The genomic landscape of Mongolian hepatocellular carcinoma
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE144269 | GEO | 2020/08/04
REPOSITORIES: GEO
Similar Datasets
Project description:Mongolia has the world’s highest incidence of hepatocellular carcinoma (HCC), with ~100 cases/105 inhabitants. We molecularly characterize the Mongolian (n=192) compared to Western HCCs (n=187) by RNA-seq and WES. Mongolian patients were predominantly younger, female, with HBV-HDV non-cirrhotic livers. Mongolian HCCs had higher rates of protein-coding mutations (121 vs 70 mut /tumor in West), and mutations in known (i.e. APOB) and putative HCC drivers (TSC2). A novel mutational signature (SBS Mongolia) was identified in 25% of cases associated with the carcinogenic DMS genotoxic signature. Two unique molecular classes enriched in HBV-HDV infection, female gender and inflamed tumors are described.
| EGAS00001005364 | EGA
Project description:The genomic landscape of Mongolian hepatocellular carcinoma
| PRJNA603277 | ENA
Project description:The genomic landscape of Mongolian hepatocellular carcinoma
| PRJNA615694 | ENA
Project description:The genomic landscape of Mongolian hepatocellular carcinoma
| PRJNA615695 | ENA
Project description:Hepatocellular carcinoma (HCC) is a highly heterogeneous disease, and prior attempts to develop genomic-based classification for HCC have yielded highly divergent results, indicating difficulty in identifying unified molecular anatomy. We performed a meta-analysis of gene expression profiles in data sets from eight independent patient cohorts across the world. In addition, aiming to establish the real world applicability of a classification system, we profiled 118 formalin-fixed, paraffin-embedded tissues from an additional patient cohort. A total of 603 patients were analyzed, representing the major etiologies of HCC (hepatitis B and C) collected from Western and Eastern countries. We observed three robust HCC subclasses (termed S1, S2, and S3), each correlated with clinical parameters such as tumor size, extent of cellular differentiation, and serum alpha-fetoprotein levels. An analysis of the components of the signatures indicated that S1 reflected aberrant activation of the WNT signaling pathway, S2 was characterized by proliferation as well as MYC and AKT activation, and S3 was associated with hepatocyte differentiation. Functional studies indicated that the WNT pathway activation signature characteristic of S1 tumors was not simply the result of beta-catenin mutation but rather was the result of transforming growth factor-beta activation, thus representing a new mechanism of WNT pathway activation in HCC. These experiments establish the first consensus classification framework for HCC based on gene expression profiles and highlight the power of integrating multiple data sets to define a robust molecular taxonomy of the disease. Surgically resected 118 tumor tissues from patients with hepatocellular carcinoma (HCC)
2009-09-08 | E-GEOD-10186 | biostudies-arrayexpress
Project description:Mongolian gerbil (Meriones unguiculatus) is an ideal animal model for non-alcoholic fatty liver disease/nonalcoholic steatohepatitis (NAFLD/NASH) which is under development. Currently, the research and application of Mongolian gerbils have been largely limited due to the lack of genomic and transcriptome information. In the present study, we sought to better understand the underlying mechanism of the rapid development of NASH in high-fat diet (HFD)-fed Mongolian gerbils by analyzing the transcriptome profilings of different modeling times. Eight hub genes CD44, APP, CDC42, CD68, CXCR4, CSF1R, ADGRE1 and FERMT3 were obtained, which are all involved in inflammation response and CDC42 and FERMT3 are associated with hepatocellular carcinoma (HCC). Most of the hub genes showed high expression levels in the first stage of modeling-building (HFD for 4 weeks). We observed that feeding HFD for 4 weeks is sufficient to induce high expression of pro-fibrotic factors such as PDGFB and CTGF and to form collagen deposits. Intriguingly, we found four significant independent prognostic factors for HCC: GPC1, ARPC1B, DAB2 and CFL exhibiting high expression levels during the modeling time. Our findings indicated that, Mongolian gerbil is an ideal NAFLD model with rapid progression in inflammation and fibrosis. Prolonging the modeling time may lead to the formation of NAFLD-related HCC and further research is needed to investigate this possibility.
