有效地检测和治疗癌症需要掌握它作为体细胞和肿瘤宏进化的疾病特性。这种认识对于避免引发不良反应的治疗方案至关重要，以防止产生不可治疗和致命的肿瘤群体。宏进化与微进化不同，主要是通过核型变化而不是局部化的突变作为遗传变异的主要来源。癌细胞展示了重大的多位点染色体重排列，这些重排列似乎在肿瘤进化历史的许多不同情况下突然发生。这些基因组重构事件有助于解释标记癌症进展中的主要转折点的跃变宏进化变化。至少两种不随机的快速多位点基因组重构模式——染色体破碎和染色体编织——在基因组内的分布以及负责其发生的压力诱导过程的细胞生物学方面明显不同。这些观察结果告诉我们，真核细胞具有在灾难情况下快速重组其基因组的能力。由于染色体破碎和染色体编织已经在人类生殖线和其他真核生物中被鉴定出来，它们提供了一个模型，用于应对导致大规模灭绝的各种应激压力的生物宏进化。 版权所有© 2021 Elsevier Ltd。保留所有权利。

Detecting and treating cancer effectively involves understanding the disease as one of somatic cell and tumor macroevolution. That understanding is key to avoid triggering an adverse reaction to therapy that generates an untreatable and deadly tumor population. Macroevolution differs from microevolution by karyotype changes rather than isolated localized mutations being the major source of hereditary variation. Cancer cells display major multi-site chromosome rearrangements that appear to have arisen in many different cases abruptly in the history of tumor evolution. These genome restructuring events help explain the punctuated macroevolutionary changes that mark major transitions in cancer progression. At least two different nonrandom patterns of rapid multisite genome restructuring - chromothripsis ("chromosome shattering") and chromoplexy ("chromosome weaving") - are clearly distinct in their distribution within the genome and in the cell biology of the stress-induced processes responsible for their occurrence. These observations tell us that eukaryotic cells have the capacity to reorganize their genomes rapidly in response to calamity. Since chromothripsis and chromoplexy have been identified in the human germline and in other eukaryotes, they provide a model for organismal macroevolution in response to the kinds of stresses that lead to mass extinctions.Copyright © 2021 Elsevier Ltd. All rights reserved.