Interaction of Hepatitis B virus with cellular processes in liver carcinogenesis.
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.
Rabe
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Department of Medicine I, University of Bonn, Germany.
Caselmann
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D000595:Amino Acid Sequence; D017209:Apoptosis; D001483:Base Sequence; D002471:Cell Transformation, Neoplastic; D002472:Cell Transformation, Viral; D004260:DNA Repair; D006515:Hepatitis B virus / Q000472:pathogenicity*; D006801:Humans; D008113:Liver Neoplasms / Q000473:pathology* / Q000821:virology*; D008969:Molecular Sequence Data; D015398:Signal Transduction; D015533:Transcriptional Activation; D014764:Viral Proteins / Q000737:chemistry / Q000235:genetics / Q000502:physiology
D014764:Viral Proteins