| Project/Area Number |
07457322
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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 | Saitama Medical School |
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Principal Investigator |
MATSUTANI Masao Saitama Medical School. Neurosurgery. Professor., 医学部, 教授 (90010454)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIKAWA Ryo Saitama Medical School. Neurosurgery. Assistant Professor., 医学部, 講師 (90237678)
SUGIYAMA Satoru Saitama Medical School. Neurosurgery. Assistant Professor, 医学部, 講師 (50154498)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥4,900,000 (Direct Cost: ¥4,900,000)
Fiscal Year 1996: ¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | astrocytoma / glioblastoma / p53 / EGFR / 染色体 |
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| Research Abstract |
The purpose of this study is to clarify the progression of astrocytic tumors fromclinical and basic research.
p53 mutation appears in similar proportion (-50%) of low grade astrocytoma (AS) and high grade astrocytic tumors (anaplastic astrocytoma (AA) and glioblastoma (GM) ), while the amplification of EGFR gene appears mainly in GM.These observations lead to the hypothesis that the p53 mutation is an early event in the multi-step process of astrocytic tumor progression and the amplification of EGFR confers malignant phenotype of GM.Samples of 61 astrocytic tumors were stained immunohistochemically with antibodies against mutated p53-protein and EGFR.
Result : (1)Five of seven EGFR (-) /p53 (+) AS with long follow-up period had recurred as AA/GM,one is alive for 7 years without recurrence, and the other one has recurred after 5 years as AS.(2)Among the four cases of AS with EGFR (-) /p53 (-) , two are alive, and the other two had progressed to AA/GM clinically. (3)Five of seven "secondary GM" were EGFR (-) /p53 (+) , and the other two were EGFR (+) /p53 (+) .
Conclusion : Five of seven EGFR (-) /p53 (+) AS showed malignant progression, which suggested the clinical significance of p53 immunopositivity as an possible prognostic factor of AS.On the contrary, two ofEGFR (-) /p53 (-) AS progressed to AA/GM,which suggested certain limitations of clinical application. Genetic alterations occurring in EGFR (-) /p53 (-) AS need to be elucidat xed to understand the mechanisms of malignant progression among those cases.
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