| Project/Area Number |
26670710
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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 |
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| Co-Investigator(Kenkyū-buntansha) |
TOYOSHIMA Masafumi 東北大学, 大学病院, 助教 (70451581)
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| Co-Investigator(Renkei-kenkyūsha) |
KITATANI Kazuyuki 東北大学, 東北メディカル・メガバンク機構, 助教 (40539235)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 卵巣がん / 漿液性腺癌 / p53変異 / 卵管采 / DNA損傷 / トランスフェリン / 卵胞液 / 循環腫瘍DNA |
|---|
| Outline of Final Research Achievements |
Serous adenocarcinoma is the most common tissue type of ovarian cancer, and is thought to be originated from tubal fimbria in recent years. We are focusing on DNA damage response, which is considered the cause of p53 mutations, because serous ovarian cancer has p53 mutations even at the precursor lesions. Using γ-H2AX as a marker of DNA2 double strand breaks, we found that transferrin cause DNA damage response in cells. We confirmed that this is specifically dependent on transferrin receptor 1 by siRNA knockdown. The above results were published in the oncogene, and are considered to be a significant achievement in understanding the pathogenesis of ovarian cancer.
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