Margolis Robert L
Institut de Biologie Structurale J-P Ebel (CEA-CNRS-UJF), 41 rue Jules Horowitz, 38027 Grenoble Cedex 1, France.
Cancer Cell. 2005 Nov;8(5):353-4. doi: 10.1016/j.ccr.2005.10.017.
In tumorigenesis, aneuploidy is frequently preceded by tetraploidy. Major issues include how tetraploidy arises and how cells can effectively respond to this state. Two recent papers address these issues. Shi and King demonstrate that nondisjunction of chromosomes in mitosis frequently results in tetraploidy through mitotic cleavage failure. Fujiwara et al. demonstrate that p53 null tetraploid cells are highly competent to induce tumors in nude mice. Together, these papers emphasize the unique hazard of tetraploidy and the fact that p53 status has an intrinsic capacity to eliminate tetraploid cells and suppress tumorigenesis. This p53-dependent elimination may represent a checkpoint control.
在肿瘤发生过程中,非整倍体常常先于四倍体出现。主要问题包括四倍体是如何产生的,以及细胞如何有效地应对这种状态。最近的两篇论文探讨了这些问题。施和金证明,有丝分裂中染色体不分离常常通过有丝分裂分裂失败导致四倍体。藤原等人证明,p53缺失的四倍体细胞在裸鼠中具有很高的致瘤能力。总之,这些论文强调了四倍体的独特危害,以及p53状态具有消除四倍体细胞和抑制肿瘤发生的内在能力这一事实。这种p53依赖的消除可能代表一种检查点控制。