| Project/Area Number |
09672046
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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 |
Surgical dentistry
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| Research Institution | OSAKA CITY UNIVERSITY MEDICAL SCHOOL (1998)
Osaka University (1997) |
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Principal Investigator |
MORITA Takashi OSAKA CITY UNIVERSITY MEDICAL SCHOOL,PROFESSOR, 医学部, 教授 (70150349)
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| Co-Investigator(Kenkyū-buntansha) |
IWAI Soichi OSAKA UNIVERSITY,FACULTY OF DENTISTRY,
岩井 聡一 大阪大学, 歯学部・附属病院, 医員
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1997: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | embryonal carcinoma cell / cisplatin / apoptosis / cell cycle / RecA / Rad51 / antisense DNA / 抗癌剤耐性 / p53 / DNA修復 / 分化 / 相同組み換え |
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| Research Abstract |
(1) We demonstrated that cisplatin induced growth suppression followed by induction of differentiation in teratocarcinoma F9 cells. In this study, we investigated the mechanism of the effect of cisplatin for cell cycle progression in F9 cells focusing on the change of p34^<cdc2>. By the treatment, the level of the expressionof cdc2 mRNA did not change, but the half life of p34^<cdc2> was greatly reduced, which would result in the arrest the cell cycle at the late S to G2/M.
(2) The mammalian Rad51 gene is a homolog of the yeast Rad5l and E.coli RecA genes, which are related to the repair of DNA double-strand breaks and are also involved in recombination repair and various SOS responses to DNA damage by g-irradiation and alkylating agent like anticancer agent. In this study, we demonstrated that Rad51 antisense oligonucleotides enhances the radiosensityivity of mouse malignant gliomas in vivo and in vitro, suggesting the potentiation for radiation therapy in malignant gliomas by inhibiting DNA double-strand break repair.
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