Molecular alterations in hepatocellular carcinoma associated with hepatitis B and hepatitis C infections

Research output: Contribution to journalArticle

Abstract

Chronic infections with hepatitis B (HBV) and hepatitis C viruses (HCV) are the leading cause of cirrhosis and hepatocellular carcinoma (HCC) worldwide. Both viruses encode multifunctional regulatory proteins activating several oncogenic pathways, which induce accumulation of multiple genetic alterations in the infected hepatocytes. Gene mutations in HBV- and HCV-induced HCCs frequently impair the TP53, Wnt/b-catenin, RAS/RAF/MAPK kinase and AKT/mTOR pathways, which represent important anti-cancer targets. In this review, we highlight the molecular mechanisms underlying the pathogenesis of primary liver cancer, with particular emphasis on the host genetic variations identified by high-throughput technologies. In addition, we discuss the importance of genetic alterations, such as mutations in the telomerase reverse transcriptase (TERT) promoter, for the diagnosis, prognosis, and tumor stratification for development of more effective treatment approaches.

Original languageEnglish
Pages (from-to)25087-25102
Number of pages16
JournalOncotarget
Volume7
Issue number18
DOIs
Publication statusPublished - May 1 2016

Keywords

  • Genetic alteration
  • hepatitis B virus (HBV)
  • Hepatitis C virus (HCV)
  • Hepatocellular carcinoma (HCC)
  • Somatic mutation

ASJC Scopus subject areas

  • Oncology

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