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Radiation-Induced Delayed Genome Instability and Hypermutation in Mammalian Cells
https://repo.qst.go.jp/records/58417
https://repo.qst.go.jp/records/584178f7e318a-eae3-4529-b2c9-fc543531b9d8
| Item type | 一般雑誌記事 / Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2014-02-14 | |||||
| タイトル | ||||||
| タイトル | Radiation-Induced Delayed Genome Instability and Hypermutation in Mammalian Cells | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | article | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Allen, Christopher
× Allen, Christopher× Fujimori, Akira× Okayasu, Ryuichi× Nickoloff, Jac× 藤森 亮× 岡安 隆一 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | 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, sug- gesting that an early step in carcinogenesis is the acquisition of a “genome instabil- ity” (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 gen- erations 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. | |||||
| 書誌情報 |
Stress-Induced Mutagenesis 発行日 2013-09 |
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| 出版者 | ||||||
| 出版者 | Springer Science+Business Media | |||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | DOI 10.1007/978-1-4614-6280-4_9 | |||||
