中文摘要：

目的探讨白细胞介素（IL）6基因启动子区-572位点多态性与男性肝细胞癌（HCC）发生的关系。方法采用以医院为基础的病例对照研究，以500例经肝组织病理学诊断为HCC，且无其他器官肿瘤史的男性患者作为病例组，以同期来自相同医院创伤骨科和眼科的无肿瘤病史、无长期慢性疾病史的男性患者590例作为对照组。应用ABI 7500fast实时荧光定量PCR仪对IL-6基因启动子区-572位点多态性进行分型。采用z。检验和非条件logistc回归模型比较携带不同基因型人群罹患HCC的风险，logistic回归模型进行交互作用分析。结果-572位点G／C等位基因、各基因型频率在病例组和对照组中的分布差异均无统计学意义（P〉0．05）；多因素logistc回归分析发现，男性携带G等位基因个体（CG＋GG）HCC发生风险是CC基因型的1．31倍（95％CI为1．00～1．71）。分层分析显示，在HBV感染者中与CC基因型相比，男性携带CG基因型能增加HCC发生的风险（OR；1．60，95％CI为1．14～2．24）；趋势x2检验结果显示，个体HCC发生风险随携带等位基因G数量的增加而升高织删〈0．05）。Breslow-Day一致胜检验发现HBV感染与IL-6多态性具有交互作用（P〈0．05），HBV感染与携带G等位基因同时存在时的OReg=5．95（95％CI为3．99～8．87），且为超相乘交互作用。结论男性IL-6基因启动子区-572位点多态性可能与HCC发生相关。男性携带G等位基因与HBV感染有超相乘交互作用，两者同时存在可能增加男性HCC发生的风险。

英文摘要：

Objective To study the relationship between the interleukin （IL）6 -572G/C polymorphism and risk of hepatoceUular carcinoma （HCC） in men. Methods A hospital-based case-control study was conducted with 500 male HCC patients without tumor history in other organs and 590 healthy male controls without history of tumors or chronic diseases. All HCC cases were diagnosed by histopathology. The controls were recruited from the Department of Orthopedic Trauma and Ophthalmology at the same hospital. The IL-6 promoter -572G/C polymorphism and its genotype variants were detected by real-time fluorescence quantitative PCR. The Chi-squared test and unconditional logistic regression analyses were applied to determine the risk of HCC among men carrying the different genotype variants. Results The frequencies of alleles and distribution of genotypes in the -572G/C loci were not significantly different between the HCC cases and controls （P〉 0.05）. The Chi-squared test indicated that the polymorphisms of the loci were not associated with HCC in our male population. However, after adjusting by multivariate logistic regression, the odds ratio （OR） of HCC for the G allele （CG＋GG genotypes） carriers was 1.31 （95% confidence interval （CO： 1.00 - 1.71） compared with the CC genotype. Among the male HBV carriers, the CG genotype increased HCC risk significantly （OR = 1.60, 95% C/： 1.14 - 2.24） compared with the CC genotype. A trend test indicated that HCC risk was significantly increased with the numbers of G alleles （P~d 〈 0. 05）. Breslow-Day tests of homogeneity of the ORs indicated an interaction between hepatitis B virus （HBV） infection and polymorphisms of IL-6 （/＇〈0.05）. The synthetic odds ratio （ORog） of I-IBV infection and harboring a G allele was 5.95 （95% C1： 3.99-8.87）, which represented a super multiplication interaction. Conclusion Polymorphism of the IL-6 promoter -572 loci may be associated with HCC occurrence in men. Moreover, there is a super multiplication i