Cancer development and therapy resistance are driven by chromosomal instability (CIN), which causes chromosome gains and losses (i.e., aneuploidy) and structural chromosomal alterations. Technical limitations and knowledge gaps have delayed therapeutic targeting of CIN and aneuploidy in cancers. However, our toolbox for creating and studying aneuploidy in cell models has greatly expanded recently. Moreover, accumulating evidence suggests that seven conventional antimitotic chemotherapeutic drugs achieve clinical response by inducing CIN instead of mitotic arrest, although additional anticancer activities may also contribute . In this review, we discuss these recent developments. We also highlight new discoveries, which together show that 25 chromosome arm aneuploidies (CAAs) may be targetable by 36 drugs across 14 types of cancer. Collectively, these advances offer many new opportunities to improve cancer treatment.

中文翻译：

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针对癌症中的染色体不稳定性和非整倍性

癌症的发展和治疗耐药性是由染色体不稳定性（CIN）驱动的，它会导致染色体的获得和丢失（即非整倍性）和染色体结构改变。技术限制和知识差距延迟了癌症中 CIN 和非整倍性的治疗目标。然而，我们用于在细胞模型中创建和研究非整倍性的工具箱最近已大大扩展。此外，越来越多的证据表明，七种传统的抗有丝分裂化疗药物通过诱导 CIN 而不是有丝分裂停滞来实现临床反应，尽管额外的抗癌活性也可能有所贡献。在这篇评论中，我们讨论了这些最新进展。我们还重点介绍了一些新发现，这些发现共同表明 25 条染色体臂非整倍体 (CAA) 可能是 14 种癌症中 36 种药物的靶点。总的来说，这些进步为改善癌症治疗提供了许多新的机会。