| Project/Area Number |
10670163
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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 |
Human pathology
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
IWAKI Toru Graduate School of Medical Sciences, Kyushu University, Professor, 大学院・医学系研究科, 教授 (40221098)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Satoshi o Graduate School of Medical Sciences, Kyushu University, Instructor, 大学院・医学系研究科, 助手 (90294917)
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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 |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | brain tumor / ependymoma / oncogene / SV40 / p53 / MDM2 |
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| Research Abstract |
Ependymomas rarely show p53 gene alteration and the tumorigenic mechanism of ependymomas still remains to be elucidated. We herein investigated the amplification and overexpression of mdm2 gene, whose product (MDM2) is considered to be one of the major cellular regulators of p53-mediated growth control, in 26 specimens of ependymomas obtained from 20 patients. The majority of the ependymomatous samples (96%) showed at least focal immunopositivity for MDM2 ; however, only 8% of the samples were immunopositive for p53. Mdm2 gene amplification was detected in 35% of the samples by differential polymerase chain reaction, all of which overexpressed MDM2. These results suggest that the amplification and/or overexpression of mdm2 may thus be one of the major molecular events occurring in the tumorigenesis of ependymomas.
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