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目的探讨染色体着丝粒点(Cd)的变异与AN3CA细胞和BMDC1细胞染色体非整倍性畸变的关系。方法肿瘤细胞株传代后用常规方法制备染色体,用直接法制备胚胎绒毛组织染色体标本,采用Cd-NOR同步银染分析技术研究AN3CA细胞和BMDC1细胞染色体Cd的变异。结果 1.AN3CA细胞染色体Cd缺失率为1.87%、Cd迟滞复制率为0.19%、小Cd率为1.52%、Cd-NOR融合率为1.88%、与正常人胚胎绒毛细胞染色体Cd相比较,AN3CA细胞染色体Cd缺失、Cd-NOR融合显著升高(P<0.0125),而小Cd、Cd迟滞复制其差异无统计学意义。2.BMDC1细胞染色体Cd缺失率为1.13%、Cd迟滞复制率为1.52%、小Cd率为1.53%、Cd-NOR融合率为0.57%、与正常人胚胎绒毛细胞染色体Cd相比较,BMDC1细胞染色体Cd缺失、Cd迟滞复制显著升高(P<0.0125),而小Cd、Cd-NOR融合其差异无统计学意义。结论 1.AN3CA细胞染色体非整倍性畸变可能主要源于Cd缺失、Cd-NOR融合;2.BMDC1细胞染色体非整倍性畸变可能主要源于Cd缺失、Cd迟滞复制。
Objective To investigate the relationship between chromosome centromere (Cd) mutation and chromosomal aneuploidy aberrations in AN3CA and BMDC1 cells. Methods Chromosomes were prepared by conventional methods after being passaged. Chromosome samples from embryonic chorionic villi were prepared by direct method. The variation of chromosomal Cd in AN3CA cells and BMDC1 cells was analyzed by Cd-NOR synchronous silver staining. Results 1. The rate of chromosome deletion in AN3CA cells was 1.87%, the rate of Cd delayed hysteresis was 0.19%, the rate of small Cd was 1.52%, and the rate of Cd-NOR fusion was 1.88%. Compared with the normal human chorionic villi chromosomes, AN3CA cells Chromosomal Cd was absent, and Cd-NOR fusion was significantly increased (P <0.0125), while no significant difference was found between Cd and Cd hysterosalities. The chromosome deletion rate of BMDC1 cells was 1.13%, the rate of Cd hysteresis replication was 1.52%, the rate of small Cd was 1.53%, and the rate of Cd-NOR fusion was 0.57%. Compared with the normal human chorionic villi chromosome Cd, There was no significant difference between Cd and Cd-NOR fusion in Cd-deficient and Cd-delayed replication (P <0.0125). Conclusion 1.A3CA cell chromosome aneuploidy may be mainly due to Cd deletion, Cd-NOR fusion; 2.BMDC1 cells chromosome aneuploidy may be mainly due to Cd deletion, Cd lag replication.