| Project/Area Number |
10671282
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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 |
Cerebral neurosurgery
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| Research Institution | University of Tsukuba |
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Principal Investigator |
TAKANO Shingo Institute of Clinical Medicine, University of Tsukuba Assistant professor, 臨床医学系, 講師 (50292553)
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| Co-Investigator(Kenkyū-buntansha) |
MITSUI Youji Natl Inst of Biosci & Human - Technol, Chief senior researcher, 生命工学技術研究所, 主席研究官
TSUBOI Koji Institute of Clinical Medicine, University of Tsukuba Assistant professor, 臨床医学系, 講師 (90188615)
OKUDA Yukichi Institute of Clinical Medicine, University of Tsukuba Associate professor, 臨床医学系, 助教授 (60211132)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 1999: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1998: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | angiogenesis / glioma / VEGF / Theobromin / pentoxifyllin / cranial window model / thrombospondin / interferon-β / promoter / thrombospondin 1 / thymidine phosphorylase / IP10 / interferon-β |
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| Research Abstract |
1) Angiogenic balance in gliomas : Expression of various angiogenic factor and inhibitors was investigated in a series of glioma tissues and glioma cells. The expression balance of VEGF / thrombospondin-1 controlled glioma angiogenesis. Interferon β resulted in inhibition of VEGF expression as well as angiogenic inhibitor, IP10
2) Overexpression of thrombospondin in glioma cells : Thronbospondin-1 expressed plasmid DNA has been used for the transfection (ripofectin method & electroporation). The experiment has been repeated in order to acquire the stable transfectant.
3) Mouse & human VEGF / reporter plasmid was constructed. Using luciferase assay, the materials that inhibit VEGF promoter activity was investigated. Thrombospondin, genistein, mithramycin, and theobromin inhibited the VEGF promoter activity, resulting in inhibition of VEGF mRNA and protein expression of glioma cells and glioma induced endothelial cell migration. Pentoxyfillin also inhibited VEGF mRNA and protein expression of glioma cells, resulting in inhibition of glioma induced endothelial cell migration.
4) Using mouse cranial window model implanted U87 tumor fragment, above-mentioned inhibitors of VEGF activity have been investigated for their intravital anti-angiogenic activity.
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