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Inhibition of Mammary Tumor Growth by Dexamethasone in Rats in the Presence of High Serum Prolactin Levels¹

Department of Physiology, Neuroendocrine Research Laboratory, Michigan State University, East Lansing, Michigan 48824

Female Sprague-Dawley rats with established 7,12-dimethylbenz(a)anthracene-induced mammary tumors were given daily s.c. injections of 50 µg dexamethasone per rat, 0.5 mg haloperidol per kg, or both for 3 weeks. Control rats received the injection vehicles only. Mammary tumor growth was measured at weekly intervals for 21 days, and blood was collected on Days 10 and 21 of treatment for assay of prolactin. Dexamethasone produced significant regression of mammary tumors and reduced serum prolactin levels, whereas haloperidol significantly increased mammary tumor growth and greatly elevated serum prolactin levels. When dexamethasone and haloperidol were injected together, there was significant regression of mammary tumors despite markedly elevated serum prolactin levels. No significant differences in specific prolactin binding to membrane preparations of mammary tumors from these animals were observed in any treatment group. These results indicate that dexamethasone, a synthetic glucocorticoid, can directly inhibit mammary tumor growth in the presence of elevated serum prolactin levels produced by haloperidol, and this inhibition is not due to a reduction of prolactin binding sites in the tumor tissue.

¹ Published with the approval of the Michigan Agricultural Experiment Station as Journal Article 9239.

² NIH Postdoctoral Fellow, supported by Grant AM06034 from the National Institute of Arthritis, Metabolism and Digestive Diseases.

³ Aided by NIH Grants CA10771 from the National Cancer Institute and AM04784 from the National Institute of Arthritis, Metabolism and Digestive Diseases.

Received 11/30/79. Accepted 2/28/80.

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