Mechanism of anticancer agents and carcinogenesis in glioblastoma detected with markers for DNA damege
| Project/Area Number |
23590472
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Hirosaki University |
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Principal Investigator |
KUROSE Akira 弘前大学, 医学(系)研究科(研究院), 教授 (70244910)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | DNA損傷 / DNA修復 / 脳腫瘍 / 核異型 / 多形性 / 増殖能 / γH2AX / 悪性化 / DNA傷害 / DAN二本鎖断裂 / ヒストン / H2AX / グリオーマ / 再発 / 抗癌剤 / テモゾロミド / フローサイトメトリー |
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| Research Abstract |
gamma-H2AX is a useful marker for DNA double strand breaks. Present study revealed that effects of anti-cancer drugs in glioma depend on cell lines, and cell cycle arrest and/or senescence play major roles in the effects. Progression of malignancy in glioma might be associated with inhibition of cell responses for DNA damages, since pathological specimens of glioma showed increasing positivity for H2AX as the grade of the glioma increased. In glioma, lots of nuclei with significant pleomorphism demonstrated both severe DNA damage and positivity for a cell-prolirerating marker. These results implies severe DNA damage induces nuclear pleomorphism and nuclear pleomorphism is not necessarily a direct evidence for malignancy.
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Report
(4 results)
Research Products
(27 results)
