Mutational Analysis of β‐Catenin Gene in Japanese Ovarian Carcinomas: Frequent Mutations in Endometrioid Carcinomas

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Abstract
To investigate the contribution of the β‐catenin gene to the development of ovarian carcinomas, mutational analysis of exon 3 of the β‐catenin gene was conducted. We analyzed 61 primary ovarian carcinomas, consisting of 49 non‐endometrioid‐type and 12 endometrioid‐type tumors, for genetic alteration of the β‐catenin gene. Five carcinomas showed β‐catenin mutations (S37C, T41I, T41A), including 4 (33%) of 12 endometrioid‐type tumors and 1 (14%) of 7 mucinous‐type tumors. All of these mutations altered at the serine/threonine residues that are potential sites of GSK3‐β phosphorylation. We detected no carcinomas with interstitial deletion involving exon 3 of β‐catenin. Furthermore, we immunohistochemically studied 27 of the 61 ovarian carcinomas. Both nuclear and cytoplasmic β‐catenin expressions were demonstrated in 4 of the 27 ovarian carcinomas for which tissue samples were available for examination. All 4 cases exhibited mutations in exon 3 of β‐catenin, including a mucinous carcinoma. Our results suggested that β‐catenin gene mutation at potential GSK3‐β phosphorylation sites results in accumulation of β‐catenin protein within the cells and its translocation to nuclei. Accumulated β‐catenin protein may be involved in the development of endometrioid‐type ovarian carcinomas, and some mucinous‐type ovarian carcinomas.