| Project/Area Number |
07671515
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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 | Osaka University |
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Principal Investigator |
HIRAGA Shoju Osaka University Medical School, Assistant Professor, 医学部, 助手 (40243232)
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| Co-Investigator(Kenkyū-buntansha) |
HAYAKAWA Toru Osaka University Medical School, Professor, 医学部, 教授 (20135700)
OHNISHI Takanori Osaka University Medical School, Assistant Professor, 医学部, 助手 (70233210)
瀧 琢有 大阪大学, 医学部・附属病院, 医員
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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 |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1996: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1995: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | astroglia / immortalization / gene / transformation / carcinogenesis / Astrocyte / Immortalization / Gene / Cloning / Carcinogenesis |
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| Research Abstract |
We have obtained 5 immortalized astroglial cells of which growth and morphological characters are indistinguishable from normla ones but express carcinoembryonic tenascin and have strong motility to glial motility factor. The cells have intermediate characters between transformed and normal cells. We investigated genes responsible for immortalization and transformation of type 1 astroglia. Differental hybridization was performed between the normal and immortalized cells and we obtained 26 genes. We excluded fibronectin, intergrins, heat shock proteins and mortalin genes by gene homology survey and 6 genes which have unreported DNA sequences were candidated for astroglial immortalization. Likewise, 4 genes were subcloned and candidated for the transformation of astroglia using differential display method. The former genes are introduced to senescent cells and recovery from the senescence of the cells were now under investigation. The latter subclones are also introduced to immortalized cells. We reported that tumor suppressor p53 gene correlated with transformation and not with immortalization of astroglia. Moreover, we are subcloning human homologic genes to the above mentioned genes. Thus, investigation of our astroglial carcinogenesis model contribute to simplifying and elucidating pathophysiology of human glioma development and progression.
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