Abstract
Endometrial carcinoma is a prevalent disease in the Western world and is experiencing an upward trend in developing countries as well. Endometrial hyperplasia is regarded as a precancerous lesion. Apoptosis plays an important role in the neoplastic transformation of cells, with Bcl-2 serving as an anti-apoptotic cellular marker. It is possible that Bcl-2 may plays an important role in the development of endometrial carcinoma. The objective was to evaluate and compare the expression of the Bcl-2 markers accross the spectrum of normal endometrium endometrial hyperplasia and endometrial adenocarcinoma. A total of 50 cases were included in this study, comprising of 10 cases of normal endometrium, 10 cases of endometrial hyperplasia without atypia, 10 cases of atypical endometrial hyperplasia and 20 cases of endometrial adenocarcinomas. The cases were collected from January 2017 to June 2018. Immunohistochemical staining with Bcl-2 was performed and the results were subsequently analyzed. Bcl-2 staining demonstrated a notable increase in cases exhibiting with strong staining intensity, from 20% in normal endometrial tissue to 75% in cases of endometrial hyperplasia. However, there was a notable decline in the number of cases exhibiting with strong intensity Bcl-2 staining as the lesions progressed from endometrial hyperplasia to endometrial carcinoma (30% of the cases). The results were statistically significant (P =0.00309). However, there was no significant association was observed between staining and either atypical hyperplasia or endometrial carcinomas (p=0.429), or between the degree of carcinoma and staining (p=0.6903). Bcl-2 expression demonstrated an increase from cases of normal endometrium to endometrial hyperplasia, which supports the hypothesis that there is an increase in anti-apoptotic activity in endometrial hyperplastic lesions. The observed decrease in Bcl-2expression in endometrioid adenocarcinoma when compared to endometrial hyperplasia may indicate the involvement of alternative mechanisms of carcinogenesis, potentially beyond the failure of apoptosis.