| Project/Area Number |
15H04808
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
大島 茂 東京医科歯科大学, 医学部附属病院, 助教 (50376787)
渡辺 守 (渡邉 守) 東京医科歯科大学, 大学院医歯学総合研究科, 教授 (10175127)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥17,810,000 (Direct Cost: ¥13,700,000、Indirect Cost: ¥4,110,000)
Fiscal Year 2017: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2016: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥8,450,000 (Direct Cost: ¥6,500,000、Indirect Cost: ¥1,950,000)
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| Keywords | Atoh1 / 炎症発癌 / 自然免疫応答 / 持続炎症刺激モデル / 持続炎症 / 炎症性腸疾患 / シグナルスパイラル |
|---|
| Outline of Final Research Achievements |
Patients with ulcerative colitis are increasing in Japan, since it has been concerned the increase of the patients with UC-related colon cancer. However, the molecular mechanism of UC-related carcinogenesis is still unclear. In this study, we therefore built a continuation inflammation stimulation model using the primary culture system of the mouse colonic epithelium stem cell for the first time in the world. We then found that innate immuno-responce was in a spiral state by stimulation for a long term, indicating that this model might be UC model. In addition, we identified molecular mechanism of mucinous cancer formation during UC-related carcinogenesis, which has more malignant potential.
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