Desoxycorticosterone acetate, mammary gland growth, and carcinogenesis in mice.

Whether the carcinogenic action of estrogen is an expression solely of its ability to establish and sustain a mammary gland or whether this hormone has in addition to mammary stimulation an independent carcinogenic property per se has been questioned (5). Desoxycortieosterone acetate has been reported to be as effective as estrogen in stimulating the development of mammary glands in young male mice of cancer-susceptible strains (6). If desoxycorticosterone acetate were to sustain mammary stimulation as effectively as estrogen and yet lack carcinogenic potency, it would support the thesis that estrogens are mammary-stimulating and in addition are in a direct sense carcinogenic. It has been reported that sustained treatment of mice with desoxycorticosterone acetate did not lead to mammary tumors (3, 4). Because in the latter reports (3, 4) no evidence was presented concerning the extent of mammary stimulation, the experiments described here were undertaken to check whether sustained and adequately frequent treatment with dcsoxycortieosterone acetate 1 would produce verifiable, sustained stimulation of the mammary gland and still not produce tumors. Male C3H mice from the same stock (colony K. B. DeOme) which developed a high incidence of mammary tumors after treatment with the estrogen triphenylethy]ene (2) were injected subcutaneously 4 times weekly with 0.05 cc. or 0.1 cc. of 0.5 per cent desoxycortieosterone acetate in sesame oil. Thirty-three animals were injected. Four to six