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  • Title: Mutations of beta-catenin and AXIN I genes are a late event in human hepatocellular carcinogenesis.
    Author: Park JY, Park WS, Nam SW, Kim SY, Lee SH, Yoo NJ, Lee JY, Park CK.
    Journal: Liver Int; 2005 Feb; 25(1):70-6. PubMed ID: 15698401.
    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 beta-catenin and AXIN I genes, and immunohistochemistry for beta-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 beta-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 beta-catenin immunostaining was observed in 30 of 81 HCCs, but not in dysplastic nodules. CONCLUSION: Taken together, our data suggest that beta-catenin stabilization because of either beta-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.
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