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Influence of Prolactin on Carcinogen-induced Leukemogenesis in Long-Evans Rats¹

Department of Anatomy, Michigan State University, East Lansing, Michigan 48824 [C. W. W., S. H.], and the Ben May Laboratory for Cancer Research, University of Chicago, Chicago, Illinois 60637 [C. B. H.]

Hypophysectomy of rats bearing 7,12-dimethylbenzanthracene-induced leukemia has been reported to result in a prompt and persistent regression of the leukemia. The purpose of this study was to determine whether or not marked alterations in prolactin secretion would influence this neoplastic process. To determine this, immature male and female Long-Evans rats were divided into three groups: Group 1, controls; Group 2, pituitary grafted (hyperprolactinemia); and Group 3, 2-bromo--ergocryptine-treated (hypoprolactinemia). Two weeks after the initial treatment and at 2-week intervals thereafter (6 total), each rat was given a single intragastric intubation of 7,12-dimethylbenzanthracene (10 mg/rat). Two months after the initial carcinogen treatment and at 2- to 3-week intervals thereafter, all rats had liver biopsies for the identification of leukemia. Results clearly show that despite nearly 10-fold difference in mean serum prolactin levels in the three groups of female rats and nearly a 20-fold difference in the level of this hormone in male rats, no significant differences in the magnitude of this leukemogenic process could be detected. Thus, striking changes in prolactin secretion do not appear to influence significantly this leukemogenic process.

¹ Supported by NIH Research Grant CA-13777 and American Cancer Society Research Grant ET-59.

² Recipient of NIH Research Career Development Award CA-35027. To whom requests for reprints should be addressed.

³ Recipient of NIH Research Grant CA-11603, Jane Coffin Childs Memorial Fund for Cancer Research, and the American Cancer Society.

Received 6/ 9/75. Accepted 8/26/75.