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Effect of High-Dose Progesterone on Growth of Rat Mammary Carcinoma¹

Research Institute of the Hospital for Joint Diseases, Mount Sinai School of Medicine, New York, New York 10035

Growth of the transplantable rat mammary carcinoma, MTW9, is stimulated by elevated serum prolactin concentrations. When serum prolactin is increased by coimplantation with a mammosomatotropic tumor, the mammary tumor, MTW9-MtT, does not regress after ovariectomy, but rapid growth ceases. In contrast, when MTW9 is grown in rats with high serum prolactin produced by p.o. administration of perphenazine, the tumor, MTW9-P, does regress after ovariectomy. When perphenazine treatment is discontinued, the tumor, now referred to as MTW9-PD, stops growing but still regresses after ovariectomy.

The present report examines the effects of progesterone on growth of MTW9 mammary tumors in ovariectomized rats. Administration of progesterone (10 mg/day) to rats bearing MTW9-PD completely prevented ovariectomy-induced regression but did not stimulate tumor growth or increase serum prolactin. Cessation of progesterone administration caused tumor regression. Administration of neither estrogens nor 17-hydroxyprogesterone caproate, a synthetic progestin, prevented tumor regression. Administration of progesterone (4 mg/day) to hosts of MTW9-MtT after ovariectomy permitted continued rapid mammary tumor growth, whereas estrogens failed to affect growth.

When estradiol benzoate (5 µg/day) was combined with progesterone, the ability of progesterone to stimulate growth of MTW9-MtT after ovariectomy was lost. Progesterone (10 mg/day) also retarded the rapid and complete regression of MTW9-MtT which occurs when ovariectomy is combined with surgical removal of the mammosomatotropic tumor. No effects of progesterone were observed on growth of either MTW9-MtT or MTW9-PD in intact rats. Progesterone may inhibit mammary tumor regression and stimulate tumor growth after ovariectomy by acting directly on tumor cells or indirectly by stimulating the secretion of a pituitary growth factor.

¹ This investigation was supported by Grants CA 14194 and CA 10064 of the National Cancer Institute, and, in part, by BRSG Grant RR 5589 of the Biomedical Research Support Grant Program, Division of Research Resources. NIH.

² Present address: Department of Obstetrics and Gynecology, University of South Alabama, College of Medicine, 2451 Fillingim Street, Mobile, Ala. 36617.

³ To whom requests for reprints should be addressed.

Received 7/13/79. Accepted 1/ 4/80.