Ectopic Pituitary Grafts in Mice: Hormone Levels, Effects on Fertility, and the Development of Adenomyosis Uteri, Prolactinomas, and Mammary Carcinomas*

R A Huseby, Robert A. Huseby, Michael J. Soares, M J Soares, Frank Talamantes, F Talamantes
Endocrinology · 1985 · vol. 116(4) , pp. 1440–1448 · doi:10.1210/endo-116-4-1440 · PMID:3971922 · W2015597679
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Ectopic pituitary grafts in mice caused hyperprolactinemia, altered progesterone levels, reduced corpora lutea, and increased adenomyosis and mammary carcinomas, particularly in hybrids.

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Abstract

Some endocrinological consequences of grafting hypophyses of mice to sites distant from the hypothalamic-pituitary portal vessels were investigated. Serum PRL levels in recipients rose within 3 weeks to levels seen during pregnancy, resulting in a premature increase in serum progesterone (P) levels. After 7 weeks, luteolytic effects were evident in BALB/c females, and P values had plateaued in the range of those seen in normal adult animals, while in BALB/c X C3H F1 hybrids, this effect was delayed, and P values rose, reaching, in some animals, levels reported during pregnancy. Despite continuing hyperprolactinemia, the fertility of graft-bearing females was reduced only slightly. By the 6th month, lesions of adenomyosis were frequent in uteri of C3H and F1 hybrids, but essentially absent from BALB/c animals. The number of corpora lutea was reduced in all experimental groups, yet serum P values were somewhat elevated in hybrid females and BALB/c animals bearing three grafts. Evidence is presented indicating that PRL enhances the action of P on both the estrogen-stimulating vagina and uterus. Small groups of grafted BALB/c and hybrid females not infected with exogenous mouse mammary tumor virus were allowed to survive until mammary cancers developed or until they reached 18 months of age. The grafts in the hybrids routinely became adenomatous, producing serm PRL levels of 1-21 X 10(3) ng/ml; only one secreted excessive GH. Adenomyosis wained in the aged hybrids, apparently due to declining ovarian function. The majority of the animals developed adenoid cystic mammary cancers that seemed to arise from areas of hyperplasia within dilated ducts rather than from alveolar hyperplasias, as is most frequently the case in mice carrying exogenous mouse mammary tumor virus.

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Condition tags

mesh:D004715adenomyosis

MeSH descriptors

Carcinoma Endometriosis Fertility Hormones Mammary Glands, Animal Pituitary Gland Pituitary Neoplasms Prolactin Aging Animals Breeding Carcinoma Endometriosis Female Hormones Male Mammary Glands, Animal Mammary Neoplasms, Experimental Mammary Neoplasms, Experimental Mice

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