| Project/Area Number |
26670711
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Tohoku University |
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Principal Investigator |
Ito Kiyoshi 東北大学, 災害科学国際研究所, 教授 (70241594)
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| Co-Investigator(Kenkyū-buntansha) |
鈴木 貴 東北大学, 医学系研究科, 教授 (10261629)
三木 康宏 東北大学, 災害科学国際研究所, 講師 (50451521)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | estrogen / 子宮内膜癌 / 子宮内膜増殖症 / androgen / dihydrotestosterone / 5α-reductase / 17β-HSD / 閉経後 / endometrial carcinoma / endometrial hyperplasia / androgen receptor / 17β-HSD2 |
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| Outline of Final Research Achievements |
We indicated that estrogen-dependent carcinoma progression is suppressed by dihydrotestosterone (DHT)-androgen receptor pathway in post-menopausal endometrioid endometrial carcinoma. Among the enzymes required for local biosynthesis of androgen, 5α-reductase type1 is the principal enzyme in the formation of DHT in endometrial carcinoma. The expression of this enzyme may play the important role for suppressing the carcinoma progression. In addition, We found that 17β-hydroxysteroid dehydrogenase type2, which catalyzes E2 to E1, is induced by DHT in post-menopausal endometrioid endometrial carcinoma.
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