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

V. S. Tharayil, Lewis Rowland Roberts

Research output: Contribution to journalArticle

1 Citation (Scopus)

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 2006

Fingerprint

Hepatitis B virus
Hepatocellular Carcinoma
Therapeutics
Carcinogenesis
Allelic Imbalance
Virus Integration
Aflatoxins
Chronic Hepatitis B
Virus Diseases
Molecular Biology
Genome
Gene Expression
DNA
Growth

Keywords

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

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Molecular targets for therapy of hepatitis B virus-induced hepatocellular carcinoma. / Tharayil, V. S.; Roberts, Lewis Rowland.

In: Minerva Gastroenterologica e Dietologica, Vol. 52, No. 4, 12.2006, p. 387-406.

Research output: Contribution to journalArticle

@article{e45a9af2f51f4dbca7cc856059838376,
title = "Molecular targets for therapy of hepatitis B virus-induced hepatocellular carcinoma",
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.",
keywords = "Hepatitis B virus infections, diagnosis, Hepatitis B virus infections, drug therapy, Hepatitis B virus infections, physiopatology, Hepatocellular carcinoma",
author = "Tharayil, {V. S.} and Roberts, {Lewis Rowland}",
year = "2006",
month = "12",
language = "English (US)",
volume = "52",
pages = "387--406",
journal = "Minerva Gastroenterologica",
issn = "0026-4776",
publisher = "Edizioni Minerva Medica S.p.A.",
number = "4",

}

TY - JOUR

T1 - Molecular targets for therapy of hepatitis B virus-induced hepatocellular carcinoma

AU - Tharayil, V. S.

AU - Roberts, Lewis Rowland

PY - 2006/12

Y1 - 2006/12

N2 - 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.

AB - 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.

KW - Hepatitis B virus infections, diagnosis

KW - Hepatitis B virus infections, drug therapy

KW - Hepatitis B virus infections, physiopatology

KW - Hepatocellular carcinoma

UR - http://www.scopus.com/inward/record.url?scp=33846541908&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33846541908&partnerID=8YFLogxK

M3 - Article

C2 - 17108869

AN - SCOPUS:33846541908

VL - 52

SP - 387

EP - 406

JO - Minerva Gastroenterologica

JF - Minerva Gastroenterologica

SN - 0026-4776

IS - 4

ER -