New development of pancreatic cancer stromal control based on the molecular analysis
| Project/Area Number |
24791430
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Digestive surgery
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| Research Institution | Kyushu University |
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Principal Investigator |
FUJITA Hayato 九州大学, 医学(系)研究科(研究院), 共同研究員 (40611281)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 膵癌 / 間葉系幹細胞 / 線維増生 |
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| Research Abstract |
CD90-positive fibroblasts were observed in 93% or more in the analysis of pancreatic stellate cells and this CD90 could be the key surface marker to regulate desmoplasia. In the analysis of pancreatic cancer cells, CD105-positive pancreatic cancer cells showed the specific gene expression of epithelial-mesenchymal transition and these mobility were enhanced by pancreatic stellate cells. In the case of CD166, CD166-negative pancreatic cancer cells showed strong mobility and invasiveness compared with CD166-positive cells. Furthermore, the anti-fibrotic drug "Pirfenidone" inhibited pancreatic cancer desmoplasia mainly contributed by pancreatic stellate cells and it had been suggested that regulation of stroma could suppress progression for pancreatic cancer.
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Report
(3 results)
Research Products
(17 results)
