Individual response to ionizing radiation

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• 作者：Nicolas Foray^a ; ^{nicolas.foray@inserm.fr} ; Michel Bourguignon^b ; ^{michel.bourguignon@irsn.fr} ; Nobuyuki Hamada^c ; ^{hamada-n@criepi.denken.or.jp}
• 关键词：AT ; ataxia telangiectasia ; ATLD ; ataxia-telangiectasia-like disorder ; ATM ; ataxia telangiectasia mutated ; BBC3 ; B-cell lymphoma/leukemia 2 binding component 3 ; BD ; base damage ; BLM ; Bloom ; BRCA1/2 ; breast cancer susceptibility gene 1/2 ; CCNB1 ; cyclin B1 ; CDKN1A ; cyclin-dependent kinase inhibitor 1A ; CHK2 ; cell cycle checkpoint kinase 2 ; CGH ; comparative genomic hybridization ; CS ; Cockayne syndrome ; CTCAE ; common terminology criteria for adverse events ; DDR ; DNA damage response ; DSB ; DNA double-s
• 刊名：Mutation Research/Reviews in Mutation Research
• 出版年：2016
• 出版时间：October-December 2016
• 年：2016
• 卷：770
• 期：part_PB
• 页码：369-386
• 全文大小：901 K
• 卷排序：770

文摘

The human response to ionizing radiation (IR) varies among individuals. The first evidence of the individual response to IR was reported in the beginning of the 20th century. Considering nearly one century of observations, we here propose three aspects of individual IR response: radiosensitivity for early or late adverse tissue events after radiotherapy on normal tissues (non-cancer effects attributable to cell death); radiosusceptibility for IR-induced cancers; and radiodegeneration for non-cancer effects that are often attributable to mechanisms other than cell death (e.g., cataracts and circulatory disease). All the molecular and cellular mechanisms behind IR-induced individual effects are not fully elucidated. However, some specific assays may help their quantification according to the dose and to the genetic status. Accumulated data on individual factors have suggested that the individual IR response cannot be ignored and raises some clinical and societal issues. The individual IR response therefore needs to be taken into account to better evaluate the risks related to IR exposure.