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Increased Incidence of Spontaneous Mammary Tumors in Female Rats with Induced Hypothalamic Lesions¹

Departments of Anatomy [C. W. W.] and Physiology [H. N., J. M.], Michigan State University, East Lansing, Michigan 48823

Forty-four multiparous, mammary tumor-free, Sprague-Dawley rats, 10 months old, were divided into two groups as follows: Group 1, sham-operated controls; and Group 2, bilateral electrolytic lesions placed in the median eminence area of the hypothalamus. After 25 weeks, the animals were killed, the number of palpable mammary tumors was determined, and blood was withdrawn for prolactin analysis by radioimmunoassay. Mammary tumor incidence and blood prolactin levels were significantly increased in median eminence-lesioned rats (12/23, 52%; 179.8 ± 23.9 mµg/ml) in contrast to the controls (4/21, 19%; 50.9 ± 9.6 mµg/ml). These results demonstrate that disruption of the final common pathway from the hypothalamus to the anterior pituitary can significantly enhance spontaneous mammary tumorigenesis in the female rat. The increased blood levels of prolactin observed in the median eminence-lesioned rats provide further evidence that this is the principal hormonal factor in mammary tumorigenesis in the rat.

¹ Supported in part by NSF Research Grant GB-17034 and NIH Research Grant CA-10771. Reported at the Annual Meetings of the American Association for Cancer Research, Philadelphia, Pennsylvania, April 1970.

² Postdoctoral Research Training Fellow of International Agency for Research on Cancer, World Health Organization. Present address: National Cancer Institute, Tokyo, Japan.

Received 3/ 2/70. Accepted 5/ 8/70.