| Project/Area Number |
23592435
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Chiba University |
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Principal Investigator |
USUI Hirokazu 千葉大学, 医学(系)研究科(研究院), 講師 (90375634)
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| Co-Investigator(Renkei-kenkyūsha) |
SHOZU Makio 千葉大学, 大学院医学研究院, 教授 (30226302)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 侵入奇胎 / 雄核発生奇胎 / トロホブラスト / 絨毛外栄養膜細胞 / 低酸素 / インプリント遺伝子 / p57KIP2 / マイクロアレイ |
|---|
| Research Abstract |
We planned to identify the specific gene of invasive mole development, compared the expression pattern of primary culture cell of extravillous trophoblasts between the case of gestational trophoblastic neoplasia (GTN) development and the case primary remission. We purified 15 cases of EVTs cells. Among them, only one case developed to GTN. The case that became the invasive mole was not enough for the original purpose.
We compared the expression of key genes in the villus differentiation between the purified EVTs and uncultured villous tissue. In addition, we confirmed a methylation status of the imprinted gene, KvDMR, which controlled the expression of p57KIP2. The increased expression level of p57KIP2 was regulated by the possible mechanism except for the methylation of imprinted gene, KvDMR.
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