@misc{oai:repo.qst.go.jp:00072750,
 author = {Xue Lian and 于, 冬 and Yajima, Hirohiko and Furusawa, Yoshiya and Liu, Cuihua and Fujimori, Akira and Wang, Bing and 于 冬 and 矢島 浩彦 and 古澤 佳也 and 劉 翠華 and 藤森 亮 and 王 冰},
 month = {Apr},
 note = {In the past HIMAC experiments, we proved that besides ATM, ATR signaling also participated in the early G2/M checkpoint after ionizing radiation. ATR pathway was found to be more efficiently activated by heavy ion beams compared with X rays in not only ATM deficient/mutant cells but also normal cells. As ATR pathway is overactivated in hepatocellular carcinoma, we further explored whether inhibition of ATR pathway can exhibit radiosensitive effects under different types of radiation (low and high LETs) in hepatocellular carcinoma. Last year, we did some experiments with hepatoma carcinoma cells-HepG2 (p53 wide type), Hep3B (p53 null) and Huh7 (p53 mutant), which indicated that ATR inhibitor had radiosensitizing effects in hepatoma carcinoma cells with different p53 background under different types of radiation. Meanwhile, ATR inhibitor could induce more apoptosis in hepatoma carcinoma cells under X ray irradiation., 平成29 年度HIMAC 共同利用研究成果発表会},
 title = {Differential processing of low and high LET radiation induced DNA damage: Investigation of switch from ATM to ATR signaling},
 year = {2018}
}