Mechanisms of Development of Prolactin-Induced Adenomyosis in Mice
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Ectopic pituitary transplantation induced adenomyosis in mice, characterized by stromal fibroblast and uterine gland invasion into the myometrium, suggesting mechanisms for prolactin-induced pathological uterine changes.
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Abstract
Ectopic (intrauterine and under the renal capsule) pituitary transplantation induced a high incidence of adenomyosis with subserous nodules in both SHN and SLN strains of mice. Early signs of the development were the invasion of stromal fibroblasts into the myometrium along the branches of blood vessels, followed by uterine gland invasion of the musculature to the serosa. Pituitary grafting did not modify the effects of carcinogens on the uterus. Mechanisms of the development of adenomyosis and hormonal milieu facilitating these pathological changes of the uterus are discussed.
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- Suppression of normal and preneoplastic mammary growth and uterine adenomyosis with reduced growth hormone level in SHN mice given monosodium glutamate neonatally 1985
- Endometriosis and Various Pelvic Lesions Associated with H‐perprolactinemia 1985
- Ectopic Pituitary Grafts in Mice: Hormone Levels, Effects on Fertility, and the Development of Adenomyosis Uteri, Prolactinomas, and Mammary Carcinomas* 1985
- Ultrastructural changes in uterine myometrium of mice with experimentally-induced adenomyosis 1984
- Endometriosis associated with hyperprolactinaemia 1984
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