clearly classified normal livers, cirrhosis and HCC in 3 different groups. 961 genes were significantly hypermethylated in HCC compared to cirrhotic and 3942 genes showed hypermethylation in cirrhotic compared to normal liver tissue. 163 genes showed stepwise significant hypermethylation from normal to cirrhotic to HCC, including well described (p16, SOCS2, SFRP5, RBP1) and potential (SRD5A2, PCDH8, IGF-1R, UCHL1) TSGs, and the miR-10a. 133 genes were specifically hypermethylated in HCC. Among them the transcription factors GATA2, DLX1, and KLF14, all significantly inversely correlated to gene expression (p=0.003, p=0.03, and p=0.007, respectively). The methylation status of SOCS2 (p=0.025) and DLX1 (p=0.025) was significantly correlated to phosphorylation of IGFR1. Samples with RBP1 hypermethylation showed significantly higher AFP serum levels (p=0.018). Conclusion: Whole genome methylation analysis markedly classifies normal, cirrhotic and HCC samples. 8 TSGs play a key role in this stepwise progression of hypermethylation in the development of HCC and could be a promising point of action in anticancer therapy.
2013-09-27 | GSE44970 | GEO
Project description:Epigenetic modifications, such as DNA methylation, play an important role in carcinogenesis. In a recent NTP study, chronic exposure of B6C3F1/N mice to Ginkgo biloba extract (GBE) resulted in a high incidence of hepatocellular carcinomas (HCC). Genome-wide promoter methylation profiling on GBE-exposed HCC (2000 mg/kg group), spontaneous HCC (vehicle-control group) and age-matched vehicle control liver was performed to identify differentially methylated genes in GBE-exposed HCC and spontaneous HCC. DNA methylation alterations were correlated to the corresponding global gene expression changes to identify differentially methylated promoter regions of relevant cancer genes altered in GBE-exposed HCC compared to spontaneous HCC.
2020-01-01 | GSE132577 | GEO