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Estrogen-Prolactin Dependency in 7,12-Dimethylbenz(a)anthracene-induced Tumors¹

Department of Surgery, University of Oregon Medical School, Portland, Oregon 97201

Hormonal influences on dimethylbenz(a)anthracene-induced tumor growth were investigated in detail by endocrine ablation and replacement of hormones. The majority of tumors regressed following ablation and most of them were reactivated by subsequent administrations of estrogen (0.1 to 5 µg) or prolactin (2 mg). Increasing numbers of tumors, however, were not stimulated by prolactin when administration was delayed, and a basal level of estradiol (0.01 µg) in addition to prolactin was required for reactivation of tumors. Nafoxidine hydrochloride, a competitor of estrogen at the receptor sites, arrested growth of a large portion of dimethylbenz(a)anthracene-induced tumors in intact animals but failed to retard growth of prolactin-stimulated tumors. On withdrawal of prolactin-nafoxidine, rapid regression of tumor occurred and readministration of prolactin failed to activate most of the tumors for as long as 28 days. Our results give good supporting evidence that estrogen plays a primary role in tumor growth. The interactions of prolactin and estrogen at tumor sites are necessary for regulatory events related to tumor growth.

¹ This work was supported in part by research grants from the Oregon Division of the American Cancer Society and by Grant RR-334 from the General Clinical Research Centers Branch of the Division of Research Resources, NIH, Bethesda, Md. Results were presented at the 56th Annual Meeting of the Endocrine Society, Atlanta, Ga., June 1974.

² Associate Professor of Surgery; Director, Clinical Research Center Core Laboratory. To whom requests for reprints should be sent, at Department of Surgery, University of Oregon Medical School, 3181 S. W. Sam Jackson Park Road, Portland, Ore. 97201.

³ Surgical Research Fellow.

⁴ Student Research Assistant.

Received 8/ 2/74. Accepted 11/14/74.

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