Expression of death receptor and death ligand in human astrocytic brain tumors
| Project/Area Number |
10671288
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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 | Kanazawa University |
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Principal Investigator |
TACHIBANA Osamu Department of Neurosurgery Kanazawa University School of Medicine Assistant Professor, 医学部, 講師 (40211362)
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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 |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | necrogenesis / apoptosis / glioblastoma / death receptor / caspase-3 / 壊死巣 / death receptor 5 / Caspase-3 / PARP |
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| Research Abstract |
In the present study, I assesed the expression of death receptor, including Fas/APO-1 (CD95), DR4, and DR5, death ligand (Fas ligand, TRAIL), and decoy receptor, and its relation to necrosis phenotype in glioblastomas. I previously reported that Fas expression is predominantly induced in perinecrotic glioma cells, suggesting that Fas induction is associated with apoptosis and necrosis formation, a histological hallmark of glioblastomas. In this study, DR5 expression is induced in large necrosis, like Fas expression. Fas L and TRAIL were expressed in glioblastoma cells. Caspase-3 overexpression and activated appears to correlate with small necrosis area. These results suggested that necrosis phenotype in glioblastoma were different cell death pathway, and small necrosis was dependent to caspase-3 activation and large necrosis dependent to death receptors.
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Report
(3 results)
Research Products
(1 results)
