| Project/Area Number |
25461024
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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 | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
MIZUMOTO Kazuhiro 九州大学, 大学病院, 准教授 (90253418)
SAKAI Hiroshi 九州大学, 医学研究院, 共同研究員 (80611665)
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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 |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 膵癌 / ペリサイト / 膵星細胞 / 薬剤送達 / 血管内皮細胞 / 腫瘍血管 / 間質 / NG2 / PDGFRβ |
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| Outline of Final Research Achievements |
Antiangiogenic agents have been shown to be effective in the treatment of cancers such as colon cancer and lung cancer, but not in pancreatic cancer. In this study, we aimed to develop a new treatment of pancreatic cancer targeting pericytes, which cover and stabilize the tumor vessels.
In our study, pericytes were prevalent in the stroma of pancreatic cancer specimen. Then we conducted this study focused on pancreatic stellate cells(PSCs),which play a crucial role in desmoplasia, considering the possiblity that tumor vascular permeability is caused by the abundant tumor stroma.
Stromal CD51 expression in the resected pancreatic cancer specimens was associated with shorter patients survival time, and knockdown of CD51 in PSCs led to suppression of proliferation and migration of PSCs in vitro. In addition, tumor growth was inhibited in nude mice co-transplanted with pancreatic cancer cells and CD51 knocked down PSCs, compared with those co-transplanted with control PSCs.
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