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目的探讨8号染色体短臂(8p22)的杂合性缺失(LOH)在慢性粒细胞白血病(CML)发生和演变中的作用。方法采用多聚酶链反应(PCR)扩增、聚丙烯酰胺凝胶电泳和硝酸银染色技术,检测8p22上D8S511和D8S258位点的LOH。结果22例慢性期和8例加速期CML病人在8p22D8S511和D8S258位点均未发生LOH。4例急变期CML病人在D8S511位点上均未检出LOH,仅1例在D8S258位点发生LOH。5例正常对照组均未发生LOH。结论8p22上D8S511位点的LOH与CML各期的发生和演变无关;D8S258位点的LOH与CML慢性期和加速期的发生和演变无关,但可能与CML急变有关。
Objective To investigate the role of heterozygosity deletion (LOH) on chromosome 8 short arm (8p22) in the pathogenesis and evolution of chronic myeloid leukemia (CML). Methods The LOH of D8S511 and D8S258 on 8p22 was detected by polymerase chain reaction (PCR) amplification, polyacrylamide gel electrophoresis and silver nitrate staining. Results In 22 cases of chronic phase and 8 cases of accelerated CML patients, no LOH occurred at 8p22D8S511 and D8S258 sites. Four cases of acute phase CML patients did not detect LOH at D8S511 locus, only one case had LOH at D8S258 locus. None of the 5 normal controls had LOH. Conclusion The LOH of D8S511 locus on 8p22 has nothing to do with the occurrence and evolution of CML stages. LOH at D8S258 site has nothing to do with the occurrence and evolution of CML chronic phase and accelerated phase, but may be related to CML.