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Article type: Research Article
Authors: Madden, Charles R. | Slagle, Betty L.
Affiliations: Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030, USA
Note: [] Department of Molecular Virology and Microbiology, Mailstop BCM-385, One Baylor Plaza, Baylor College of Medicine, Houston, TX 77030-3411, USA. Tel.: +1 713 798 3006; Fax: +1 713 798 5075; E-mail: bslagle@bcm.tmc.edu
Abstract: Chronic infection with the hepatitis B virus (HBV) is a known risk factor in the development of human hepatocellular carcinoma (HCC). The HBV-encoded X protein, HBx, has been investigated for properties that may explain its cancer cofactor role in transgenic mouse lines. We discuss here recent data showing that HBx is able to induce hepatocellular proliferation {\it in vitro} and {\it in vivo}. This property of HBx is predicted to sensitize hepatocytes to other HCC cofactors, including exposure to carcinogens and to other hepatitis viruses. Cellular proliferation is intimately linked to the mechanism(s) by which most tumor-associated viruses transform virus-infected cells. The HBx alteration of the cell cycle provides an additional mechanism by which chronic HBV infection may contribute to HCC.
Journal: Disease Markers, vol. 17, no. 3, pp. 153-157, 2001
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