| Project/Area Number |
01480551
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Saga Medical School |
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Principal Investigator |
TABUCHI Kazuo Saga Medical School, Neurosurgery, Professor, 医学部, 教授 (50116480)
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| Co-Investigator(Kenkyū-buntansha) |
SHIRAISHI Tetsuya Saga Medical School, Neurosurgery, Assistant, 医学部, 助手 (70206275)
TSUJI Takehisa Saga Medical School, Neurosurgery, Assistant, 医学部, 助手 (40217302)
ABE Masamitsu Saga Medical School, Neurosurgery, Instructor, 医学部, 講師 (20136427)
植田 清隆 佐賀医科大学, 医学部, 講師 (50144738)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1990: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Brain tumor / Oncogene / Anti-oncogene / PCR-SSCP / Cell growth related antigen p53 / KI-67 / Kiー67 / 癌遺伝子産物 / 免疫組織化学 / ウエスタンブロッティング / RFLPs |
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| Research Abstract |
Previous studies have demonstrated that the allelic deletions of the short arm of chromosome seventeenth (17p) and the long arm of the tenth (10q) are closely associated with the tumorigenesis of human malignant gliomas. Recent studies have shown that the cellular p53, which is encoded on chromosome17p13.1, may function as a suppressor of neoplastic growth and play an important role in the pathogenesis of human glial tumors. We have focused on the genetic abnormalities of p53 in relation to the development of human glial tumors, and investigated the structure and expression of p53 protein in glial tumors as well as the mutations of p53 gene. Our study demonstrated that several glioma cell lines had an aberrant form of p53 protein not only in its expression but also its molecular structure, and that p53 abnormalities might be an essential event associated with development of glial tumors. Immunoelectron microscopic study revealed that positive reaction for Ki-67 was on the granular and dense components of nucleolus, indicating that Ki-67 might participate in the processing and assembly of preribosmal particles. On the other hand, PCR-SSCP (polymerase chain reaction-single strand conformation polymorphism) analysis disclosed nucleotide substitution in 3 out of 7 human glial cell lines examined in exon 7 or 8 of the p53 gene, which were generally conserved over species. We assume these genetic alterations in coding sequence of the p53 gene are quite responsible mutations, because their products show prolonged half-life and are constantly expressed in the nuclei of human glial tumor cells. In view of these points, the genetic alterations of p53 gene appear to play a significant role in the development of glial cell neoplasia.
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