TNF-α 启动子多态性在沙利度胺联合地塞米松治疗多发性骨髓瘤中的作用及其对临床结局的影响。
Role of the TNF-α promoter polymorphisms for development of multiple myeloma and clinical outcome in thalidomide plus dexamethasone.
机构信息
The Key Laboratory of Developmental Genes and Human Disease of Education Ministry, Genetics Research Center, Southeast University Medical School, Nanjing, China.
出版信息
Leuk Res. 2010 Nov;34(11):1453-8. doi: 10.1016/j.leukres.2010.01.011. Epub 2010 Jan 31.
The role of TNF-α promoter polymorphisms in the development of multiple myeloma (MM) were tested in 210 patients and 218 healthy individuals and their impact on the clinical outcome were evaluated in 98 patients treated with thalidomide and dexamethasone (Thal+Dex) regimen. MM patients carrying the GA genotype (P=0.01) or GA+AA genotypes (P=0.02) at the TNF-α -308 polymorphism were associated with a reduced risk for MM. The TNF-α -238 GA+AA genotypes were associated with a significant enhancement in the progression-free survival (PFS) (P=0.009) and a better overall survival (OS) (P=0.088).
研究人员在 210 名多发性骨髓瘤（MM）患者和 218 名健康个体中检测了 TNF-α 启动子多态性在 MM 发病机制中的作用，并在接受沙利度胺和地塞米松（Thal+Dex）方案治疗的 98 名患者中评估了其对临床结局的影响。TNF-α -308 多态性中 GA 基因型（P=0.01）或 GA+AA 基因型（P=0.02）的 MM 患者患 MM 的风险降低。TNF-α -238 GA+AA 基因型与无进展生存期（PFS）的显著改善（P=0.009）和更好的总生存期（OS）（P=0.088）相关。
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