| Project/Area Number |
20590915
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
|
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| Research Institution | Niigata University |
|---|
Principal Investigator |
KAGAMU Hiroshi Niigata University, 医歯学系, 講師 (30418686)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NAKATA Kou 新潟大学, 医歯学総合病院, 教授 (80207802)
YOSHIZAWA Hirohisa 新潟大学, 医歯学総合病院, 准教授 (50282984)
TANAKA Hiroshi 新潟大学, 医歯学総合病院, 特任助教 (80463991)
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| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
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| Keywords | 非閉塞性肺疾患 / 肺線維症 / 呼吸器感染症 / その他 / Th17 / 制御性T細胞 / 小細胞肺癌 |
|---|
| Research Abstract |
To elucidate the SCLC antigens that are recognized by Th17 cells, we examine surface molecules of SCLC cells and found that the floating SCLC cells express CD133, which is one of putative cancer stem cell (CSC) markers. Proteome analyses revealed DEAD/H (Asp-Glu-Ala-Asp/His) box polypeptide 3, X-linked (DDX3X) as a novel CSC-specific protein. An anti-DDX3X vaccination induced anti-CSC effector T cells that mediated antitumor therapeutic efficacy. DDX3X was highly expressed in human CD133^+ SCLC cells but not in normal epithelial cells. These results indicate that anti-DDX3X, immunotherapy to induce Th17 is a promising treatment option in the clinical setting.
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