HBV induced carcinogenesis

Recent genetic studies have provided insight into the mechanisms underlying viral-associated hepatocarcinogenesis. It has been shown that the rate of chromosomal alterations is significantly increased in HBV-related tumours compared with tumours associated with other risk factors. HBV might therefore play a role in enhancing genomic instability. Inactivation of p53 by mutations and regional allelic deletions is found more frequently in tumours associated with HBV infection. By contrast, HBV related tumours harbour a low rate of β-catenin mutations. Together, these data strongly support the notion that chronic HBV infection might trigger specific oncogenic pathways, thus playing a role beyond stimulation of host immune responses and chronic necro-inflammatory liver disease.