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肿瘤坏死因子基因多态性与多发性骨髓瘤的临床相关关系[J]. 肿瘤防治研究, 2005, 32(12): 764-767. DOI: 10.3971/j.issn.1000-8578.582
引用本文: 肿瘤坏死因子基因多态性与多发性骨髓瘤的临床相关关系[J]. 肿瘤防治研究, 2005, 32(12): 764-767. DOI: 10.3971/j.issn.1000-8578.582
Clinical Relationship between Tumor Necrosis Factor Genetic Polymorphisms and Multiple Myeloma[J]. Cancer Research on Prevention and Treatment, 2005, 32(12): 764-767. DOI: 10.3971/j.issn.1000-8578.582
Citation: Clinical Relationship between Tumor Necrosis Factor Genetic Polymorphisms and Multiple Myeloma[J]. Cancer Research on Prevention and Treatment, 2005, 32(12): 764-767. DOI: 10.3971/j.issn.1000-8578.582

肿瘤坏死因子基因多态性与多发性骨髓瘤的临床相关关系

Clinical Relationship between Tumor Necrosis Factor Genetic Polymorphisms and Multiple Myeloma

  • 摘要: 目的 探讨肿瘤坏死因子α(Tumor necrosis factor alpha,TNFα)基因-308位和淋巴毒素(Lymphotoxin-α,LTα)基因+252住基因多态性与多发性骨髓瘤(Multiple Myeloma,MM)发病、临床及预后的相关关系。方法 用聚合酶链反应(PCR)、限制性内切酶消化及电泳技术,对32名MM患者和72名正常对照者的TNFα和LTα基N的单碱基突变多态性进行检测,并收集病人组的临床资料,进行生存状况分析。结果 (1)MM病人TNF两位点基因型频率、等住基因频率、联合单倍体分型中各型的频率与对照组比较差异均无统计学意义(P〉0.05);(2)比较MM病人两位点联合单倍体分型在不同性别、分期、肿瘤负荷、血红蛋白、血钙、血肌酐中的分布,没有发现显著性差异(P〉0.05);(3)用KaplanMeier方法进行生存分析,没有发现高危型与低危型的总生存时间有显著性差异:在高危型组和低危型组,2年生存率和4年生存率差异无统计学意义(P〉0.05);Cox回归模型显示两位点联合单倍体分型不是影响预后的危险因素(P〉0.05)。结论 本组研究显示TNFα-308位、LTα+252住基因多态性在MM病人发病的易感性、临床和预后中可能不起重要作用。

     

    Abstract: Objective  This study was designed to investigate the relationship between-308bp polymorphism in tumor necrosis factor-α( TNFα) gene and + 252bp in lymphotoxin-α(L Tα) gene and the pathogenesis, clinical course and outcome of multiple myeloma (MM) . Methods  The single base change polymorphism in TNFα gene and L Tα gene were analyzed among 32 chinese patient s with MM and 72 normal controls by using PCR-rest rictive f ragment length polymorphism ( RFL P) . The clinical data were collected and survival analysis was performed. Results  (1) The difference of dist ribution of genotypes, alleles of TNFα ( 3/ 308), L Tα( + 252) and TNF/ L T polymorphic extended haplotypes between the MM patients and control group were not statistically significant ( P > 0. 05) . (2) In patients group, no statistically significant association was found between the presence of a given TNF/ L T haplotype status and clinical characters such as sex, age, clinical stags, myeloma burthen, hemoglobin, creatinine. (3) The estimated 22year and 42year overall survival rates in the groups of patient s carrying high-risk and low-risk haplotypes were not statistically significant ( P > 0. 05) using Kaplan-Meier method. In multivariate Cox regression models the TNF/L T haplotype status was not found to be risk factors for outcome ( P > 0. 05) . Conclusion  These data suggest that genetic polymorphisms in the TNFα( 3/308), L Tα( + 252) are not crucial in the pathogenesis, clinical course, outcome of MM patients.

     

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