白血病患者外周血淋巴细胞微核分析

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目的:应用微核分析技术检测初诊白血病患者的遗传损伤。方法:应用细胞周期阻断法检测54例初诊白血病患者(CML11例,AML-M1 7例,AML-M2 6例,AML-M3 4例,AML-M4 2例,AML-M5 4例,AML-M6 2例,ALL18例)和30例健康人外周血,以微核率(micronucleus rate,MNR)、微核细胞率(micronucleus cell rate,MCR)、核芽(nuclear bud,Bud)率、核质桥(nucleoplasmic bridge,NPB)率、核分裂指数(nucleus division index,NDI)、凋亡细胞(apoptotic cells,AC)率结合染色体中期分析、融合基因和基因重排检测作为染色体损伤指标分析初诊白血病患者的遗传损伤。结果:54例初诊白血病患者外周血的MNR[(17.368±1.305)‰vs(7.368±0.844)‰]、MCR[(15.418±1.212)‰vs(5.887±1.101)‰]、Bud率[(8.142±0.132)%vs(0.404±0.404)%]、NPB率[(5.724±0.874)%vs(0.034±0.034)%]、NDI[(1.722±0.062)%vs(2.282±0.324)%]、AC率[(2.167±0.333)%vs(0.167±0.667)%]、异常染色体检出率(24.00%)、融合基因或基因重排阳性率(18.00%)均明显异于健康人(P<0.05或P<0.01)。结论:白血病患者发病初期即有不同程度的遗传损伤,提示染色体不稳定造成的遗传损伤与白血病发病密切相关。 Objective: To detect the genetic damage of newly diagnosed leukemia patients by micronucleus analysis. Methods: A total of 54 patients with newly diagnosed leukemia were studied by cell cycle arrest (CML 11, AML-M1 7, AML-M2 6, AML-M3 4, AML-M4 2, AML- M6 in 2 cases and ALL in 18 cases) and 30 healthy volunteers. The micronucleus rate (MNR), micronucleus cell rate (MCR), nuclear bud (Bud) (NPB) rate, nucleus division index (NDI), apoptotic cells (AC) rate combined with chromosomal metaphase analysis, fusion gene and gene rearrangement as chromosomal damage markers in patients with newly diagnosed leukemia Genetic damage. Results: The MNR of the peripheral blood of 54 newly diagnosed leukemia patients was significantly higher than that of the untreated leukemia patients (MNR [(17.368 ± 1.305) ‰ vs (7.368 ± 0.844) ‰] and MCR [(15.418 ± 1.212) 0.132% vs 0.404 ± 0.404%, NPB rate (5.724 ± 0.874)% vs (0.034 ± 0.034)%, NDI (1.722 ± 0.062)% vs (2.282 ± 0.324)%, (2.167 ± 0.333)% vs (0.167 ± 0.667)%, the rate of abnormal chromosome (24.00%) and the positive rate of fusion gene or gene rearrangement (18.00%) were significantly different from those in healthy people (P <0.05 or P < 0.01). Conclusion: The onset of leukemia patients have different degrees of genetic damage, suggesting that chromosomal instability caused by genetic damage and the incidence of leukemia are closely related.
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