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ZHAO Hong-yun, CHEN Yun-xian, ZHONG Xue-yun, HUANG Ying-qiang. 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: ZHAO Hong-yun, CHEN Yun-xian, ZHONG Xue-yun, HUANG Ying-qiang. 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

Clinical Relationship between Tumor Necrosis Factor Genetic Polymorphisms and Multiple Myeloma

  • 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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