[Contribution of immunohistochemistry and flow-cytometry in the study of endometrial pathology].

Endometrioid endometrial carcinoma is characterized by hyperestrogenism and high sensitivity to progestogens. Our study was designed in order to demonstrate the hormonal influences in neoplastic endometrium, by investigating steroid receptors expression and their correlation with proliferation activity, with matrix enzymes expression, and with susceptibility to apoptosis inducers, from hyperplasia to carcinoma. 13 cases were included in our study, 7 endometrial hyperplasias, and 6 endometrial carcinomas. Immunohistochemistry technique was performed, using antibodies against ER-á, PR, PCNA, MMP-2, MMP-9, Fas, and FasL molecules. Flow-cytometry was complementary used, for steroid receptors, PCNA and MMPs. Endometrial hyperplasias were positive for both hormonal receptors, in epithelial and stromal cells. An evident decrease of the percent of positive cells and of the staining intensity of both ER and PR was observed in poorly differentiated endometrial carcinomas. Endometrial hyperplasias presented a similar proliferative index with differentiated endometrioid endometrial carcinomas. Poorly differentiated endometrial carcinomas showed the highest PCNA index. Both types of investigated MMPs were evident, with similar aspect of localisation for both MMP-2 and MMP-9. The staining intensity for MMP-9 was higher than that of MMP-2, and was identified both in epithelial and in stromal cells. Fas and FasL expressions were identified in glandular epithelium of endometrial hyperplasias and carcinomas, although the staining intensity was reduced. Flow-cytometry showed a correlation between qualitative and quantitative data concerning hormonal receptors, PCNA and MMPs. Our study emphasises that neoplastic endometrial cells express several molecules correlated with malignant transformation and tumoral progression, by coordinated intervention of steroids, proliferating factors, gelatinases, in opposition with systems involved in apoptosis initiation.