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Role of Prolactin in the Promotion of Dimethylbenz[a]anthracene-induced Mammary Tumors by Dietary Fat¹

Department of Breast Surgery and Breast Cancer Research Unit, Roswell Park Memorial Institute, Buffalo 14263, [C. I., P. Y.], and Division of Endocrinology, Veterans Administration Medical Center, Buffalo, New York 14215 [L. L. B.]

Following 7,12-dimethylbenz[a]anthracene (DMBA) administration, increased tumor incidence and tumor yield were observed in intact rats fed a 20% corn oil diet compared to those fed a 0.5% corn oil diet. Elevated serum prolactin levels (determined at proestrus) were also found in the former group of animals. In order to delineate whether this was responsible for the promoting effect of dietary fat in DMBA-induced mammary carcinogenesis, rats fed these two diets were subjected to electrolytic lesion of the median eminence that resulted in higher circulating prolactin concentrations. Sham-operated animals were used as controls. Results showed that this endocrine manipulation increased the tumor incidence in the low-fat group nearly 3-fold, but it failed to elicit further enhancement in the high-fat rats. Although the serum prolactin level in the low-fat-lesioned rats was comparable to that in the high-fat-lesioned rats, the tumor incidence in the former group still lagged behind that in the latter (33.3 versus 70.4%). Thus, it can be concluded that, although increased circulating prolactin in rats fed the high-fat diet may be partly responsible for the higher tumor incidence, other factors besides prolactin may be involved in the promoting effect of dietary fat in mammary carcinogenesis.

¹ This work was supported in part by Grant CA 14812-05 from the National Cancer Institute, NIH and by Grant 76-84381 from the National Science Foundation.

² Recipient of an award from the Biomedical Research Support Grant, Roswell Park Memorial Institute, in partial support of this work. To whom requests for reprints should be addressed, at Roswell Park Memorial Institute, 666 Elm Street, Buffalo, N. Y. 14263.

Received 8/17/79. Accepted 11/ 1/79.