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机构地区:[1]重庆医科大学遗传优生教研室,重庆400016
出 处:《癌变.畸变.突变》2004年第6期335-337,共3页Carcinogenesis,Teratogenesis & Mutagenesis
摘 要:背景与目的:探讨HepG2瘤细胞染色体着丝粒点(Cd)的变异与其非整倍性畸变的关系。材料与方法:用Cd-NOR同步银染分析技术研究HepG2细胞染色体Cd的变异。 结果:HepG2细胞染色体Cd缺失率为2.30%、Cd迟滞复制率为1.02%、小Cd率为2.58%、Cd-NOR融合率为0.64%;与正常人胚胎绒毛细胞染色体Cd变异相比较,HepG2细胞染色体Cd缺失、Cd迟滞复制和小Cd升高,而Cd-NOR融合差异无显著性。结论:HepG2细胞染色体非整倍性畸变的途径可能主要涉及Cd缺失、Cd迟滞复制、小Cd。BACKGROUND & AIM: Centromeric dots(Cd) variation of HepG2 cells and its relation with aneuploidy aberration were studied. MATERIAL AND METHODS: A Cd-NOR in-phase argentums dye analysis technique modified by this laboratory was used to study centromeric dots (Cd) variation of HepG2 cells. RESULTS: Frequency of Cd loss in HepG2 cells was 2.30 % , Frequency of Cd duplication laggard was 1.02 % , Frequency of little Cd was 2.58 %, Frequency of Cd-NOR amalgamation was 0.64 %. Frequency of Cd loss, frequency of Cd duplication laggard and frequency of little Cd in HepG2 cells were significantly higher than that of normal embryonic villi cells(P < 0.05) . Frequency of Cd-NOR amalgamation showed no difference between HepG2 cells and normal embryonic villi. CONCLUSION: Cd loss, Cd duplication laggard and little Cd might be related with aneuploidy aberration of HepG2 cells.
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