2022-02-23 | GSE157169 | GEO
Project description:SUMMARY: Hepatocellular carcinoma(HCC) is one of the most malignant tumors in the world. In this study, we used microarray analysis to develop gene expression profile of HCC patients in Taiwan.We showed the gene expression signature between tumor and normal samples.
2019-07-31 | GSE101685 | GEO
Project description:Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death in the world. Mitochondrial fission regulator 2 (MTFR2) is involved in the development of various cancers. However, the roles of MTFR2 in HCC remain unknown. In this study, we conducted a comprehensive analysis of MTFR2 in HCC, which was generated from integrative MTFR2 analyses of eight HCC cell lines, and three datasets (public dataset, real-world dataset, immunotherapy dataset) derived from bulk HCC tissues, survival and immunotherapy data. We demonstrated that the expression level of MTFR2 is up-regulated in HCC, leading to poor prognosis. MTFR2 is positively correlated with the level of immune cell infiltration, multiple immune checkpoints and immunotherapy response prediction pathways, and act important role in cancer-immunity cycle. In conclusion, our work indicates that MTFR2 can shape a barrier of immune microenvironment and result in poor prognosis in hepatocellular carcinoma, but the immune barrier may be broken by immunotherapy.
2022-09-01 | GSE212529 | GEO
Project description:Hepatocellular carcinoma (HCC) is a highly heterogeneous disease, and prior attempts to develop genomic-based classification for HCC have yielded highly divergent results, indicating difficulty in identifying unified molecular anatomy. We performed a meta-analysis of gene expression profiles in data sets from eight independent patient cohorts across the world. In addition, aiming to establish the real world applicability of a classification system, we profiled 118 formalin-fixed, paraffin-embedded tissues from an additional patient cohort. A total of 603 patients were analyzed, representing the major etiologies of HCC (hepatitis B and C) collected from Western and Eastern countries. We observed three robust HCC subclasses (termed S1, S2, and S3), each correlated with clinical parameters such as tumor size, extent of cellular differentiation, and serum alpha-fetoprotein levels. An analysis of the components of the signatures indicated that S1 reflected aberrant activation of the WNT signaling pathway, S2 was characterized by proliferation as well as MYC and AKT activation, and S3 was associated with hepatocyte differentiation. Functional studies indicated that the WNT pathway activation signature characteristic of S1 tumors was not simply the result of beta-catenin mutation but rather was the result of transforming growth factor-beta activation, thus representing a new mechanism of WNT pathway activation in HCC. These experiments establish the first consensus classification framework for HCC based on gene expression profiles and highlight the power of integrating multiple data sets to define a robust molecular taxonomy of the disease.
2009-09-08 | GSE10186 | GEO
Project description:Hepatocellular carcinoma (HCC) is a highly heterogeneous disease, and prior attempts to develop genomic-based classification for HCC have yielded highly divergent results, indicating difficulty in identifying unified molecular anatomy. We performed a meta-analysis of gene expression profiles in data sets from eight independent patient cohorts across the world. In addition, aiming to establish the real world applicability of a classification system, we profiled 118 formalin-fixed, paraffin-embedded tissues from an additional patient cohort. A total of 603 patients were analyzed, representing the major etiologies of HCC (hepatitis B and C) collected from Western and Eastern countries. We observed three robust HCC subclasses (termed S1, S2, and S3), each correlated with clinical parameters such as tumor size, extent of cellular differentiation, and serum alpha-fetoprotein levels. An analysis of the components of the signatures indicated that S1 reflected aberrant activation of the WNT signaling pathway, S2 was characterized by proliferation as well as MYC and AKT activation, and S3 was associated with hepatocyte differentiation. Functional studies indicated that the WNT pathway activation signature characteristic of S1 tumors was not simply the result of beta-catenin mutation but rather was the result of transforming growth factor-beta activation, thus representing a new mechanism of WNT pathway activation in HCC. These experiments establish the first consensus classification framework for HCC based on gene expression profiles and highlight the power of integrating multiple data sets to define a robust molecular taxonomy of the disease.
2009-09-08 | GSE10393 | GEO