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Original Article
April 1957

Incorporation of P32 into Mouse Mammary Cancer: Influence of Estrogen and Testosterone

Author Affiliations


From the Surgical Service, Peter Bent Brigham Hospital, and the Department of Gynecology, Harvard Medical School.; Clinical Professor of Gynecology, Harvard Medical School (Dr. Sturgis); Research Fellow, American Cancer Society, 1954-1955 (Dr. Vasicka). Present address of Dr. Vasicka: City Hospital, Cleveland, Ohio.

AMA Arch Surg. 1957;74(4):606-609. doi:10.1001/archsurg.1957.01280100124022

Introduction  The effect of estrogens and androgens on some neoplasms of the human reproductive system, though unpredictable, has been sufficiently dramatic to warrant continued investigation. The growth rate of mammary carcinoma in particular appears to be subject to modification by these hormones in a substantial number of cases. The mechanism of action, however, is unknown. Strains of mice developing spontaneous mammary cancer in a high proportion of the females offer an appropriate laboratory preparation for the study of basic growth mechanisms involved. These tumors can be readily grafted into males of the same strain. Endogenous estrogen or androgen production can be reduced by castration in both sexes, and the influence of exogenous hormone on basic biochemical alterations is then more clearly defined. We have chosen to study the effect of 17β-estradiol and testosterone propionate on incorporation of P32 into the total nucleic acids of these tumors. In a previous

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