Mutations of β-catenin and AXIN I genes are a late event in human hepatocellular carcinogenesis
Article first published online: 15 DEC 2004
Volume 25, Issue 1, pages 70–76, February 2005
How to Cite
Park, J. Y., Park, W. S., Nam, S. W., Kim, S. Y., Lee, S. H., Yoo, N. J., Lee, J. Y. and Park, C. K. (2005), Mutations of β-catenin and AXIN I genes are a late event in human hepatocellular carcinogenesis. Liver International, 25: 70–76. doi: 10.1111/j.1478-3231.2004.0995.x
- Issue published online: 7 FEB 2005
- Article first published online: 15 DEC 2004
- Received 21 July 2003, accepted 15 January 2004
- AXIN I;
- hepatocellular carcinogenesis;
- Wnt pathway
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.