| Project/Area Number |
15K10185
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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 | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
藤田 逸人 九州大学, 医学研究院, 助教 (40611281)
坂井 寛 九州大学, 医学研究院, 共同研究員 (80611665)
水元 一博 九州大学, 大学病院, 准教授 (90253418)
大内田 研宙 九州大学, 大学病院, 講師 (20452708)
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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 |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 膵癌 / 間質細胞 / 膵星細胞 / 腹膜中皮細胞 / 湿潤・転移 / 腹膜播種 / リモデリング / 転移 / Endo180 / 膵臓癌 / 繊維芽細胞 / 播種 |
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| Outline of Final Research Achievements |
Pancreatic stellate cells reorganize matrix components and lead pancreatic cancer invasion via the function of Endo180. Cancer-associated peritoneal mesothelial cells lead the formation of pancreatic cancer peritoneal dissemination by cancer interstitial interaction and microenvironment alteration. Furthermore, we identified autophagy was involved in the activation of pancreatic stellate cells. In the mouse model, suppression of autophagy of pancreatic stellate cells reduced tumor development and metastasis. From these results, we clarified the possibility of a new treatment targeting stroma.
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