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Effects of Cryptorchidy, Parabiosis, and Estrogen Administration upon Leydig Cell Tumorigenesis in Fischer Rats¹

AMC Cancer Research Center and Hospital, Lakewood, Colorado 80214, and the Oncology Research Laboratory, Department of Medicine, Henry Ford Hospital, Detroit, Michigan 48202

The effects on Leydig cell tumorigenesis of surgical cryptorchidy, parabiotic union with a castrate male partner, and a combination of the two procedures as well as of the continuous exposure to a high level of diethylstilbestrol stimulation were studied in the high-tumor Fischer rat. Localized foci of adenomatous hyperplasia were found to have developed in the scrotal testes of most animals by 13.5 months of age. Parabiosis with a castrate male partner did not appear to alter the process significantly, but surgical cryptorchidy, even when combined with parabiosis, completely prevented the development of this pretumorous lesion as did the chronic administration of diethylstilbestrol. Furthermore, intraabdominal residency throughout the life span of animals was found to inhibit Leydig cell tumor formation almost completely. Comparative end organ weights as well as plasma testosterone determinations reported earlier indicated that, with continued intraabdominal residency 3 months and longer, the Leydig cells in this strain of rat became significantly less responsive to stimulation by pituitary gonadotropic hormones.

The data are interpreted as indicating that the endocrine stimuli most centrally involved in the genesis of this tumor type are quite different in the mouse and the rat, an abnormal response to gonadotropic stimulation being pivotal in the rat while reaction to estrogens is the most significant factor in the mouse.

¹ This research was initiated under USPHS Contract PH 43-62-171 from the Cancer Chemotherapy National Service Center and continued with the aid of USPHS Research Grant CA 05191 from the National Cancer Institute and by a grant from the Matilda R. Wilson Fund.

² To whom requests for reprints should be addressed, at Department of Medicine, Henry Ford Hospital, Detroit, Mich. 48202.

Received 12/18/80. Accepted 5/11/81.

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