Analysis of roles of autophagy in pancreatic cancer using mouse models
| Project/Area Number |
23591011
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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 |
Gastroenterology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
IKENOUE Tsuneo 東京大学, 医科学研究所, 准教授 (80396712)
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| Co-Investigator(Kenkyū-buntansha) |
IJICHI Hideaki 東京大学, 医学部附属病院, 助教 (70463841)
FURUKAWA Yoichi 東京大学, 医科学研究所, 教授 (20272560)
FUJII Tomoaki 東京大学, 医科学研究所, 特任研究員 (10511420)
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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: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 膵癌 / オートファジー / 膵臓癌 |
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| Research Abstract |
To develop new therapy for pancreatic cancer, it is essential to understand biological features of this disease. Autophagy is one of major protein degradation systems that were reportedly involved in tumorigenesis. To elucidate roles of autophagy in pancreatic cancer development, we deleted Atg5 gene, which is essential for autophagy, in pancreatic cancer mouse models. Our results demonstrated that autophagy has a suppressive role in initiation but a promotive role in progression of pancreatic cancer.
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Report
(4 results)
Research Products
(17 results)
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[Journal Article] Erlotinib prolongs survival in pancreatic cancer by blocking gemcitabine-induced MAPK signals2013
Author(s)
Miyabayashi K, Ijichi H, Mohri D, Tada M, Yamamoto K, Asaoka Y, Ikenoue T, Tateishi K, Nakai Y, Isayama H, Morishita Y, Omata M, Mo HL, Koike K.
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Journal Title
Cancer Research
Volume: 73
Pages: 2221-2234
Related Report
Peer Reviewed
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