簇状的DNA损伤，也称为多重损伤位点，是电离辐射的标志。它定义为两个或多个损伤的组合，包括链断裂，氧化产生的碱基损伤，一个或两个DNA螺旋匝内的无碱基位点，这些损伤是由单个辐射轨道的通过造成的。DSB聚集的病变将DSB与附近的几个基础损伤和无碱基位点相关联，并被复杂的DSB吸收。非DSB簇状病变包括单链断裂，碱基损伤和无碱基位点。在具有低线性能量转移（LET）的辐射下，例如X射线或γ射线，簇状的DNA损伤比DSB丰富3-4倍。随着LET的增加，它们的比例和复杂性也会增加；它们可能代表了对DNA损害的很大一部分。研究体外使用日益复杂的工程化簇状DNA损伤大大增强了我们对非DSB簇状损伤如何处理的理解。基础切除修复受到损害，在簇内病变的处理中观察到的层次结构导致形成SSB或DSB作为修复中间体，并延长了病变的寿命。结果，突变的机会急剧增加。复杂的DSB，无论是通过辐射直接形成还是通过非DSB簇状病变的处理而形成，都可以通过缓慢的动力学修复或不修复，从而导致细胞死亡或有丝分裂。在存活的细胞中，观察到大的缺失，易位和染色体畸变。

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Clustered DNA lesions, also called Multiply Damaged Sites, is the hallmark of ionizing radiation. It is defined as the combination of two or more lesions, comprising strand breaks, oxidatively generated base damage, abasic sites within one or two DNA helix turns, created by the passage of a single radiation track. DSB clustered lesions associate DSB and several base damage and abasic sites in close vicinity, and are assimilated to complex DSB. Non-DSB clustered lesions comprise single strand break, base damage and abasic sites. At radiation with low Linear Energy Transfer (LET), such as X-rays or γ-rays clustered DNA lesions are 3–4 times more abundant than DSB. Their proportion and their complexity increase with increasing LET; they may represent a large part of the damage to DNA. Studies in vitro using engineered clustered DNA lesions of increasing complexity have greatly enhanced our understanding on how non-DSB clustered lesions are processed. Base excision repair is compromised, the observed hierarchy in the processing of the lesions within a cluster leads to the formation of SSB or DSB as repair intermediates and increases the lifetime of the lesions. As a consequence, the chances of mutation drastically increase. Complex DSB, either formed directly by irradiation or by the processing of non-DSB clustered lesions, are repaired by slow kinetics or left unrepaired and cause cell death or pass mitosis. In surviving cells, large deletions, translocations, and chromosomal aberrations are observed. This review details the most recent data on the processing of non-DSB clustered lesions and complex DSB and tends to demonstrate the high significance of these specific DNA damage in terms of genomic instability induction.