Studies on Correlation Between Single-Nucleotide Polymorphisms of Tumor Necrosis Factor Gene and Different Stages of Ankylosing Spondylitis

To examine if there is any correlation between ankylosing spondylitis (AS) and TNF-α gene promoter single-nucleotide polymorphisms (SNP) and their associated haplotypes. Using restriction fragment length polymorphism—polymerase chain reaction method, the polymorphism of TNF-α-238, -308, -850, -857,...

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Published in:Cell biochemistry and biophysics 2013-12, Vol.67 (3), p.915-922
Main Authors: Ji, Yinghua, Yang, Xiaoyu, Yang, Lin, Wu, Dapeng, Hua, Fangfang, Lu, Tan, Jia, Jinling, Ma, Chao, Liang, Qiudong
Format: Article
Language:English
Subjects:
Adult
Alleles
Base Sequence
Biochemistry
Biological and Medical Physics
Biomedical and Life Sciences
Biophysics
Biotechnology
Cell Biology
Female
Frequency distribution
Gene Frequency
Genotype
Genotypes
Haplotypes
Humans
Life Sciences
Linkage Disequilibrium
Lymphotoxin-alpha - blood
Lymphotoxin-alpha - genetics
Male
Middle Aged
Original Paper
Pharmacology/Toxicology
Polymorphism, Single Nucleotide
Promoter Regions, Genetic
Severity of Illness Index
Spondylitis, Ankylosing - genetics
Spondylitis, Ankylosing - pathology
Tumor Necrosis Factor-alpha - blood
Tumor Necrosis Factor-alpha - genetics
Young Adult
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description To examine if there is any correlation between ankylosing spondylitis (AS) and TNF-α gene promoter single-nucleotide polymorphisms (SNP) and their associated haplotypes. Using restriction fragment length polymorphism—polymerase chain reaction method, the polymorphism of TNF-α-238, -308, -850, -857, -863 locus, and TNF-β +252 were analyzed in patients with progressive AS, stable AS and control. (1) Neither the genotypes nor the allele frequencies of TNF-α (-308), (-238), (-863), and TNF-β +252 showed differences in each group. TNF-α (-850) CC genotype and C allele frequency distribution was significantly higher in healthy controls group than in the stable and progressive groups. TNF-α (-857) CT, CC genotype, and C, T allele frequency showed differences in all groups. (2) Polymorphism linkage equilibrium test revealed that association of six TNF-α, β gene SNPs with haplotype GACTCG in progressive group is significantly higher than in the stable group and healthy control group ( P  
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Using restriction fragment length polymorphism—polymerase chain reaction method, the polymorphism of TNF-α-238, -308, -850, -857, -863 locus, and TNF-β +252 were analyzed in patients with progressive AS, stable AS and control. (1) Neither the genotypes nor the allele frequencies of TNF-α (-308), (-238), (-863), and TNF-β +252 showed differences in each group. TNF-α (-850) CC genotype and C allele frequency distribution was significantly higher in healthy controls group than in the stable and progressive groups. TNF-α (-857) CT, CC genotype, and C, T allele frequency showed differences in all groups. (2) Polymorphism linkage equilibrium test revealed that association of six TNF-α, β gene SNPs with haplotype GACTCG in progressive group is significantly higher than in the stable group and healthy control group ( P  &lt; 0.05). TNF-α (-857), (-850) gene polymorphism may increase the susceptibility to AS, but do not reflect the disease active state. 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Using restriction fragment length polymorphism—polymerase chain reaction method, the polymorphism of TNF-α-238, -308, -850, -857, -863 locus, and TNF-β +252 were analyzed in patients with progressive AS, stable AS and control. (1) Neither the genotypes nor the allele frequencies of TNF-α (-308), (-238), (-863), and TNF-β +252 showed differences in each group. TNF-α (-850) CC genotype and C allele frequency distribution was significantly higher in healthy controls group than in the stable and progressive groups. TNF-α (-857) CT, CC genotype, and C, T allele frequency showed differences in all groups. (2) Polymorphism linkage equilibrium test revealed that association of six TNF-α, β gene SNPs with haplotype GACTCG in progressive group is significantly higher than in the stable group and healthy control group ( P  &lt; 0.05). TNF-α (-857), (-850) gene polymorphism may increase the susceptibility to AS, but do not reflect the disease active state. The CC genotype and C allele may play a protective role in the pathogenesis of AS. TNF-α (-308) may be a weak indicator reflecting the active state of AS. Haplotype GACTCG may indicate both the susceptibility and the activity of AS.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>23861136</pmid><doi>10.1007/s12013-013-9582-z</doi><tpages>8</tpages></addata></record>
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ispartof Cell biochemistry and biophysics, 2013-12, Vol.67 (3), p.915-922
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subjects Adult
Alleles
Base Sequence
Biochemistry
Biological and Medical Physics
Biomedical and Life Sciences
Biophysics
Biotechnology
Cell Biology
Female
Frequency distribution
Gene Frequency
Genotype
Genotypes
Haplotypes
Humans
Life Sciences
Linkage Disequilibrium
Lymphotoxin-alpha - blood
Lymphotoxin-alpha - genetics
Male
Middle Aged
Original Paper
Pharmacology/Toxicology
Polymorphism, Single Nucleotide
Promoter Regions, Genetic
Severity of Illness Index
Spondylitis, Ankylosing - genetics
Spondylitis, Ankylosing - pathology
Tumor Necrosis Factor-alpha - blood
Tumor Necrosis Factor-alpha - genetics
Young Adult
title Studies on Correlation Between Single-Nucleotide Polymorphisms of Tumor Necrosis Factor Gene and Different Stages of Ankylosing Spondylitis
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