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Department of Anatomy, Michigan State University, E. Lansing, Michigan 48824 [C. W. W.], and Pharmacology Division, National Cancer Center Research Institute, Tsukiji 5-chome, Chuo-ku, Tokyo, Japan [H. N.]
It is unequivocal that prolactin is an influential hormone in murine mammary tumorigenesis. The Berenblum hypothesis (7), a well-known theoretical model of tumorigenesis that depicts this oncogenic process as a two-step mechanism, i.e., initiation and promotion, is a conceptual scheme in which the action of prolactin in mammary tumorigenesis may be understood. According to this conceptual model, prolactin would participate in both the initiation and promotion steps of mammary tumorigenesis. In the initiation phase, variations in prolactin secretion appear to influence the metabolism of the mammary epithelium, so that the epithelium would be either more receptive to or refractory to an initiating agent (e.g., chemical carcinogens, physical carcinogens, oncogenic viruses, etc.), i.e., a permissive action. In the promotion phase, prolactin may act as either a promoter or an antipromoter of the "transformed" mammary epithelium. In promotion, the hormone may either directly or indirectly (via the ovary) stimulate mitotic activity of the "transformed" epithelium. In antipromotion the hormone, in the presence of requisite hormones (e.g., glucocorticoids), may synergistically induce differentiation (e.g., lactation) in the "transformed" epithelium. A tumor would result in the former (promotion) but not in the latter (anti-promotion) case.
Whether or not prolactin is significantly influential in human breast tumorigenesis remains to be determined. This is an extremely important area of research which is justifiably receiving increased attention. For if prolactin can be shown to influence human breast epithelium in a manner similar to its effect on rodent mammary tissue, then prophylactic and/or chemotherapeutic control of human breast tumorigenesis may be feasible by appropriate drug-mediated prolactin suppression.
1 Supported in part by American Cancer Society Research Grant ET-59 and the NIH Research Grant CA-13777 from The National Cancer Institute. USPHS (National Cancer Institute) Research Career Development Awardee, CA-35027.
2 Supported by research grants from the Japanese Ministry of Health and Welfare; the Ministry of Education, Science and Culture; and the Society for Promotion of Cancer Research.
Received 9/20/76. Accepted 12/16/76.
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