Molecular targets for therapy of hepatitis B virus-induced hepatocellular carcinoma

V. S. Tharayil, L. R. Roberts

Research output: Contribution to journalArticle

1 Scopus citations

Abstract

Chronic hepatitis B virus (HBV) infection is the most frequent risk factor for development of hepatocellular carcinoma (HCC) worldwide. Studies of the molecular genetics and pathophysiology of HCC suggest that there are significant differences in the allelic imbalance, genome copy number, and gene expression patterns of HBV-induced HCC as compared to HCCs from other causes, which are presumably reflected to differences in the mode of presentation and outcomes of HBV induced HCCs. Unique features of HBV-induced carcinogenesis include the role of HBV DNA integration in carcinogenesis and the powerful synergism between HBV and dietary aflatoxins in the pathogenesis of HCC. A more complete understanding of the biology of HBV-induced HCCs may reveal well-defined differences in the molecular pathways that regulate growth of these HCCs and allow better-targeted approaches to prevention and therapy of HBV-induced HCCs. This review will attempt to summarize the current knowledge about carcinogenic pathways in HBV-induced HCCs, review the agents currently in development for targeted therapy of HCCs, and propose potentially novel approaches to therapy of HBV-induced HCC.

Original languageEnglish (US)
Pages (from-to)387-406
Number of pages20
JournalMinerva Gastroenterologica e Dietologica
Volume52
Issue number4
StatePublished - Dec 1 2006

Keywords

  • Hepatitis B virus infections, diagnosis
  • Hepatitis B virus infections, drug therapy
  • Hepatitis B virus infections, physiopatology
  • Hepatocellular carcinoma

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics
  • Gastroenterology

Fingerprint Dive into the research topics of 'Molecular targets for therapy of hepatitis B virus-induced hepatocellular carcinoma'. Together they form a unique fingerprint.

  • Cite this