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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, OBJECTIVE, METHODS, RESULTS. Meshes: Adult, Aged, Aged, 80 and over, Axin Protein, Carcinoma, Hepatocellular, Cytoskeletal Proteins, DNA Primers, DNA, Neoplasm, Female, Hepatocytes, Humans, Liver Neoplasms, Male, Middle Aged, Mutation, Polymorphism, Single-Stranded Conformational, Repressor Proteins, Trans-Activators, beta Catenin.
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Are mutations of beta-catenin and AXIN I genes a late event in human hepatocellular carcinogenesis? Context: Hepatocellular carcinoma (HCC) is a well-known cancer involving the Wnt pathway in its carcinogenesis. However, it is not clear whether these genetic changes are early genetic events in hepatocarcinogenesis or not. 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). 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.
assistant
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. Final Decision: yes