@misc{oai:repo.qst.go.jp:00062522,
 author = {Vares, Guillaume and Bing, Wang and Murakami, Masahiro and Tanaka, Kaoru and KAKIMOTO, AYANA and Eguchi-Kasai, Kiyomi and Nenoi, Mitsuru and Ｇｕｉｌｌａｕｍｅ Ｖａｒｅｓ and 王 冰 and 村上 正弘 and 田中 薫 and 柿本 彩七 and 笠井 清美 and 根井 充},
 month = {Nov},
 note = {In a variety of in vitro and in vivo models, pre-exposure to low priming dose of ionizing radiations is well known to decrease the biological effects of a subsequent higher challenging dose. However, very few data exist concerning the possibility of inducing this phenomenon, called radiation-induced adaptive response (AR), when using high-LET accelerated heavy-ion radiation. In this study, cultured human lymphoblastoid cells (with different p53 status: TK6, AHH-1, NH32) were exposed to X-rays, carbon-ion and neon-ion radiation at various LETs (ranging from 20 to 150 keV/micrometer). Mutation frequency at HPRT locus, radiation-induced cell death, cell cycle effects after irradiation, as well as estimation of DNA double-strand breaks induction and repair by measuring gamma-H2AX phosphorylation kinetics were compared in primed and unprimed cells. Our results suggest that the biological effects resulting from exposure to priming and challenging radiations vary according to irradiation type and LET. An AR to mutagenic effects of heavy-ion radiation at higher LET was observed when cells were exposed to priming doses of X-rays. The ability of low dose and low dose-rate heavy-ion radiation to trigger an AR was also assessed., 日本放射線影響学会　第50回大会},
 title = {Prospective study on adaptive response induction by heavy-ion radiation in human lymphoblastoid cell lines},
 year = {2007}
}