Abstract
Hepatocellular carcinoma (HCC) is the third leading cause of cancer death worldwide. In this context, chronic viral hepatitis B (HBV) infection represents the most common etiology of HCC. Notably, although other common causes of HCC including chronic viral hepatitis C and chronic alcoholic liver disease are mediated by progression through cirrhosis, the pathogenesis of HCC in HBV infection does not entirely depend on this mechanism. A major proposed pathway by which HCC may arise from chronic HBV infection is the integration of HBV DNA into the host genome, resulting in oncogene activation, tumor-suppressor gene inactivation, or other predisposition to chromosomal instability (1).
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