Integrating the Epigenome to Identify Novel Drivers of Hepatocellular Carcinoma
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA445291 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description: Not available
| S-EPMC6351162 | biostudies-literature
Project description:Gene expression, histone modification, DNA methylation, and DNA hydroxymethylation from normal, cirrhotic, and HCC livers
2018-09-09 | GSE112221 | GEO
Project description:Cancer is a genetic disease with frequent somatic alterations in DNA. Study of recurrent copy number aberrations (CNAs) in human cancers would enable the elucidation of disease mechanisms and the identification of key oncogenic drivers with causal roles in oncogenesis. We have comprehensively and systematically characterized CNAs and accompanied gene expression changes in the tumors and their matched non-tumor liver tissues from 286 hepatocellular carcinoma (HCC) patients. Our analysis identified 29 recurrently amplified regions and 22 deleted regions with a high level of copy number changes, harboring established oncogenes and tumor suppressors, including CCND1, MET, CDKN2A and CDKN2B, as well as many other genes not previously reported to be involved in liver carcinogenesis. Cis-acting genes in the amplification and deletion peaks were enriched in core cancer pathways, including cell cycle, p53, PI3K, MAPK, Wnt and TGFβ signaling in large proportions of HCCs. We further validated two candidate driver genes, BCL9 and MTDH, from the recurrent focal amplification peaks and showed that they play a significant role in HCC growth and survival. In summary, we have demonstrated that characterizing the CNA landscape in HCC will facilitate the understanding of disease mechanisms and the identification of oncogenic drivers that may serve as potential therapeutic targets for the treatment of this devastating disease. Two hundred and eighty-six hepatocellular carcinoma tumors and their matched non-tumor adjacent liver tissue samples were genotyped using Illumina HumanOmni1-Quad BeadChip to estimate their somatic copy number profiles.
2013-05-22 | E-GEOD-38323 | biostudies-arrayexpress
Project description:Cancer is a genetic disease with frequent somatic alterations in DNA. Study of recurrent copy number aberrations (CNAs) in human cancers would enable the elucidation of disease mechanisms and the identification of key oncogenic drivers with causal roles in oncogenesis. We have comprehensively and systematically characterized CNAs and accompanied gene expression changes in the tumors and their matched non-tumor liver tissues from 286 hepatocellular carcinoma (HCC) patients. Our analysis identified 29 recurrently amplified regions and 22 deleted regions with a high level of copy number changes, harboring established oncogenes and tumor suppressors, including CCND1, MET, CDKN2A and CDKN2B, as well as many other genes not previously reported to be involved in liver carcinogenesis. Cis-acting genes in the amplification and deletion peaks were enriched in core cancer pathways, including cell cycle, p53, PI3K, MAPK, Wnt and TGFβ signaling in large proportions of HCCs. We further validated two candidate driver genes, BCL9 and MTDH, from the recurrent focal amplification peaks and showed that they play a significant role in HCC growth and survival. In summary, we have demonstrated that characterizing the CNA landscape in HCC will facilitate the understanding of disease mechanisms and the identification of oncogenic drivers that may serve as potential therapeutic targets for the treatment of this devastating disease. Thirty hepatocellular carcinoma cell lines were genotyped using Illumina HumanOmni1-Quad BeadChip to estimate their copy number profiles relative to pooled Hapmap samples.
2013-05-22 | E-GEOD-38207 | biostudies-arrayexpress
Project description:Cooperation between distinct cancer drivers dictates inter-tumor heterogeneity in hepatocellular carcinoma
| PRJNA624109 | ENA
Project description:The purpose of this experiment of high-coverage DNA sequencing of 58 frequently mutated genes in hepatocellular carcinoma (HCC) is to confirm clonal distribution of the known HCC drivers in samples corresponding to multiple regions of a tumor.
