Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA279498 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We molecularly characterized a class of histologically aggressive childhood liver cancers and showed that these tumors are clinically aggressive and that their observed histological features are associated with underlying recurrent molecular features. We proposed a diagnostic algorithm to identify these cancers using a combination of histological and molecular features, and our analysis suggested that these cancers may benefit from specialized treatment strategies that may differ from treatment guidelines for hepatoblastomas and hepatocellular carcinomas.
2022-07-15 | GSE208217 | GEO
Project description:We molecularly characterized a class of histologically aggressive childhood liver cancers and showed that these tumors are clinically aggressive and that their observed histological features are associated with underlying recurrent molecular features. We proposed a diagnostic algorithm to identify these cancers using a combination of histological and molecular features, and our analysis suggested that these cancers may benefit from specialized treatment strategies that may differ from treatment guidelines for hepatoblastomas and hepatocellular carcinomas.
2022-09-24 | GSE214074 | GEO
Project description:GENOMIC ANALYSIS OF FIBROLAMELLAR HEPATOCELLULAR CARCINOMA REVEALS A UNIQUE MOLECULAR PROFILE
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Project description:GENOMIC ANALYSIS OF FIBROLAMELLAR HEPATOCELLULAR CARCINOMA REVEALS A UNIQUE MOLECULAR PROFILE
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Project description:Genomic analysis of Fibrolammellar Hepatocellular Carcinoma reveals an unique molecular profile [Test set]
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Project description:Genomic analysis of Fibrolammellar Hepatocellular Carcinoma reveals an unique molecular profile [Training set]
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Project description:Hepatoblastomas carry few genetic alterations, and we hypothesize that epigenetic changes could be relevant to their onset. DNA methylation profile of hepatoblastomas was explored in relation to liver development using the HM450K platform. Seven paired samples of hepatoblastomas and adjacent non-tumoral livers were studied, with biologicaland results validation validated in an independent group (12 hepatoblastomas) that confirmed 1,359 differentiated methylated CpG sites (DMSs) in hepatoblastomas compared to controls, associated with 979 genes. Hepatoblastomas also exhibited a global low-level hypomethylation when compared with differentiated livers, especially at non-repetitive intergenic DNA (~55% of the hypomethylated CpGs); conversely, most of the hypermethylated CpGs were located in CpG islands. Functional analyses revealed an enrichment in signaling pathways involved in metabolism, negative regulation of cell differentiation, liver development, cancer, and the WNT pathway. Strikingly, an important overlap was observed between hepatoblastomas DMSs and the CpG sites reported to exhibit methylation changes through liver development. Genes with differential methylation were related to maintenance of undifferentiated cell state, cell transformation and tumor progression, and the methylation profile of tumors resembled that of fetal livers. Altogether, our results suggest an arrest at early stages of liver cell differentiation, in line with the hypothesis that hepatoblastoma ontogeny involves the disruption of liver development.
2017-04-03 | GSE78732 | GEO
Project description:The cell of origin of hepatoblastoma in humans and mice (HB) is unknown; it has been hypothesized to be a transformed hepatocyte, an oval cell, or a multipotent hepatic progenitor cell. In mice, the current dogma is that HBs arise within hepatocellular neoplasms as a result of further transformation from a neoplastic hepatocyte. However, there is little evidence in the literature to support a direct relationship between these two cell types. Furthermore, due to differences in etiology and development of hepatoblastoma between mice and humans, many have questioned the relevance of these tumors in hazard identification and risk assessment. In order to better understand the relationship between hepatocellular carcinoma and hepatoblastoma, as well as better determine the molecular similarities between mouse and human hepatoblastoma, global gene expression analysis and targeted Hras and Ctnnb1 mutation analysis were performed using concurrent hepatoblastoma, hepatocellular carcinoma, and associated normal adjacent liver (in the context of vehicle control liver) samples from a recent National Toxicology Program chronic bioassay. The data from this study provides a better understanding of the origins of hepatoblastoma in the B6C3F1 mice and the relevance of mouse hepatoblastoma to humans when considering chemical exposures of potential human cancer risk. Compare mouse hepatoblastoma versus adjacent hepatocellular carcinomas versus adjacent non-tumor liver and vehicle control normal liver, 6 replicates each group.
2015-09-01 | E-GEOD-67316 | biostudies-arrayexpress
Project description:To characterize the genetic alterations that instigate hepatitis C virus-induced hepatocellular carcinoma (HCC), we conducted an integrative genomic analysis of 103 HCCs. Most tumors harbored 1q gain, 8q gain or 8p loss, with occasional alterations in 13 additional chromosome arms. In addition to amplifications at 11q13 in 6 tumors, 4 tumors harbored focal gains at 6p21 incorporating VEGFA, which were confirmed in 4 of 113 HCC in an independent validation set. Strikingly, this locus overlapped with copy gains in 4 of 371 lung adenocarcinomas. Overexpression of VEGFA via 6p21 gain suggested a cell-nonautonomous mechanism of oncogene activation. Hierarchical clustering of gene expression among 91 tumors identified 5 classes, including ‘Wnt-CTNNB1’, ‘proliferation’ and ‘interferon-related’ gene classes. We also discovered a novel class defined by polysomy of chromosome 7, gains of which were associated with early tumor recurrence after resection. These findings reveal key alterations in HCC pathogenesis and implicate potential therapeutic targets. Keywords: disease state analysis 103 hepatocellular carcinomas and 95 adjacent cirrhotic, non-tumoral liver tissue were obtained at the time of surgical resection of orthotopic transplantation.
2008-06-21 | E-GEOD-9845 | biostudies-arrayexpress