Multiple Endocrine Syndrome in SHN Mice: Mammary Tumors and Uterine Adenomyosis

In: Comparative Aspects of Tumor Development · 1989 · pp. 121–130 · doi:10.1007/978-94-009-1091-1_18 · W109275818
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Mammary gland and uterine proliferation in rodents depend on prolactin and ovarian steroid hormones.

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This paper (a 1989 chapter) reviews and synthesizes experimental findings that in SHN laboratory mice, endocrine regulation via prolactin and ovarian steroid hormones controls both mammary gland growth and uterine proliferation, with abnormal outcomes including mammary tumors and uterine adenomyosis. At a high level, it draws on studies using hormone manipulations and pituitary grafts/strains to link prolactin signaling with adenomyosis development and with mammary tumorigenesis, emphasizing strain-dependent and schedule-dependent effects. A key caveat is that the chapter’s evidence is primarily from animal experimental systems and related prior literature, so it does not present new mechanistic data in humans or a direct clinical translation. This paper is centrally about endometriosis and adenomyosis — uterine adenomyosis in SHN mice is discussed as part of a “multiple endocrine syndrome” driven by prolactin, directly relating to adenomyosis biology (and to the endometriosis corpus through shared hormonal/immunologic pathways).

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Abstract

It is recognized that in laboratory rodents normal and neoplastic mammary gland growth is dependent upon prolactin and the ovarian steroid hormones (estrogen and progesterone) (2, 37, 41). Normal and abnormal proliferation of the uterus is also under the control of similar hormones (6, 8, 14, 25), although the mechanism is not always well understood. Preview Unable to display preview. Download preview PDF. Similar content being viewed by others

References

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Multiple Endocrine Syndrome in SHN Mice: Mammary Tumors and Uterine Adenomyosis. In: Kaiser, H.E. (eds) Comparative Aspects of Tumor Development. Cancer Growth and Progression, vol 5. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-1091-1_18 Download citation DOI: https://doi.org/10.1007/978-94-009-1091-1_18 Publisher Name: Springer, Dordrecht Print ISBN: 978-94-010-6981-6 Online ISBN: 978-94-009-1091-1 eBook Packages: Springer Book Archive

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