Prolonged lactation in mice and its effect on mammary tumorigenesis.

Abstract

AbstractProlongation of lactation was induced by litter replacement in MTV‐infected (♀ C3H × ♂ O20) F 1 mice, each bearing two pituitary isografts under the kidney capsule. Measurement of litter‐growth revealed that milk production occurs in cycles of 2–3 weeks' duration.Examination of intact and thelectomized mammary glands during prolonged lactation suggested that in the thelectomized glands there exists an “alveolar cycle”. Recently proliferated alveoli reached a size comparable to that of those in the intact lactating glands. Following distension without milk removal degenerative changes and pigment deposition occurred. It is believed that proliferation occurs in the thelectomized glands because of the presence of fat tissue. In the non‐lactating mice, also bearing pituitary grafts, the size of the alveoli was smaller.Following a regression period it was observed that thelectomized glands contained hyperplastic nodules and pigment. In the contralateral intact glands, which had a lactation history, pigment was absent and only a few nodules were seen. Hyperplastic nodules were always devoid of pigment.Tumours appeared with the same rapidity in intact glands of non‐lactating mice and in thelectomized glands of both lactating and non‐lactating mice. Tumorigenesis was retarded only in the lactating glands. Thelectomy had no effect on tumorigenesis in non‐lactating mice.It is postulated that lactation inhibits noduligenesis and thus tumorigenesis by protecting the gland against the growth‐stimulating effect of hormones.On a observé qu'après une période de régression les glandes thélectomisées contenaient des nodules hyperplasiques et du pigment. Dans les glandes controlatérales intactes qui avaient produit du lait, le pigment était absent et on ne trouvait qu'un petit nombre de nodules. Il n'y avait jamais de pigment dans les nodules hyperplasiques.l'auteur émet L'HYPothèse que la lactation inhibe la formation des nodules et des tumeurs en protégeant la glande contre la stimulation de croissance produite par les hormones.