| Project/Area Number |
23592006
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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 |
Digestive surgery
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| Research Institution | Kyoto University |
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Principal Investigator |
KOIZUMI Masayuki 京都大学, 医学(系)研究科(研究院), その他 (90512351)
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| Co-Investigator(Kenkyū-buntansha) |
MASUI Toshihiko 京都大学, 医学研究科, 助教 (20452352)
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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 |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥130,000 (Direct Cost: ¥100,000、Indirect Cost: ¥30,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | インクレチン / GIP / 膵癌 / 膵発生 / 発癌 / 糖尿病 / GLP-1 |
|---|
| Research Abstract |
There are several similarities between organogensis and carcinogenesis. In this study, we focused on one of the incretin family, GIP(glucose-dependent insulinotropic polypeptide) and analyzed the role of GIP on pancreatogenesis as well as on carcinogenesis of the panreas. Loss of GIP receptor in mouse embryo shows transition of the beta cell to the alpha cell in the developing pancreas, which implies GIP comittment on beta cell development. In the pancreatic cancer specimen, the expression of GIP receptor but not of GIP itself diminishes as the tumor develops from low grade PanIN to the authentic carcinoma. Moreover, the expression of GIP receptor concomitantly diminishes as the Pdx1 decreases in the pancreatic cancer. We previously reported Pdx1 tp be an unfavorable prognostic factor, and these results suggest that the GIP develops pancreatic cancer through Pdx1 during the initial stage of the pancreas carcrinogenesis.
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