| Project/Area Number |
22590756
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | The University of Tokyo |
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Principal Investigator |
SASAHIRA Naoki 東京大学, 医学部附属病院, 助教 (30401102)
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| Co-Investigator(Kenkyū-buntansha) |
TADA Minoru 東京大学, 医学部附属病院, 講師 (80302719)
IJICHI Hideaki 東京大学, 医学部附属病院, 助教 (70463841)
ASAOKA Yoshinari 東京大学, 医学部附属病院, 助教 (90431858)
池上 恒雄 東京大学, 医科学研究所, 准教授 (80396712)
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| Co-Investigator(Renkei-kenkyūsha) |
IKENOUE Tsuneo 東京大学, 医科学研究所, 准教授 (80396712)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 膵癌 / マウスモデル / 薬剤耐性 / 遺伝子異常 / 胆道学、膵臓学 |
|---|
| Research Abstract |
We generated pancreatic cancer mouse model by inducing pancreas-specific expression of activated Kras and deletion of Pten. All the mice died from pancreas tumor in six weeks. We analyzed the effect of mTOR inhibitor, rapamycin, on pancreatic cancer cell lines with PTEN deletion or AKT2 amplification. Rapamycin had no anti-tumor effect using as a single agent or combination with gemcitabine. We discovered that low glucose medium predisposed these cells to apoptosis and rapamycin prevented this phenomenon. The result suggested that, under some conditions, mTOR inhibition could not exert anti-tumor effect even on PTEN-PI3K-AKT activated cancer.交付決定額（
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