A testable hypothesis for the role of hormones in mammary carcinogenesis with implications for other endocrine-related carcinogenesis is presented. The hypothesis is based on these observations: (a) hormones are involved, directly or indirectly, in regulating cell division in normal mammary cells; (b) emergence of overt mammary tumors requires hormonal stimulation of cells receiving carcinogenic stimulus; (c) normal mammary cells are of finite divisional capabilities, whereas neoplastic cells appear to have infinite divisional life; and (d) normal cells, when present in large quantities relative to the neoplastic cells, inhibit the growth of the latter cells. According to the hypothesis hormones play at least two roles in mammary carcinogenesis induced by diverse agents, such as viruses, chemicals, and radiation. First, hormones are necessary for DNA synthesis and mitosis of initial transformed cells for their conversion into fixed transformed cells with heritable characteristics. Second, hormones, by increasing the rate of cell division, shorten the reproductive life span of normal cells, eventually causing a reduction in the normal to transformed cell ratio in the population — a condition that allows the emergence of tumor cells by overriding the inhibitory influence of normal cells.


Presented at the John E. Fogarty International Center Conference on Hormones and Cancer, March 29 to 31, 1978, Bethesda, Md. This investigation was supported by Grant CA05388 awarded by the National Cancer Institute, Department of Health, Education, and Welfare.

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