Recent advances in hepatitis B viruses and hepatocellular carcinoma.
The data reviewed at this meeting reinforce the notion that HBV may contribute to the development of liver cancer through a variety of mechanisms, including activation of oncogenes (c-myc and N-myc) by insertional mutagenesis, expression of viral proteins (X and pre-S2/S) that function as trans-activators and possibly oncoproteins, and introduction of chromosomal defects through enzymatically mediated integration into the host genome. Not all of these mechanisms appear to be active in every tumor, however. Thus, future work will be aimed at characterizing each mechanism in more detail and determining its relative importance in the carcinogenic process.
Rogler
C E
CE
Department of Medicine, and Microbiology/Immunology, Albert Einstein College of Medicine, Bronx, New York 10461.
D000818:Animals; D006528:Carcinoma, Hepatocellular / Q000235:genetics / Q000382:microbiology*; D002471:Cell Transformation, Neoplastic / Q000235:genetics; D015611:Hepatitis B Virus, Duck / Q000235:genetics; D006515:Hepatitis B virus / Q000235:genetics*; D006801:Humans; D008113:Liver Neoplasms / Q000235:genetics / Q000382:microbiology*; D015534:Trans-Activators / Q000235:genetics; D014764:Viral Proteins / Q000235:genetics; D054334:Viral Regulatory and Accessory Proteins
D015534:Trans-Activators; D014764:Viral Proteins; D054334:Viral Regulatory and Accessory Proteins; C057628:hepatitis B virus X protein