IMR Press / FBL / Volume 12 / Issue 1 / DOI: 10.2741/2061

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

Oncogenesis and transforming viruses: the hepatitis B virus and hepatocellularcarcinoma – the etiopathogenic link

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1 Division of Medical Sciences, National Cancer Center, Singapore
2 Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
Academic Editor:Kuan-Teh Jeang
Front. Biosci. (Landmark Ed) 2007, 12(1), 234–245; https://doi.org/10.2741/2061
Published: 1 January 2007
(This article belongs to the Special Issue Human cancer causing viruses)
Abstract

Hepatocellular carcinoma (HCC) is one of the world's leading fatal malignancies. Chronic infection with the hepatitis B virus (HBV) has been implicated with the development of HCC. For the past three decades, intensive research has focused on the role of HBV in hepatocarcinogenesis. Various HBV-associated models have emerged, but increasing evidence points to two major HBV-specific mechanisms that contribute to the development of HCC. The first is the integration of the viral genome into the host chromosome causing cis-effects, resulting in loss of tumor suppressor gene functions, and/or activation of tumor-promoting genes. The second mechanism involves the expression of trans-activating factors derived from the HBV genome, which have the potential to influence intracellular signal transduction pathways and alter host gene expression. A major player involved in this form of viral transactivation is the X protein (HBx). The HBx protein was found to display pleiotropic functions and has been implicated in the malignant transformation of chronically-infected liver cells. By disrupting cellular gene expression, viral products such as HBx may modulate cellular growth, repair and death, consequently resulting in the transformation of hepatocytes to an oncogenic state.

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