beta-catenin is a continuously expressed cytoplasmic protein that has an important role is both E-cadherin-mediated cell-cell adhesion and in activation of Wnt/Wingless transcriptional pathway. The accumulation of stabilized beta-catenin caused by the mutation of the exon 3 of beta-catenin gene can stimulate the T-cell factor/Lymphoid enhancing factor-mediated transcriptional activation. The activation of transcriptional pathway may through oncogenes is an important step of the oncogenesis in solid tumors. In this study we analyzed mutations in exon 3 of the beta-catenin gene in 18 sporadic epithelial ovarian tumors. Three mutations were found from these 18 ovarian tumor samples which contained 8 serous, 3 mucinous, 5 endometrioid, one malignant Brenner-type tumor and one transitional cell carcinoma. Two mutations occurred in endometrioid-type (in 47 and 55 codons) and one in serous-type (in 47 codon) ovarian carcinomas, and both mutations were missense and somatic. The patients with mutated beta-catenin gene appeared from the younger patients under the age of 50. Our results suggest that the stabilization of beta-catenin protein by the mutation of CTNNB1 gene can contribute to the multistep process of the oncogenesis of epithelial ovarian tumors. Furthermore these mutations mostly occurs in the endometrioid-type of EOT, but can appear in other types such as serous-type ovarian tumor.
|Translated title of the contribution||Mutation analysis of the beta-catenin gene in epithelial carcinomas of the ovaries|
|Number of pages||5|
|Publication status||Published - May 21 2000|
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