title: [Associations of signal transducer and activators of transcription 3 polymorphism with the susceptibility to hepatitis B virus-related hepatocellular carcinoma].
abstract: OBJECTIVE
  To evaluate the association of signal transducer and activators of transcription 3 (STAT3) -1096G/C polymorphism in promoter region with the susceptibility to HBsAg positive hepatocellular carcinoma (HCC).
  
  
  METHODS
  A total of 632 patients with HCC and 723 HBV-infected subjects without HCC treated at Changhai Hospital of Shanghai from 2009 to 2012 were included in this case-control study. The polymorphism of STAT3 -1096 G/C was genotyped by Fluorescent probe-Real time quantitative PCR. Univariate analysis was used to calculate the odds ratio (OR) and its 95% confidence interval (CI).
  
  
  RESULTS
  The frequency of genetic allele STAT3 -1096G/C (GC+CC) of control group and case group were 61.83% (447/723) and 60.60% (383/632), while difference of HCC risk was not found among different genotypes (OR = 0.95, 95%CI: 0.76-1.18). When stratified by sex, the frequency of genetic allele STAT3 -1096C (GC+CC) of control group and case group were 62.18% (314/505) and 61.75% (331/536) in men, 61.01% (133/218) and 54.17% (52/96) in women, respectively, while difference of HCC risk was not found among different genotypes (OR = 0.98, 95%CI: 0.77-1.26; OR = 0.76, 95%CI: 0.47-1.26, respectively). When stratified by HBV genotypes, the frequency of genetic allele STAT3 -1096C (GC+CC) of control group and case group were 61.45% (110/179) and 53.13% (34/64) in HBV genotype B, 62.87% (276/439) and 60.27% (226/375) in HBV genotype C, respectively, while difference of HCC risk was not found among different genotypes (OR = 0.71, 95%CI: 0.40-1.26; OR = 0.90, 95%CI: 0.68-1.19, respectively).
  
  
  CONCLUSIONS
  STAT3 -1096G/C polymorphism was not associated with the susceptibility to HCC for the HBV-infected subjects without HCC.
authors.affiliation: Department of Preventive Medicine, Bethune Military Medical NCOs School, Shijiazhuang 050081, China. Email: xiejiaxin1006@163.com.
authors.forename: Jiaxin
authors.initials: J
authors.lastname: Xie
authors.forename: Qiuju
authors.initials: Q
authors.lastname: Gao
authors.forename: Dan
authors.initials: D
authors.lastname: Yang
authors.forename: Tianpeng
authors.initials: T
authors.lastname: Liu
authors.affiliation: Email:gcao@smmu.edu.cn.
authors.forename: Guangwen
authors.initials: G
authors.lastname: Cao
mesh_terms: D000368:Aged; D000483:Alleles; D006528:Carcinoma, Hepatocellular; D016022:Case-Control Studies; D002681:China; D004198:Disease Susceptibility; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006509:Hepatitis B; D006515:Hepatitis B virus; D006801:Humans; D008113:Liver Neoplasms; D008297:Male; D016017:Odds Ratio; D011110:Polymorphism, Genetic; D020641:Polymorphism, Single Nucleotide