A subset of chromosomal translocations related to B cell malignancy in human patients arises due to DNA breaks occurring within defined 20–600 base pair (bp) zones. Several factors influence the breakage rate at these sites including transcription, DNA sequence, and topological tension. These factors favor non-B DNA structures that permit formation of transient single-stranded DNA (ssDNA), making the DNA more vulnerable to agents such as the enzyme activation-induced cytidine deaminase (AID) and reactive oxygen species (ROS). Certain DNA lesions created during the ssDNA state persist after the DNA resumes its normal duplex structure. We propose that factors favoring both formation of transient ssDNA and persistent DNA lesions are key in determining the DNA breakage mechanism.

人类患者中与B细胞恶性肿瘤相关的染色体易位子集是由于在20-600个碱基对（bp）区域内发生DNA断裂而引起的。有几个因素会影响这些位点的断裂速率，包括转录，DNA序列和拓扑张力。这些因素有利于允许形成瞬时单链DNA（ssDNA）的非B DNA结构，从而使DNA更容易受到诸如酶激活诱导的胞苷脱氨酶（AID）和活性氧（ROS）等物质的破坏。在DNA恢复其正常的双链体结构后，在ssDNA状态期间产生的某些DNA损伤仍然存在。我们建议有利于瞬时ssDNA的形成和持续性DNA损伤的因素是确定DNA断裂机制的关键。