| Project/Area Number |
14370439
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Kumamoto University (2004)
Kagoshima University (2002-2003) |
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Principal Investigator |
KURATSU Jun-ichi Kumamoto University, Faculty of Medical and Pharmacentical Sciences, Professor, 大学院・医学薬学研究部, 教授 (20145296)
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| Co-Investigator(Kenkyū-buntansha) |
NIIRO Masaki Kumamoto University, Graduate School of Medical and Dental Sciences, Associate Professor, 大学院・医歯学総合研究科, 助教授 (30172612)
TAKESHIMA Hideo Kagoshima University Hospital, Faculty of Medicine and Dentistry, Lecturer, 大学院・医歯学総合研究科, 講師 (70244134)
HIRANO Hirofumi Kagoshima University Hospital, Faculty of Medicine and Dentistry, Lecturer, 大学院・医歯学総合研究科, 講師 (00264416)
NAKAMURA Hideo Kagoshima University Hospital, Research Associate, 医学部附属病院, 助手 (30359963)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥14,000,000 (Direct Cost: ¥14,000,000)
Fiscal Year 2004: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2003: ¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥7,900,000 (Direct Cost: ¥7,900,000)
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| Keywords | glioma / macrophage / apoptosis / integrin / MCP-1 / NF1 / angiogenesis / グリオーマ / インテグリン / PTEN / ドコサヘキサエンサン / アポトーシス / c-kit / 胚細胞腫 / NF-1 / p53 / EGF-R / NO / ケモカイン / トロンビン / 血管新生 / 浸潤 |
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| Research Abstract |
1.Vascular endothelial growth factor(VEGF) play an important role in the angiogenesis of glioma. We found that there are two mechanisms of angiogenesis by VEGF in malignant glioma, one is via VEGF produced by macrophages infiltrated by monocyte chemoattractant protein 1(MCP-1) derived from glioma cells and the other is via VEGF stimulated by thrombin converted from pro-thrombin derived from glioma cells. Furthermore, we found that docosahexaenoic acid contained in the necrotic tissue suppressed the antitumor activity of macrophages infiltrated in the glioma.
2.We reported that the increased activity and expression of Integrin-linked kinase(ILK) activity is regulated by PTEN. The transfection into the glioblastoma cells altered the localization of ILK in the cell membrane ; transfection with PTEN down-regulated PKB/Akt phosphorylation of ILK-singnaling. We assume that ILK is critical for the PTEN-sensitive regulation of PKB/Akt-dependent cell survival. The COX-2 inhibitor was capable of down-regulating ILK and PKB/Akt phosphorylation.
3.We retrospectively analyzed the relationship between treatment outcomes and EGF-R gene, homozygous deletion of p16 gene in newly diagnosed glioblastoma adult patients. We found that EGF-R and homozygous deletion of p16 gene are of significant prognostic value for predicting survival in glioblastoma patients.
4.Neurofibromin which is a NF1 gene product. We found the mutural regulation of cellular neurofibromin is essential for normal neuronal differentiation and that abnormal regulation in neuronal cells may be implicated in NF1-related learning and memory disturbance.
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