@misc{oai:repo.qst.go.jp:00062881,
 author = {Okayasu, Ryuichi and Kato, Takamitsu and Sekine, Emiko and Okada, Maki and Okabe, Atsushi and 岡安 隆一 and 加藤 宝光 and 関根 絵美子 and 岡田 真希 and 岡部 篤史},
 month = {Oct},
 note = {High LET heavy ion radiation has been successfully used for an alternative radiation treatment for cancer and is also an important component for space radiation. The biological effectiveness of high LET radiation (up to 200keV/um) is, in general, higher than that of low LET radiation such as X-rays and r-rays. One of the main causes of this is thought to be the difference in the way how cells process DNA damage, particularly DNA double strand breaks (DSBs). We have recently shown that the repair of DSBs depends on LET values, and DSB repair deficient cells show less dependency on LETs for their cell survival as well as DSB repair process. The inefficient repair of DSB associated with high LET radiation was also confirmed by a sensitive method, rH2AX assay. This inefficiency seems to result in misrejoining of chromosomes, leading to further severe biological consequences such as cell death and mutation. The misrepair/misrejoining could be shown by fluorescence in situ hybridization (FISH) of chromosomes in irradiated cells. 
\nThe phosphorylation and de-phosphorylation of DNA-PKcs, a key protein for non-homologous end joining (NHEJ), was significantly delayed by irradiation of high LET carbon and iron ions when compared to X-rays. Of interest, this phenomenon was further accentuated in the human NHEJ defective 180BR cells (shown below, Ref.: Radiat. Res. 165: 59-67 (2006)), 第7回　放射線生物学に関する日仏ワークショップ},
 title = {DNA double strand break repair under high and low LET radiation},
 year = {2008}
}