Mammary Carcinogenesis by 3-Methylcholanthrene. I. Hormonal Aspects in Tumor Induction and Growth

Abstract

Our experiments confirm the observation of Huggins and associates that 3-methylcholanthrene rapidly induces mammary carcinoma in rats. In addition, we demonstrate that pregnancy promotes the growth rate of tumors and that regression of cancer occurs after parturition. Regression of tumor after parturition is independent of lactation, because retardation of growth occurs in rats when lactation is suppressed and when lactation has never occurred. The failure to induce mammary cancer in male rats suggests that estrogens are important in mammary carcinogenesis induced by 3-methylcholanthrene. Furthermore, it seems that increased progesterone stimulation constitutes an essential factor in the rapid induction of tumors during pregnancy since pseudopregnancy produces similar effects. The failure to enhance tumor production in rats fed 3-methylcholanthrene during pregnancy suggests that an initiating process for the induction of “latent tumor cells” by the carcinogen is necessary. The increased hormone production in pregnancy is inconsequential to tumor production in the absence of a prior initiating process provided by the carcinogen. The data seem to indicate that if pregnancy occurs before the administration of 3-methylcholanthrene it retards the induction of mammary tumors. In mammary carcinogenesis in rats, hormones regulate the promoting process by 3-methylcholanthrene.