2006 Fiscal Year Final Research Report Summary
Development of innovated radiation therapy applying the molecular mechanisms of double strand break repair.
| Project/Area Number |
17591248
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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 |
Radiation science
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| Research Institution | Chiba University |
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Principal Investigator |
KAWAKAMI Hiroyuki Chiba University, University Hospital, Research Associate, 医学部附属病院, 助手 (30296701)
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| Co-Investigator(Kenkyū-buntansha) |
川田 哲也 千葉大学, 大学院医学研究院, 講師 (60234077)
KAWATA Tetsuya Chiba University, Graduate School of Medicine, Assistant Professor, 大学院医学研究院, 講師 (60234077)
UNO Takashi Chiba University, Graduate School of Medicine, Associate Professor, 大学院医学研究院, 助教授 (30302540)
ISOBE Koichi Chiba University, University Hospital, Assistant Professor, 医学部附属病院, 講師 (80334184)
ITO Hisao Chiba University, Graduate School of Medicine, Professor, 医学部附属病院, 教授 (20095574)
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| Project Period (FY) |
2005 – 2006
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| Keywords | Radiation / DNA repair / ATM / non-homologous end-joining |
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| Research Abstract |
Ionizing radiation induces DNA damages, of which double strand breaks (dsbs) are believed to be the most crucial if not repaired. It is believed that ATM is known to be the one of the most early responding genes. We focused the role of ATM in repairing dsbs through NHEJ and HR. When confluent normal and AT cells are irradiated and subcultured immediately or 24-hour after repair, dsbs are repaired using NHEJ. 24-h repair time reduced chromosome aberrations to around a half compared to immediate plating in normal cells, but similar for AT cells, suggesting that ATM plays an important factor in NHEJ. When exponentially growing cells are irradiated and chromosome aberrations were scored, the frequency of chromatid breaks was a little higher for AT cells compared to normal cells but that of chromatid exchanges was relatively similar between two cell lines, suggesting that ATM may not play an important role in repairing G2 chromatid breaks. siRNA for ATM was used for tumor cells to induce misrepair after irradiation, but due to not enough insertion into cell nuculeus, misrepair induction was not induced this time. Further study is required to induce higher sensitivity of tumor cells by using siRNA.
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