Toledo Franck
Genetics of Tumor Suppression, Institut Curie, PSL Research University, Sorbonne University, CNRS UMR3244 Dynamics of Genetic Information, 26 rue d'Ulm, CEDEX 05, 75248 Paris, France.
Cancers (Basel). 2020 Dec 15;12(12):3783. doi: 10.3390/cancers12123783.
Understanding the mechanisms underlying cancer genome evolution has been a major goal for decades. A recent study combining live cell imaging and single-cell genome sequencing suggested that interwoven chromosome breakage-fusion-bridge cycles, micronucleation events and chromothripsis episodes drive cancer genome evolution. Here, I discuss the "interphase breakage model," suggested from prior fluorescent in situ hybridization data that led to a similar conclusion. In this model, the rapid genome evolution observed at early stages of gene amplification was proposed to result from the interweaving of an amplification mechanism (breakage-fusion-bridge cycles) and of a deletion mechanism (micronucleation and stitching of DNA fragments retained in the nucleus).
几十年来，了解癌症基因组进化的潜在机制一直是一个主要目标。最近一项结合活细胞成像和单细胞基因组测序的研究表明，相互交织的染色体断裂-融合-桥循环、微核化事件和染色体碎裂事件推动了癌症基因组的进化。在此，我将讨论基于先前荧光原位杂交数据提出的“间期断裂模型”，该模型也得出了类似结论。在这个模型中，基因扩增早期阶段观察到的快速基因组进化被认为是由一种扩增机制（断裂-融合-桥循环）和一种缺失机制（微核化以及细胞核中保留的DNA片段拼接）相互交织导致的。
