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目的探讨恶性肿瘤细胞染色体不稳定性的可能机制。方法采用本实验室建立的kinetochore-NOR同步银染技术,对SW626细胞染色体kinetochore变异进行分析。结果与正常人外周血细胞相比,SW626细胞染色体kineto-chore缺失[132(0.89%)vs26(0.18%)]、kinetochore迟滞复制[82(0.55%)vs14(0.10%)]和kinetochore-NOR融合[153(1.03%)vs51(0.37%)]频率显著升高(P<0.01),而不对称kinetochore频率二者差异性不显著(P>0.05)。此外,在某些SW626细胞染色体上还观察到多重kinetochores现象。结论 kinetochore缺失、kinetochore迟滞复制和kinetochore-NOR融合可能是SW626细胞染色体非整倍性变异起源的诱因之一;染色体多重kinetochores可能是恶性肿瘤细胞染色体结构畸变产生的重要途径之一。
Objective To investigate the possible mechanism of chromosomal instability in malignant tumor cells. Methods The kinetochore variation of SW626 cells was analyzed by kinetochore-NOR synchronous silver staining technique established in our laboratory. Results Chromosome kineto-chore deletion [132 (0.89%) vs26 (0.18%)], kinetochore hysterectomy [82 (0.55%) vs14 (0.10%)] and kinetochore-NOR fusion in SW626 cells compared with normal human peripheral blood [ 153 (1.03%) vs 51 (0.37%)] (P <0.01), while the asymmetry kinetochore frequency had no significant difference (P> 0.05). In addition, multiple kinetochores were also observed on some SW626 cell chromosomes. Conclusion Kinetochore deletion, kinetochore hysteresis replication and kinetochore-NOR fusion may be one of the inducing factors of SW626 cell chromosome aneuploidy mutation origin. Chromosome multiple kinetochores may be one of the important pathways of chromosome aberration in malignant tumor cells.