癌细胞中常见的中心粒数量增加，但中心粒扩增在癌症发展过程中的作用、发生的方式和时间尚不清楚。一种产生具有额外中心粒的癌细胞的机制是全基因组倍增（WGD），这种事件发生在超过30％的人类肿瘤中，并与预后差相关。新形成的四倍体细胞在WGD过程中可以获得额外的中心粒，而一个广泛接受的模型认为四倍体细胞中的中心粒扩增通过生成非整倍体和染色体不稳定性促进了癌症进展。然而，最近的研究结果表明，体外形成的四倍体细胞失去了多极细胞分裂，以防止其额外的中心粒。这些证据不支持持续的中心粒扩增，而是引发了一个可能性，即对于四倍体细胞来说，最初恢复中心粒数量的稳态，并且在癌症演变的后期阶段重新获得额外的中心粒可能是有益的。在本综述中，我们探讨了新形成的四倍体细胞可选的不同进化路径，它们对后代细胞中中心粒和染色体数量分布的影响，以及它们长期存活的概率。然后，我们讨论了可能改变四倍体细胞中中心粒和染色体数量的机制，以及它们与WGD后癌症进展的相关性。版权所有 ©2023 Bloomfield和Cimini。

An increase in centrosome number is commonly observed in cancer cells, but the role centrosome amplification plays along with how and when it occurs during cancer development is unclear. One mechanism for generating cancer cells with extra centrosomes is whole genome doubling (WGD), an event that occurs in over 30% of human cancers and is associated with poor survival. Newly formed tetraploid cells can acquire extra centrosomes during WGD, and a generally accepted model proposes that centrosome amplification in tetraploid cells promotes cancer progression by generating aneuploidy and chromosomal instability. Recent findings, however, indicate that newly formed tetraploid cells in vitro lose their extra centrosomes to prevent multipolar cell divisions. Rather than persistent centrosome amplification, this evidence raises the possibility that it may be advantageous for tetraploid cells to initially restore centrosome number homeostasis and for a fraction of the population to reacquire additional centrosomes in the later stages of cancer evolution. In this review, we explore the different evolutionary paths available to newly formed tetraploid cells, their effects on centrosome and chromosome number distribution in daughter cells, and their probabilities of long-term survival. We then discuss the mechanisms that may alter centrosome and chromosome numbers in tetraploid cells and their relevance to cancer progression following WGD.Copyright © 2023 Bloomfield and Cimini.