Influence of Pregnancies on the Histogenesis of Mammary Cancer in the RIII/Dm/Se Substrain of Mice2

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Abstract
An attempt was made to demonstrate how pregnancies affect histogenesis of mammary cancer in RIII mice. The behavior, incidence, number, and relationship of precancerous lesions to the age and reproductive life are compared in virgin, normal-bred, and force-bred mice. The results indicate that pregnancies enhance development of cancer through a promoting action on precancerous lesions. Data are presented which suggest that pregnancies give rise to the nodules both through a subinvolution of the functioning lobule and through a new growth of alveoli—the latter always occurring in the mammary glands of virgins. Both methods operate in the breeders, and the number of nodules in their mammary glands is higher than in the mammary glands of the virgins. Moreover, pregnancies enhance the cancerization of the nodules. Mammary glands of old breeders were not studied because they die of mammary cancer before they reach an advanced age. In the resting mammary tissue of the mammary glands of very old virgins occasional nodules are found which do not become cancers because of the lack of hormonal stimuli that promotes the change from preneoplastic lesions into cancer. Pregnancies provide the quantity of hormones sufficient to promote the cancerization of most nodules. Evidence is accumulating that pregnancies give rise to the precancerous lesion, the plaque, in which growth takes place during the second half of the pregnancy and regression occurs after parturition. The plaques represent the second source of mammary-cancer development in our force-bred mice of the RIII substrain.