| Project/Area Number |
09671430
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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 | Kagoshima University (1998)
Kumamoto University (1997) |
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Principal Investigator |
KURATSU Jun-ichi Faculty of Medicine Kagoshima University, Professor, 医学部, 教授 (20145296)
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| Co-Investigator(Kenkyū-buntansha) |
HIRANO Hirofumi Faculty of Medicine Kagoshima University, Research Associate, 医学部, 助手 (00264416)
YOKOYAMA Shunichi University Hospital Kagoshima University, Assistant Professor, 医学部・附属病院, 講師 (90191519)
TAKESHIMA Hideo Kumamoto University, Faculty of Medicine, Research Associate, 医学部, 助手 (70244134)
NISHI Toru Kumamoto University, Faculty of Medicine, Research Associate, 医学部, 助手 (00264309)
KOCHI Masato Kumamoto University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (70178218)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | MCP-1 / Glioma / Angiogenesis / Macrophage / Macrophage / グリオーマ / マクロファージ / サイトカイン |
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| Research Abstract |
We previously purified the human monocyte chemoattractant protein-1(MCP-1) from supernatant of cultured human glioma cell lines. MCP-1 is a member of the C-C chemokines that medicate monocyte chemotaxis. After cloning of the MCP-1 cDNA, ewe hacve analyzed the expression of the gene In a variety of brain tumors. We found the therewas a positive correatlon between the amount of MCP-1 expression of the tumors and the number of tumor associated macrophages. Furthermore, a transfection experiment demonstrated that excessive expression of this chemokine could induce macrophage infiltration and suppression In vivo tumor growth.
The MCP-1 receptor, designated hCCR2, is an essential co-receptor In cell entry by the human immunodeficiency virus (HIV) as , well as a receptor for MCP-1. To elucidate the molecular mechanisms for transcriptional regulation of hCCR2, we cloned and sequenced the hCCR2 gene. In the 5-flanking region, there were the typical mammalian promotor consensus elements, a CAAT box and a TATA box resulting in a single transcription-Initiation site.
Furthermore, we found that macraphages infiltrated into the glioma tissue express the tyrosine phosphorylase which play an important role on the neovascularization. We posit the regulation of MCP-1 activity and the control of the CCR2 expression of macrophages should lead to the growth control of glioma.
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