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  • Title: Immunohistochemical expression of E-cadherin and beta-catenin in the normal and malignant human endometrium: an inverse correlation between E-cadherin and nuclear beta-catenin expression.
    Author: Shih HC, Shiozawa T, Miyamoto T, Kashima H, Feng YZ, Kurai M, Konishi I.
    Journal: Anticancer Res; 2004; 24(6):3843-50. PubMed ID: 15736420.
    Abstract:
    BACKGROUND: The E-cadherin/beta-catenin complex plays a crucial role in epithelial cell-cell adhesion and in the maintenance of tissue architecture. We previously reported aberrant expression of beta-catenin in endometrial carcinomas. However, the expression and correlation of E-cadherin and beta-catenin in normal and malignant endometrial tissues are not fully understood. MATERIALS AND METHODS: Immunohistochemical expression of E-cadherin and beta-catenin was detected in 30 cases of normal endometrium and 73 cases of endometrial carcinoma. RESULTS: In the normal endometrium, the expression of E-cadherin and cytoplasmic beta-catenin in glandular cells was predominantly observed in the proliferative phase, and decreased in the secretory phase. In endometrial carcinomas, the expression of E-cadherin and cytoplasmic beta-catenin decreased compared to that in the normal proliferative endometrial glands. The expression of E-cadherin and cytoplasmic beta-catenin tended to be reduced in histologically high-grade tumors compared to low-grade tumors. Nuclear expression of beta-catenin was observed in the glandular cells in the late proliferative and early secretory phases, as well as in high-grade endometrial carcinomas. Interestingly, nuclear beta-catenin expression was associated with the loss of E-cadherin expression in normal and carcinoma cells, indicating an inverse correlation. CONCLUSION: The cyclic expression of E-cadherin and beta-catenin in the normal endometrium suggests that the adhesion complex may act to maintain the endometrial architectures. In addition, nuclear beta-catenin expression associated with loss of E-cadherin expression may be involved in the acquisition of aggressive biological behavior, especially in high-grade tumors.
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