There is unequivocal evidence that telomeres are crucial for cellular homeostasis and that telomere dysfunction can elicit genome instability and potentially initiate events that culminate in cancer. Mounting evidence points to telomeres having a crucial role in driving local and systemic structural rearrangements that drive cancer. These include the classical 'breakage-fusion-bridge' (BFB) cycles and more recently identified genome re-shaping events like kataegis and chromothripsis. In this brief review, we outline the established and most recent advances describing the roles that telomere dysfunction has in the origin of these catastrophic genome rearrangements. We discuss how local and systemic structural rearrangements enable telomere length maintenance, by either telomerase or the alternative lengthening of telomeres, that is essential to sustain cancer cell proliferation.

中文翻译：

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与异常端粒维护相关的基因组重排。

有明确的证据表明端粒对于细胞体内平衡至关重要，端粒功能障碍可引起基因组不稳定，并可能引发癌症高发事件。越来越多的证据表明端粒在驱动癌症的局部和全身结构重排中起着至关重要的作用。这些包括经典的“断裂-融合-桥”（BFB）循环，以及最近发现的基因组重塑事件，例如卡塔吉斯病和色杆菌病。在这篇简短的综述中，我们概述了已建立的最新进展，这些进展描述了端粒功能障碍在这些灾难性基因组重排起源中的作用。我们讨论了局部和全身结构重排如何通过端粒酶或端粒的替代延长来维持端粒的长度，