Ganem Neil J, Storchova Zuzana, Pellman David
Department of Pediatric Oncology, Dana-Farber Cancer Institute, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Curr Opin Genet Dev. 2007 Apr;17(2):157-62. doi: 10.1016/j.gde.2007.02.011. Epub 2007 Feb 26.
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.
非整倍体是正常细胞与癌细胞之间最明显的差异之一。然而，关于非整倍体细胞如何产生以及它们是否是肿瘤发生的原因或结果，仍存在争议。一种产生非整倍体癌细胞的途径是通过不稳定的四倍体中间体。支持这一观点的是，最近的研究表明四倍体在体内促进染色体畸变和肿瘤发生。这些四倍体细胞可通过多种机制产生，包括有丝分裂滑脱、胞质分裂失败和病毒诱导的细胞融合。此外，新的研究表明可能不存在永久阻止四倍体细胞增殖的倍性感应检查点。因此，四倍体细胞的异常分裂可能会促进导致非整倍体癌症的基因变化。
