W H Caselmann, C Rabe
Journal: Critical reviews in clinical laboratory sciences 2001;37(5):407-29
PMID: 11078055
Hepatitis B infection is strongly linked epidemiologically to hepatocellular carcinoma development. This article reviews the molecular mechanisms by which hepatitis B encoded proteins such as hepatitis B x and hepatitis B surface transactivators may interact with gene transcription, tumor suppression, apoptosis, and signalling pathways of the liver cell with the possible consequence of tumor induction. Data on the interaction between hepatitis B proteins and cellular processes are often conflicting indicating a non-specific simultaneous interaction with antagonistic cellular processes that result in the formation of escape mutants that are not subject to these selective pressures.
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