Fibloblast response to the tumor in the desmoplasia involved in the malignant potential of pancreatic cancer
| Project/Area Number |
25430106
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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 |
Tumor biology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
IJICHI Hideaki 東京大学, 医学部附属病院, 講師 (70463841)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 膵癌 / デスモプラジア / 線維芽細胞 / 腫瘍間質相互作用 / CXCR2 / CCケモカイン / CXCケモカイン |
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| Outline of Final Research Achievements |
Desmoplasia, marked fibrosis in the pancreatic cancer tissues, seems involved in the malignant potential of pancreatic cancer. We have already established a murine model recapitulating human pancreatic carcinogenesis and reported that the cancer cells produced CXCR2 ligands specifically in the tumor-stromal interaction. Here we tried to elucidate the comprehensive response of the stromal fibroblasts to the cancer cells. The cancer-associated fibroblasts produced the same CXCR2 ligands with those derived from cancer cells, in response to the cancer cells' stimuli, resulting in promoting the cancer cell invasion. The response was quite different from that of normal pancreatic fibroblasts. Thus, inhibition of CXCR2 signaling might be a potent therapeutic strategy controlling the tumor-microenvironment of pancreatic cancer. Consistent with this, heterozygous knockout of CXCR2 in the murine pancreatic cancer model showed a tendency of the prolonged survival.
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Report
(4 results)
Research Products
(4 results)
