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.

有效地检测和治疗癌症涉及将疾病理解为体细胞和肿瘤宏观进化之一。这种理解是避免引发治疗不良反应的关键，这种不良反应会产生无法治疗的致命肿瘤群。宏观进化与微观进化的不同之处在于核型变化，而不是孤立的局部突变是遗传变异的主要来源。癌细胞显示出主要的多位点染色体重排，这些重排似乎在肿瘤进化历史中的许多不同情况下突然出现。这些基因组重组事件有助于解释标志着癌症进展重大转变的间断宏观进化变化。至少有两种不同的快速多位点基因组重组的非随机模式——染色体碎裂（“染色体破碎”）和染色体复合（“染色体编织”）——在它们在基因组中的分布和负责应激诱导过程的细胞生物学中明显不同他们的发生。这些观察结果告诉我们，真核细胞有能力快速重组其基因组以应对灾难。由于在人类生殖系和其他真核生物中发现了染色体碎裂和染色体折叠，它们为生物体宏观进化提供了一个模型，以响应导致大规模灭绝的各种压力。这些观察结果告诉我们，真核细胞有能力快速重组其基因组以应对灾难。由于在人类生殖系和其他真核生物中发现了染色体碎裂和染色体折叠，它们为生物体宏观进化提供了一个模型，以响应导致大规模灭绝的各种压力。这些观察结果告诉我们，真核细胞有能力快速重组其基因组以应对灾难。由于在人类生殖系和其他真核生物中发现了染色体碎裂和染色体折叠，它们为生物体宏观进化提供了一个模型，以响应导致大规模灭绝的各种压力。