生物
非整倍体
胞质分裂
癌变
有丝分裂
癌症
倍性
染色体不稳定性
遗传学
癌症研究
癌细胞
细胞分裂
变色
细胞生物学
染色体
细胞
DNA损伤
基因组不稳定性
DNA
基因
作者
Neil J. Ganem,Zuzana Storchová,David Pellman
标识
DOI:10.1016/j.gde.2007.02.011
摘要
Aneuploidy is one of the most obvious differences between normal and cancer cells. However, there remains debate over how aneuploid cells arise and whether or not they are a cause or consequence of tumorigenesis. One proposed route to aneuploid cancer cells is through an unstable tetraploid intermediate. Supporting this idea, recent studies demonstrate that tetraploidy promotes chromosomal aberrations and tumorigenesis in vivo. These tetraploid cells can arise by a variety of mechanisms, including mitotic slippage, cytokinesis failure, and viral-induced cell fusion. Furthermore, new studies suggest that there might not be a ploidy-sensing checkpoint that permanently blocks the proliferation of tetraploid cells. Therefore, abnormal division of tetraploid cells might facilitate genetic changes that lead to aneuploid cancers.
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