Hepatitis B infection is associated with an increased risk of hepatocellular carcinoma development. Hepatitis B proteins, such as the hepatitis B x protein, the large hepatitis B surface protein, or truncated middle hepatitis B surface proteins, regulate transcription of many candidate genes for liver carcinogenesis by trans-mechanisms. They also alter mechanisms of apoptosis and interfere with nucleotide excision repair of damaged DNA. Together with an influence on cellular signaling, these mechanisms may favor the cell's clonal expansion.
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