Abstract B23: Dominant stablized ß-catenin induces adenomyosis formation and ablation of Mig-6 accelerates progress of adenomyosis formation

Adenomyosis is a common gynecological disorder defined by the presence of endometrial glands and stroma within the myometrium. Despite its frequent occurrence, the precise etiology of adenomyosis is still unknown, although it has often been associated with endometrioid adenocarcinoma. β-catenin abnormalities are common in endometrioid type endometrial carcinomas. The expression of the dominant stabilized β-catenin in the murine uterus (PRcre/+ Ctnnb1f(ex3)/+) resulted in endometrial glandular hyperplasia. In addition to the glandular hyperplasia phenotype, uteri of PRcre/+ Ctnnb1f(ex3)/+ mice exhibited an abnormal myometrial structure and proceed to develop adenomyosis. Ablation of Mig-6 in the murine uterus (PRcre/+ Mig-6f/f) leads to the development of endometrial hyperplasia and estrogen-induced endometrial cancer. Concomitant stabilization of β -catenin and ablation of Mig-6 dramatically accelerated the development of adenomyosis and glandular hyperplasia compared to stablizing β-catenin alone. The adenomyosis phenotype of ovariectomized Pffre/+ Ctnnb1f