Analysis of trmorigenesis and drug-resistance of ovarian/endometrial cancer due to imbalance of activin and inhibin.
| Project/Area Number |
20791157
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
MABUCHI Yasushi Wakayama Medical University, 医学部, 助教 (80382357)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | アクチビン・インヒビン / 卵巣癌 / アクチビン / インヒビン / 子宮内膜癌 / 抗癌剤耐性 |
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| Research Abstract |
No immunostaining for the a-subunit of inhibin was observed in ovarian endometriosis and the normal endometrium. Positive immunostaining for the βA-subunit of inhibin, activin A, activin receptors type IA, type IB, type IIA, type IIB, Smad2, Smad3 and Smad4 was observed in ovarian endometriosis and the normal endometrium.
These results suggest that activin A, but not inhibins, might be produced by ovarian endometriosis and the normal endometrium, and that the activin signal transduction system might exist in both ovarian endometriosis and the normal endometrium.
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Report
(3 results)
Research Products
(2 results)
