Gene signatures in hepatocellular carcinoma (HCC)

Andrisani, Ourania M.; Studach, Leo; Merle, Philippe

doi:10.1016/j.semcancer.2010.09.002

Cited by 54 publications

(56 citation statements)

References 68 publications

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“…In untransformed hepatocytes, Suz12 chromatin immunoprecipitation assays identified a subset of genes that are repressed by the PRC2 complex, including: BAMBI, CCND2, DLK1, EpCAM, and IGFII [69]. Interestingly, Suz12 occupancy at the promoters of these genes was significantly reduced in X-transformed cells, and up-regulated expression of these genes was detected in liver tumors from animal models of X-mediated and HBV-mediated hepatocarcinogenesis [69,70]. Significantly, these genes are up-regulated in the G1 subgroup of HBV-mediated HCCs [7] and also are expressed in hepatic cancer initiating/stem cells [71].…”

Section: Suz12 Containing Prc2 Complexmentioning

confidence: 99%

“…Significantly, these genes are up-regulated in the G1 subgroup of HBV-mediated HCCs [7] and also are expressed in hepatic cancer initiating/stem cells [71]. Intriguingly, these genes are also markers of normal hepatoblasts [70], raising a question of the mechanism allowing re-expression of hepatoblast markers during oncogenic transformation of differentiated hepatocytes. One might predict up-regulation of genes supporting re-establishment of the hepatoblast phenotype, resulting in lineage mis-specification and reversal of the differentiated phenotype.…”

Section: Suz12 Containing Prc2 Complexmentioning

confidence: 99%

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Deregulation of Epigenetic Mechanisms by the Hepatitis B Virus X Protein in Hepatocarcinogenesis

Andrisani

2013

Viruses

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This review focuses on the significance of deregulation of epigenetic mechanisms by the hepatitis B virus (HBV) X protein in hepatocarcinogenesis and HBV replication. Epigenetic mechanisms, DNA methylation, and specific histone modifications, e.g., trimethylation of H3 on lysine-27 or lysine-4, maintain ‘cellular memory’ by silencing expression of lineage-inducing factors in stem cells and conversely, of pluripotency factors in differentiated cells. The X protein has been reported to induce expression of DNA methyltransferases (DNMTs), likely promoting epigenetic changes during hepatocarcinogenesis. Furthermore, in cellular and animal models of X-mediated oncogenic transformation, protein levels of chromatin modifying proteins Suz12 and Znf198 are down-regulated. Suz12 is essential for the Polycomb Repressive Complex 2 (PRC2) mediating the repressive trimethylation of H3 on lysine-27 (H3K27me3). Znf198, stabilizes the LSD1-CoREST-HDAC complex that removes, via lysine demethylase1 (LSD1), the activating trimethylation of H3 on lysine-4 (H3K4me3). Down-regulation of Suz12 also occurs in liver tumors of woodchucks chronically infected by woodchuck hepatitis virus, an animal model recapitulating HBV-mediated hepatocarcinogenesis in humans. Significantly, subgroups of HBV-induced liver cancer re-express hepatoblast and fetal markers, and imprinted genes, suggesting hepatocyte reprogramming during oncogenic transformation. Lastly, down-regulation of Suz12 and Znf198 enhances HBV replication. Collectively, these observations suggest deregulation of epigenetic mechanisms by HBV X protein influences both the viral cycle and the host cell.

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Section: Suz12 Containing Prc2 Complexmentioning

confidence: 99%

Section: Suz12 Containing Prc2 Complexmentioning

confidence: 99%

Deregulation of Epigenetic Mechanisms by the Hepatitis B Virus X Protein in Hepatocarcinogenesis

Andrisani

2013

Viruses

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“…The existence of 2 broad categories of HCCs, one with and the other without a ‘high-proliferation' gene expression signature, has been confirmed in multiple, independent studies [24]. Most have found that tumors of the high proliferation group are more aggressive and less histologically differentiated than the group without this expression signature.…”

Section: Gene Signature Associated With Prognosismentioning

confidence: 93%

Biology of Hepatocellular Carcinoma

Villa³

2015

Dig Dis

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This chapter focuses on the identification of hepatocellular carcinoma (HCC) molecular signatures and the potentials of these signatures in prediction of HCC prognosis and driving of HCC therapeutic treatments. Progress in molecular profiling studies using DNA-microarray-based gene expression profiling has provided new insight about HCC pathogenesis, and gene signatures that can distinguish tumor subtypes assist clinical staging and predict patient outcomes. This provides the possibility to improve the stratification of HCC patients at a molecular level and, in the near future, will be potential in paving the way for tailored medicine in HCC patients.

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“…It has been reported to be involved in suppressing cell differentiation and maintaining stem cell properties. PROM1 is known to be highly related to HCC and has often served as a marker of hepatoblast and liver cancer stem cells (Katoh & Katoh, 2007;Andrisani et al, 2011).…”

Section: Shared Genes Related To Both Hbvahcc and Hbvnhccmentioning

confidence: 99%

Investigating genetic characteristics of hepatitis B virus-associated and -non-associated hepatocellular carcinoma

Lou

et al. 2016

Genet. Res.

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SummaryBackground: Hepatocellular carcinoma (HCC) is a primary liver malignancy that mainly occurs in patients with chronic liver disease and cirrhosis. Risk factors for HCC include hepatitis B virus (HBV) infection. However, the specific role of HBV infection in HCC development is not yet completely understood. In order to reveal the effects of HBV on HCC, we compare the genes of HCC patients infected with HBV with those who are not infected.Methods: We encoded the genes of these two types of HCC in databases using enrichment scores of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway terms. A random forest algorithm was employed in order to distinguish these two types in the classifier, and a series of feature selection approaches was used in order to select their optimal features. Novel HBV-associated and -non-associated HCC genes were predicted, respectively, based on their optimal features in the classifier. A shortest-path algorithm was also employed in order to find all of the shortest-paths genes connecting the known related genes.Results: A total of 54 different features between HBV-associated and -non-associated HCC genes were identified. In total, 1236 and 881 novel related genes were predicted for HBV-associated and -non-associated HCC, respectively. By integrating the predicted genes and shortest path genes in their gene interaction network, we identified 679 common genes involved in the two types of HCC.Conclusion: We identified the significantly different genetic features between two types of HCC. We also predicted related genes for the two types based on their specific features. Finally, we determined the common genes and features that were involved in both of these two types of HCC.

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Gene signatures in hepatocellular carcinoma (HCC)

Cited by 54 publications

References 68 publications

Deregulation of Epigenetic Mechanisms by the Hepatitis B Virus X Protein in Hepatocarcinogenesis

Deregulation of Epigenetic Mechanisms by the Hepatitis B Virus X Protein in Hepatocarcinogenesis

Biology of Hepatocellular Carcinoma

Investigating genetic characteristics of hepatitis B virus-associated and -non-associated hepatocellular carcinoma

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