1987 Fiscal Year Final Research Report Summary
Induction Mechanisms by Prolaction of Mammary Tumor, Uterine Adenomyosis and Pancreatic Hyperplasia in Mice
| Project/Area Number |
60540478
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
動物形態・分類学
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| Research Institution | University of Tokyo, Faculty of Science |
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Principal Investigator |
MORI Takao University of Tokyo, Faculty of Science, 理学部, 講師 (80011659)
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| Project Period (FY) |
1985 – 1987
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| Keywords | Mouse / Hyperprolactinemia / Mammary tumor / Uterine adenomyosis / pancreatic tumor / 細胞分裂 |
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| Research Abstract |
Prolactin is a versatile hormone in its physiological effects on vertebrates. However, it is also well recognized that prolactin induces an abnormal proliferation of the several organs in cooperation with the other hormones. Namely, prolactin causes to elevate the mammary gland DNA sysnthesis in mice. Acceleration of the mammary DNA synthesis is a limiting factor of the tumorigenesis. In uterus, experimentally-induced hyperprolactinemia results in an early and high incidence of the adenomyosis. The primary cause of development of adenomyosis is a disintegration of the uterine myometrium associated with proliferation of endometrial tissues. Furthermore, hyperprolactinemia also induces a marked proliferation of both endocrine and exocrine pancreatic tissues, and then results in teh hyperplastic lesions. All results indicate that the high circulating levels of prolactin may be responsible for the occurrence of abnormal proliferation of some target tissues, suggesting the participation of prolactin in the genesis of lesions and tumors.
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