Hepatitis B infection is strongly linked epidemiologically to hepatocellula
r carcinoma development. This article reviews the molecular mechanisms by w
hich hepatitis B encoded proteins such as hepatitis B x and hepatitis B sur
face transactivators may interact with gene transcription, tumor suppressio
n, apoptosis, and signalling pathways of the liver cell with the possible c
onsequence of tumor induction. Data on the interaction between hepatitis B
proteins and cellular processes are often conflicting indicating a non-spec
ific simultaneous interaction with antagonistic cellular processes that res
ult in the formation of escape mutants that are not subject to these select
ive pressures.