Abstract
Entecavir is a widely used nucleoside analogue for antiviral therapy against chronic hepatitis B virus (HBV) infection. Despite its remarkable efficacy in suppressing HBV replication, a substantial proportion of cirrhotic patients still developed hepatocellular carcinoma (HCC) after entecavir treatment (1). Presumably, it is largely attributed to the existing precancerous hepatocytes, which sturdily progresses into cancer despite effective viral suppression. HBV X (HBx) protein is a well‐known oncogenic protein. Here, we explored an alternative possibility that oncogenic‐enhancing mutations developed in HBx in HCC patients having received entecavir treatment.
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