信号传导与转录激活因子3基因多态性与肝细胞癌的关系

Associations of signal transducer and activators of transcription 3 polymorphism with the susceptibility to hepatitis B virus-related hepatocellular carcinoma

目的 探讨信号传导与转录激活因子3（signal transducer and activators of transcription 3,STAT3）基因启动子区-1096G/C多态性与乙肝表面抗原（HBsAg）阳性肝细胞癌（hepatocellular carcinoma,HCC）易感性之间的关系.方法 采用病例-对照研究方法,应用荧光探针实时定量PCR法对2009至2012年在上海某医院就诊的632例HCC患者和723名非HCC乙肝病毒（HBV）感染者的STAT3基因启动子区-1096G/C基因多态性进行检测,使用单因素分析方法确定该基因多态性OR（95％ CI）值.结果 对照组、病例组携带STAT3-1096C（GC＋ CC）基因型者分别占61.8％ （447/723）、60.6％（383/632）,不同基因型之间HCC发病风险差异无统计学意义（OR =0.95,95％ CI：0.76～1.18）.以性别进行分层分析,在男性人群中,对照组、病例组携带STAT3-1096 C（GC＋ CC）基因型者分别占62.2％（314/505）、61.8％（331/536）,在女性人群中,分别为61.0％（133/218）、54.17％ （52/96）,在男性和女性人群中,不同基因型HCC发病风险差异均没有统计学意义（OR=0.98,95％ CI：0.77～1.26;OR =0.76,95％CI：0.47 ～ 1.26）.以HBV基因型进行分层分析,在HBV B型感染者中,对照组、病例组携带STAT3-1096C（GC＋ CC）基因型者分别占61.5％（110/179）、53.1％（34/64）,在HBV C型感染者中,对照组、病例组携带STAT3-1096C（GC＋CC）基因型者分别占62.9％（276/439）、60.3％（226/375）,在HBV B或C型感染者中,不同基因型患者HCC发病风险差异没有统计学意义（OR =0.71,95％ CI：0.40～1.26;OR =0.90,95％ CI：0.68～ 1.19）.结论 STAT3-1096G/C基因多态性与HBV阳性HCC的易感性没有相关性.

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： O. 77-1.26; OR =0. 76, 95% CI： O. 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）. Conclusion STAT3 -1096G/C polymorphism was not associated with the susceptibility to HCC for the HBV-infeeted subjects without HCC.