Chromosome instability (CIN) and aneuploidy are hallmarks of cancer cells, typically associated with aggressiveness and poor outcomes. Historically, the causative link between aneuploidy and cancer has been difficult to study due to its intrinsic complexity and the poor fitness of aneuploid cells. In this issue of Genes & Development, two companion papers (Trakala and colleagues [pp. 1079–1092] and Shoshani and colleagues [pp. 1093–1108]) exploited sophisticated mouse models to study the progression of aneuploidy from early phases to established tumors. Both groups observed that, while in the early nontumoral cells aneuploidy is characterized by random chromosomal gains, established tumors display a stereotypic karyotype with recurrent gains of only a few chromosomes. Thus, aneuploidy in tumors is not random but shows reproducible patterns of chromosomal changes induced by mechanisms that these two studies are beginning to unveil.

中文翻译：

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解决癌症中非整倍性的染色体难题

染色体不稳定性 (CIN) 和非整倍性是癌细胞的标志，通常与侵袭性和不良结果有关。从历史上看，由于其内在的复杂性和非整倍体细胞的适应性差，非整倍体与癌症之间的因果关系一直难以研究。在本期《基因与发展》中, 两篇配套论文（Trakala 及其同事 [pp. 1079–1092] 和 Shoshani 及其同事 [pp. 1093–1108]）利用复杂的小鼠模型来研究非整倍性从早期阶段到确定肿瘤的进展。两组都观察到，虽然在早期的非肿瘤细胞中，非整倍体的特征是随机染色体增加，但已建立的肿瘤显示出一种刻板的核型，只有少数染色体反复增加。因此，肿瘤中的非整倍性不是随机的，而是显示出由这两项研究开始揭示的机制引起的可重复的染色体变化模式。