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      Beta-catenin mutations in hepatocellular carcinoma correlate with a low rate of loss of heterozygosity.

      Oncogene
      Aneuploidy, Cadherins, genetics, Carcinoma, Hepatocellular, Cytoskeletal Proteins, DNA Mutational Analysis, Drosophila Proteins, Genes, APC, Humans, Liver Neoplasms, Loss of Heterozygosity, Mutation, Proto-Oncogene Proteins, Trans-Activators, Wnt Proteins, Wnt1 Protein, Zebrafish Proteins, beta Catenin

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          Abstract

          To determine the frequency of Wnt/Wingless beta catenin pathway alteration in human hepatocellular carcinoma, a beta catenin and APC gene mutation screening was performed in a series of 119 tumors. An activating beta catenin mutation in exon 3 was found in 18% of the cases. Among tumors lacking beta catenin mutation, no APC mutation has been evidenced in a subset of 30 cases tested. The correlation between beta catenin mutation status and chromosome segment deletions was studied on a set of 48 hyperploid tumors. Chromosome 1p, 4q and 16p deletions were significantly associated with the absence of beta catenin mutation (P<0.05). Furthermore the Fractional Allelic Loss was significantly smaller in the beta catenin mutated tumors than in the non-mutated tumors (0.12 versus 022). Taken together, these results suggest, the existence of two carcinogenesis mechanisms. The first mechanism implies a beta catenin activating mutation associated with a low rate of loss of heterozygosity. The second mechanism, operating in a context of chromosomal instability, would involve tumor suppressor genes.

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