2020-01-16 | E-MTAB-5899 | biostudies-arrayexpress
Project description:Cancer is a genetic disease with frequent somatic alterations in DNA. Study of recurrent copy number aberrations (CNAs) in human cancers would enable the elucidation of disease mechanisms and the identification of key oncogenic drivers with causal roles in oncogenesis. We have comprehensively and systematically characterized CNAs and accompanied gene expression changes in the tumors and their matched non-tumor liver tissues from 286 hepatocellular carcinoma (HCC) patients. Our analysis identified 29 recurrently amplified regions and 22 deleted regions with a high level of copy number changes, harboring established oncogenes and tumor suppressors, including CCND1, MET, CDKN2A and CDKN2B, as well as many other genes not previously reported to be involved in liver carcinogenesis. Cis-acting genes in the amplification and deletion peaks were enriched in core cancer pathways, including cell cycle, p53, PI3K, MAPK, Wnt and TGFβ signaling in large proportions of HCCs. We further validated two candidate driver genes, BCL9 and MTDH, from the recurrent focal amplification peaks and showed that they play a significant role in HCC growth and survival. In summary, we have demonstrated that characterizing the CNA landscape in HCC will facilitate the understanding of disease mechanisms and the identification of oncogenic drivers that may serve as potential therapeutic targets for the treatment of this devastating disease.
2013-05-22 | GSE38323 | GEO
Project description:Cancer is a genetic disease with frequent somatic alterations in DNA. Study of recurrent copy number aberrations (CNAs) in human cancers would enable the elucidation of disease mechanisms and the identification of key oncogenic drivers with causal roles in oncogenesis. We have comprehensively and systematically characterized CNAs and accompanied gene expression changes in the tumors and their matched non-tumor liver tissues from 286 hepatocellular carcinoma (HCC) patients. Our analysis identified 29 recurrently amplified regions and 22 deleted regions with a high level of copy number changes, harboring established oncogenes and tumor suppressors, including CCND1, MET, CDKN2A and CDKN2B, as well as many other genes not previously reported to be involved in liver carcinogenesis. Cis-acting genes in the amplification and deletion peaks were enriched in core cancer pathways, including cell cycle, p53, PI3K, MAPK, Wnt and TGFβ signaling in large proportions of HCCs. We further validated two candidate driver genes, BCL9 and MTDH, from the recurrent focal amplification peaks and showed that they play a significant role in HCC growth and survival. In summary, we have demonstrated that characterizing the CNA landscape in HCC will facilitate the understanding of disease mechanisms and the identification of oncogenic drivers that may serve as potential therapeutic targets for the treatment of this devastating disease.
2013-05-22 | GSE38207 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE9843: Gene expression profiling of 91 hepatocellular carcinomas with hepatitis C virus etiology, Samples with "vascular invasion: Yes/No" were included in the study. GSE20017: Gene Signature to Identify Vascular Invasion in Hepatocellular Carcinoma Refer to individual Series
2011-07-30 | E-GEOD-20238 | biostudies-arrayexpress
Project description:Primary liver cancer represents a major health problem. It comprises hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC), which differ markedly with regards to their morphology, metastatic potential and therapy response. Yet, molecular actors and tissue context that commit transformed hepatic cells towards HCC or ICC are largely unknown. Here, we report that the hepatic microenvironment epigenetically shapes lineage commitment in mosaic mouse models of liver tumourigenesis. While a necroptosis associated hepatic cytokine microenvironment determines ICC outgrowth from oncogenically transformed hepatocytes, hepatocytes harbouring identical oncogenic drivers give rise to HCC if surrounded by apoptotic hepatocytes. Epigenome and transcriptome profiling of murine HCC and ICC singled out Tbx3 and Prdm5 as major microenvironment-dependent and epigenetically regulated lineage commitment factors, a function conserved in humans. Together, our study provides unprecedented insights into lineage commitment in liver tumourigenesis and explains molecularly why common liver damaging risk factors can either lead to HCC or ICC.
2018-06-28 | GSE112615 | GEO