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Immunocytochemical Study of Progesterone Receptors in Hyperplastic and Neoplastic Endometrial Tissues¹

Department of Pathology and Lady Davis Institute, The Sir Mortimer B. Davis—Jewish General Hospital and McGill University, Montreal, Quebec, Canada [C. B., A. F., G. S.], and the Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55901 [D. O. T.]

Endometrial carcinoma is the most common genital malignancy in North America. However its pathogenesis, in particular its relationship with hyperplasia is not clear. To understand steroid hormonal interactions in the genesis and growth of human endometrial hyperplasia and carcinoma, we have assayed progesterone receptors in hyperplastic and neoplastic human endometrium by immunocytochemistry. The presence of progesterone receptors in target tissues is known to be a marker of both estrogen and progesterone action. The receptors were identified in freshfrozen sections using a mouse monoclonal antiprogesterone receptor antibody (PR6). The progesterone receptor content was high in the epithelium of hyperplasia without cytological atypia and low in the epithelium of endometrial intraepithelial neoplasia (hyperplasia with cytological atypia). In carcinomas there was a heterogenous distribution of progesterone receptors in the epithelium but low as compared to hyperplastic endometria without cytological atypia. The stroma contained relatively high progesterone receptor levels irrespective of whether the epithelium was hyperplastic or neoplastic.

¹ These studies were supported by a grant from the National Cancer Institute of Canada (to G. S.). C. B. was a recipient of a fellowship from the Cancer Research Society Inc. Preliminary results have been presented, in part, at the 19th Annual Meeting of the Society of Gynecologic Oncologists, Miami, FL, 1988.

² To whom requests for reprints should be addressed, at Lady Davis Institute for Medical Research—Jewish General Hospital, 3755 Cote St-Catherine Road, Montreal, Quebec, Canada H3T 1E2.

Received 2/29/88. Revised 6/22/88. Accepted 7/29/88.

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