| Project/Area Number |
14570896
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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 | National Institute of Radiological Sciences |
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Principal Investigator |
FURUSAWA Yoshiya National Institute of Radiological Sciences, Research Center for Charged Particle, Researcher, 重粒子医科学センター, 研究員 (50260237)
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| Co-Investigator(Kenkyū-buntansha) |
AOKI Mizuho National Institute of Radiological Sciences, Research Center for Charged Particle, Researcher, 重粒子医科学センター, 研究員
KAWATA Tetsuya Chiba University, Graduate School on Medicine, Department of Radiation Oncology, Assistant Professor, 大学院・医学研究院・放射線腫瘍学, 助手 (60234077)
ANDO Koichi National Institute of Radiological Sciences, Research Center for Charged Particle, Researcher, 重粒子医科学センター, 研究員 (00159526)
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| Project Period (FY) |
2002 – 2003
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| Keywords | Radiotherapy / Radiosensitivity / DNA damage repair / Heavy-ion beams / Malignant melanomas / Squamous cell carcinomas / High-LET radiations |
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| Research Abstract |
To make clear the difference in therapeutic results of radiotherapy caused by the radiation quality and the kinds of the cancer, survival parameters on different cell lines (10 malignant melanoma : MIM, and 11 squamous cell carcinoma : SCC cells) exposed to X-rays and carbon-beams were analyzed. Ratios of the alpha/beta values or Dq values to X-rays and carbon-beams on MM and SCC cells showed different spectrum. This may suggests the difference in the response to the radiotherapy with X-rays and carbon-beams in MM and SCC. Preliminary experiments on protain expressions on those cells were performed. In addition, to expand the experiments into in vivo systems, the possibility to transplant and/or growth the cells in mice were start to stydy.
LET dependency of the radiosensitivity on each homologous recombination repair (HRR) and non-homologous end-joining (NHEJ) knock-out cells were measured. When cells were lacking both HRR and NHEJ system, or lacking NHEJ and at the cell cycle was at inactive phase of HRR, no increase in radiosensitivity with LET, which is usually observed on normal cells. This suggests the increase in RBE with LET caused by a misrepair of DNA double strand breaks. The same results were found when chromosome aberrations were analyzed, e.g. repair deficient cells showed more than ten timed higher aberrations to the wild cells, showed small LET dependency on the cells but the dependency was clearly observed on the wild cells.
It is believed that the repair of sub-lethal damage from high-LET radiation can be not observed or small. When low-LET radiations were used as the second challenge radiation, the sub-lethal damage repair was clearly observed while the LET of the first radiation is very high.
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