| Summary: | Hepatocellular carcinoma (HCC) is the most common primary liver cancer affecting adults and the second most common primary liver cancer affecting children. Recent years have seen a significant increase in our understanding of the molecular changes associated with HCC. However, HCC is a complex disease, and its molecular pathogenesis, which likely varies by aetiology, remains to be fully elucidated. Interestingly, some inherited cholestatic disorders that manifest in childhood are associated with early HCC development. This review will thus explore how three genes that are associated with liver disease in childhood (<i>ABCB11, TJP2</i> and <i>VPS33B</i>) might play a role in the initiation and progression of HCC. Specifically, chronic bile-induced damage (caused by <i>ABCB11</i> changes), disruption of intercellular junction formation (caused by <i>TJP2</i> changes) and loss of normal apical–basal cell polarity (caused by <i>VPS33B</i> changes) will be discussed as possible mechanisms for HCC development.
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