Canoy Reynand Jay, Shmakova Anna, Karpukhina Anna, Shepelev Mikhail, Germini Diego, Vassetzky Yegor
UMR 9018, CNRS, Université Paris Saclay, Institut Gustave Roussy, F-94805 Villejuif, France.
Institute of Human Genetics, National Institutes of Health, University of the Philippines Manila, Manila 1000, Philippines.
Cancers (Basel). 2022 Oct 18;14(20):5110. doi: 10.3390/cancers14205110.
Chromosomal translocations are products of the illegitimate repair of DNA double-strand breaks (DSBs). Their formation can bring about significant structural and molecular changes in the cell that can be physiologically and pathologically relevant. The induced changes may lead to serious and life-threatening diseases such as cancer. As a growing body of evidence suggests, the formation of chromosomal translocation is not only affected by the mere close spatial proximity of gene loci as potential translocation partners. Several factors may affect formation of chromosomal translocations, including chromatin motion to the potential sources of DSBs in the cell. While these can be apparently random events, certain chromosomal translocations appear to be cell-type-specific. In this review, we discuss how chromosomal translocations are formed and explore how different cellular factors contribute to their formation.
染色体易位是DNA双链断裂（DSB）异常修复的产物。它们的形成可导致细胞发生显著的结构和分子变化，这些变化可能在生理和病理方面具有相关性。诱导产生的变化可能会导致诸如癌症等严重的、危及生命的疾病。越来越多的证据表明，染色体易位的形成不仅受到作为潜在易位伙伴的基因座在空间上的紧密接近程度的影响。有几个因素可能会影响染色体易位的形成，包括染色质向细胞中DSB潜在来源的移动。虽然这些可能是明显的随机事件，但某些染色体易位似乎具有细胞类型特异性。在这篇综述中，我们讨论了染色体易位是如何形成的，并探讨了不同的细胞因子如何促成其形成。
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