2003 Fiscal Year Final Research Report Summary
Combinedtherapy with anti-angiogenic factors, low-dose anti-cancer drugs and interferons for malignant gliomas
| Project/Area Number |
14571304
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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 | Faculty of Medical Sciences, University of Fukui |
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Principal Investigator |
KUBOTA Toshihiko University of Fukui, Faculty of Medical Sciences, Professor, 医学部, 教授 (70092781)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAGAWA Takao University of Fukui Hospital, Lecturer, 医学部附属病院, 講師 (40217675)
TAKEUCHI Hiroaki University of Fukui, Faculty of Medical Sciences, Assistant Professor, 医学部, 助手 (80262624)
SATO Kazufumi University of Fukui Hospital, Associate Professor, 医学部附属病院, 助教授 (60187177)
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| Project Period (FY) |
2002 – 2003
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| Keywords | glioma / angiogenesis / cytokine / interferon / VEGF / TP / ACNU / 5-FU |
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| Research Abstract |
1)Glioma cells under hypoxic condition promoted survival of human brain microvascular endothelial cell. This protective effect included anti-apoptotic and anti-necrotic processes and required VEGF from glioma cells and NFkB activation in endothelial cells.
2)Interferon-β stimulated angiopoietin-2 expression in human glioma cells
3)cDNA microarray analysis reveals many gene expression changes in ACNU-resistant glioma cells.
4)Interferon-β induced TP/PD-ECGF expression in glioma cells, which enhanced cytotoxic activity of 5-FU.
5)TP/PD-ECGF expression in glioma cells induced by interferon-β required transcriptiona activation and mRNA stabilization dependent on JAK-STAT pathway.
6)Interferons stimulates VEGF expression in glioma cells. This process required de novo protein synthesis and depended p44/p42 MAPK in part.
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