量研学術機関リポジトリ「QST-Repository」は、国立研究開発法人 量子科学技術研究開発機構に所属する職員等が生み出した学術成果（学会誌発表論文、学会発表、研究開発報告書、特許等）を集積しインターネット上で広く公開するサービスです。 Welcome to QST-Repository where we accumulates and discloses the academic research results(Journal Publications, Conference presentation, Research and Development Report, Patent, etc.) of the members of National Institutes for Quantum Science and Technology.
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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.
Differential processing of low and high LET radiation induced DNA damage: Investigation of switch from ATM to ATR signaling
