Abstract: Background: Hepatocellular carcinoma (HCC) is a well-known cancer involving the Wnt pathway in its carcinogenesis.
Aims: However, it is not clear whether these genetic changes are early genetic events in hepatocarcinogenesis or not.
Method: In this study, we performed mutational analysis of the β-catenin and AXIN I genes, and immunohistochemistry for β-catenin in a series of 114 hepatocellular nodular lesions, including premalignant lesions such as low-grade dysplastic nodules (LGDNs) and high-grade dysplastic nodules (HGDNs). Results: In the present study, mutations of the β-catenin and AXIN I genes were detected in 16% (13 out of 81) and 6.2% (five of 81) of the HCCs, respectively. However, no mutations were found in 14 LGDNs and 19 HGDNs. Moreover, abnormal nuclear β-catenin immunostaining was observed in 30 of 81 HCCs, but not in dysplastic nodules.
Conclusion: Taken together, our data suggest that β-catenin stabilization because of either β-catenin or AXIN I mutation might be a late event for malignant progression rather than an early genetic event involving the initiation of HCC development.