中文摘要：

染色体非整倍性畸变是恶性肿瘤细胞的显著细胞遗传学特征，但其诱发染色体数目不稳定的机制一直尚未阐明。本研究从与染色体分离直接相关的动粒（kinetochore）角度，采用kinetochore—NOR同步银染技术对HEP-2细胞染色体kinetochore变异进行分析，以探讨恶性肿瘤细胞染色体数目变异的形成机制。实验共分析HEP-2细胞分裂相308个，计染色体16962条，正常对照个体外周血细胞分裂相300个，计染色体13800条。结果表明：与正常人外周血细胞相比，HEP-2细胞染色体kinetochore缺失和kinetochore迟滞复制频率显著升高（P〈0．01），而kinetochore—NOR融合频率二者没有显著差异（P〉0．05），这些结果提示kinetochore缺失和kinetochore迟滞复制可能是HEP-2细胞染色体非整倍性变异起源的诱因之一。此外，我们还在某些HEP-2细胞染色体上观察到多重kinetochore现象，并认为染色体多重kinetochore可能是恶性肿瘤细胞染色体结构畸变产生的一个新的途径。

英文摘要：

Chromosomal instability is a marked character in many tumor cells, however the mechanism of this instability has not been clarified up to now. In this study, kinetochore variation of HEP-2 cells were analysized by an improved method for staining kinetochores of human chromosomes in order to probe the mechanism of chromosomal instability of tumor cells. The metaphases of 308 （including 16 962 scored chromosomes） from HEP- 2 cells and 300 （including 13 800 scored chromosomes） from normal control were analyzed under microscope. The results showed that： 1） compared to normal cells, frequency of kinetochore loss, kinetochore duplication laggard and kinetochore dissymmetry in HEP-2 cells were significantly higher than that of control respectively （P〈0.01）. 2） a cytogenentic phenomenon of multi-kinetochores was observed in HEP-2 cells, and we suggested that it might be a new mechanism for inducing chromosomal structure abnormality in tumor cell.