@article{oai:repo.qst.go.jp:00058252,
 author = {Allen, Christopher and Fujimori, Akira and Okayasu, Ryuichi and Nickoloff, Jac and アレン クリストファー and 藤森 亮 and 岡安 隆一},
 journal = {Stress-Induced Mutagenesis},
 month = {},
 note = {Genome instability is a hallmark of cancer cells. Inherited cancer predisposition syndromes typically show defects in DNA repair or DNA damage checkpoint systems, collectively called the DNA damage response (DDR). Several mutations in key genes are required to convert a normal cell to a cancer cell, suggesting that an early step in carcinogenesis is the acquisition of a 'genome instability' (mutator) phenotype. DDR proteins suppress cancer by preventing spontaneous damage from causing excessive genome instability, and thus, normal cells display very low mutation rates and stable genomes. Genotoxins such as DNA-reactive chemicals and radiation cause DNA damage that results in small- and large-scale genetic change (mutations). Recently it has become clear that radiation, including ionizing radiation (IR) such X-rays and charged particles (heavy ion radiation), as well as nonionizing radiation (UV light) induce genome instability many cell generations after the exposure. These delayed effects are seen after high (1-10 Gy) and very low (0.01-0.1 Gy) IR doses, and include hypermutation, hyper-homologous recombination, chromosome instability, and reduced clonogenic survival (delayed death). Similar to immediate effects of radiation, delayed effects show adaptive responses. Here we focus on potential mechanisms that underlie radiation-induced delayed genome instabilities, and discuss the risks of genome destabilizing effects of occupational and accidental radiation exposures, and clinical exposures associated with radiation therapy and diagnostic imaging procedures.},
 pages = {183--198},
 title = {Radiaiton-induced delayed genome instability and hypermutation in mammalian cells},
 year = {2013}
}