| Project/Area Number |
11557105
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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 | 展開研究 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Yamaguchi University |
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Principal Investigator |
NISHIZAKI Takafumi Yamaguchi University, School of Medicine, Associate Professor, 医学部, 助教授 (10237688)
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| Co-Investigator(Kenkyū-buntansha) |
SASAKI Kohsuke Yamaguchi University, School of Medicine, Professor, 医学部, 教授 (80116722)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 2000: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1999: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | cytogenetics / CGH / LSC / SKY / meningioma / pituitary adenoma / schwannoma / genetic subgroups / spectral karyotyping / pilocyticastrocytoma / 悪性化 |
|---|
| Research Abstract |
Purpose : Little is known about genetic subgroups or genetic alterations during malignant progression in benign brain tumors. Since it is accepted that malignant tumors evolve by the accumulation of genetic aberrations during tumor progression, the investigation of genetic changes should provide some clues as to the mechanisms underlying malignant progression of benign brain tumors. In this study, we described the cytogenetic alterations detected by comparative genomic hybridization (CGH) analysis in benign brain tumors, and depicted a plausible genetic pathway for their progression. Methods : Using CGH and laser scanning cytometic (LSC) analyses, we investigated cytogenetic alterations and DNA ploidy patterns for meningiomas, pituitary adenomas, schwannomas and other brain tumors. In order to elucidate the relationship between chromosome structural disorders and DNA copy number aberrations in tumor cells, we applied the techniques of spectral karyotyping (SKY) for human glioma cell li
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nes. Results : The average number of alteration sites in each patient with typical meningioma was significantly less than those with atypical or anaplastic meningioma. The CGH findings suggest that losses of 1p, 2p, 6q, chromosome 10 and 14q, and gain of 20q are genetic changes implicated in the malignant progression of meningioma. The mean number of sites of copy gain was significantly higher in functioning adenomas than in non-functioning tumors. The DNA aneuploid adenomas showed cytogenetic changes more frequent than DNA diploid ones. Typical schwannomas displayed only a few genetic changes. Primary CNS lymphomas seem to have common genetic pathway with non-CNS ones. SKY, CGH and fluorescence in situ hybridization using yeast artificial chromosome probes for human glioma cell lines shed light on the close relationship between DNA amplification and chromosomal translocation. Conclusion : The data obtained from the further CGH analysis will allow a more definite genetic subgroups or progression pathways for benign brain tumors. Less
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