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.