| Project/Area Number |
22791332
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Research Collaborator |
坂本 規彰 University of Bonn, Department of Neuropathology, 留学生
上前 洋二 筑波大学, 大学院人間総合科学研究科, 大学院・・生
松田 真秀 筑波大学, 附属病院, 病院講師
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 血管内皮前駆細胞 / 免疫学 / 脳神経疾患 / 悪性脳腫瘍 / 神経膠腫 / 脳神経外科 / 癌幹細胞 / ワクチン / 血管内皮細胞 / ワクチン療法 / 脳腫瘍 |
|---|
| Research Abstract |
Various types of endothelial cell-targeting therapies have been developed today. The present study investigated the effect of combined vaccine from glioma cells (GL261) and endothelial cells (F-2). Tumor growth was inhibited after preventive use of the combined vaccine, prepared from GL261 and F-2 cells. Next, we investigated endothelial cell-targeting therapies using glioma initiating cells (TSG). TSG cells highly expressed CXCR4. Under specific culture condition of the glioma-initiating cells the cell morphology including high expression of CXCL12. CXCL12/CXCR-4 blockage by AMD 3100 or siRNA markedly inhibited the cell proliferation in a concentration-dependent manner. In vivo model, CXCL12 knockdown by shRNA inhibited the tumor growth. These results indicate that CXCL12 of glioma initiating cells is one of key molecules to mediate tumor growth.
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