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目的 探讨p16基因结构及启动子区CPG岛甲基化在多发性骨髓瘤 (MM)发病中的作用。方法 利用PCR 单链构象多态性、甲基化特异性PCR(MSP)技术研究骨髓瘤细胞株U2 66、LP1、KM3及MM患者p16基因结构改变及启动子区CPG岛甲基化状态。结果 KM3细胞株为p16基因外显子 2的同源缺失 ;U2 66、LP1细胞株及 5 5 .5 6%MM患者的p16基因启动子区存在CPG岛甲基化现象 ,p16基因甲基化与MM分期无关 (P >0 .0 5 )。结论 p16基因甲基化在MM中较为常见 ,这可能为MM的治疗提供借鉴。
Objective To investigate the role of p16 gene structure and promoter region CPG island methylation in the pathogenesis of multiple myeloma (MM). Methods The single strand conformation polymorphism (PCR) and methylation specific PCR (MSP) were used to study the structural changes of p16 gene and the methylation status of CPG in the promoter region of myeloma cell lines U2 66, LP1, KM3 and MM. Results KM3 cell line was homologous deletion of exon 2 of p16 gene. Methylation of CPG island was found in promoter region of p16 gene in U2 66, LP1 cell lines and 55.6% MM patients. Methylation of p16 gene No correlation with MM staging (P> 0.05). Conclusion The methylation of p16 gene is more common in MM, which may provide a reference for the treatment of MM.