文章：

细胞分裂缺陷与癌症

Cytokinesis defects and cancer

原文发布日期：2018-12-06

DOI: 10.1038/s41568-018-0084-6

类型: Review Article

开放获取: 否

英文摘要：

Whole-genome and centrosome duplication as a consequence of cytokinesis failure can drive tumorigenesis in experimental model systems. However, whether cytokinesis failure is in fact an important cause of human cancers has remained unclear. In this Review, we summarize evidence that whole-genome-doubling events are frequently observed in human cancers and discuss the contribution that cytokinesis defects can make to tumorigenesis. We provide an overview of the potential causes of cytokinesis failure and discuss how tetraploid cells that are generated through cytokinesis defects are used in cancer as a transitory state on the route to aneuploidy. Finally, we discuss how cytokinesis defects can facilitate genetic diversification within the tumour to promote cancer development and could constitute the path of least resistance in tumour evolution.

摘要翻译： 

在实验模型系统中，胞质分裂失败引发的全基因组和中心体复制能够驱动肿瘤发生。然而胞质分裂失败是否真是人类癌症的重要诱因仍未有定论。本综述中，我们总结了人类癌症中频繁观察到的全基因组倍增事件的证据，并探讨了胞质分裂缺陷对肿瘤发生的促进作用。我们概述了胞质分裂失败的潜在诱因，讨论了通过胞质分裂缺陷产生的四倍体细胞如何作为通往非整倍体途中的过渡状态促进癌症发展。最后，我们阐述了胞质分裂缺陷如何促进肿瘤内部的遗传多样性以加速癌症进展，并可能构成肿瘤进化过程中的最小阻力路径。

原文链接：

Cytokinesis defects and cancer