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白介素10基因多态性与肝细胞癌关系 被引量:5

Association of interleukin-10 gene polymorphism with hepatocellular carcinoma
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摘要 目的探讨细胞因子白介素10(IL-10)基因启动子区单核苷酸多态性和环境因素的交互作用与肝细胞癌(HCC)遗传易感性关系。方法采用以医院为基础的病例对照研究方法,选择589例HCC患者为病例组,同期在相同医院住院的597例无肿瘤患者为对照组;应用TaqMan MGB实时荧光定量PCR技术对IL-10基因-819位点和-592位点进行基因分型,采用非条件Logistic回归模型分析比较携带不同基因型者罹患HCC风险,以及基因多态性和环境因素的交互作用。结果 IL-10-819位点CC、CT、TT基因型在2组中分布差异无统计学意义(P>0.05),3种基因型与HCC患病风险无统计学关联(P>0.05);IL-10基因-592位点CC、AC、AA基因型在2组中分布差异无统计学意义(P>0.05),3种基因型与HCC患病风险无统计学关联(P>0.05);交互作用分析结果表明,IL-10基因-819和-592位点单核苷酸多态性与吸烟、饮酒、食鱼生及乙型肝炎表面抗原(HBsAg)阳性等环境因素在HCC发生中存在交互作用。结论 IL-10基因多态性在HCC发生过程中,可能无独立的危险作用,但与吸烟、饮酒、食鱼生及HBsAg阳性等环境因素的交互作用能增加HCC的患病风险。 Objective To investigate the association between interleukin-10(IL-10) promoter polymorphism and environmental factors in hereditary susceptibility to hepatocellular carcinoma.Methods A hospital-based case-control study was conducted in 589 cases with hepatocellular careicnona(HCC) and 597 controls with diseases other than tumor.IL-10 promoter single nucleotide polymorphism(SNP) was determined by real-time polymorphism chain reaction with TaqMan MGB probe.Unconditional logistic regression was used to estimate the odds ratios and 95 confidence intervals.Results For the genotypes of IL-10 on-819 and-592 site,there was no significant difference between cases and controls(P0.05).The genotypes of IL-10 were not associated with hepatocellular carcinoma.But the interaction of cytokine IL-10 promoter polymorphism and environmental factors was associated with hereditary susceptibility to hepatocellular carcinoma.Conclusion The SNPs of IL-10 on-819 and-592 site do not increase the risk of hepatocellular carcinoma themselves,but increase the risk of hepatocellular carcinoma together with environmental factors including smoking,alcohol drinking,eating uncooked fish,and hepatitis B virus infection.
出处 《中国公共卫生》 CAS CSCD 北大核心 2011年第3期309-311,共3页 Chinese Journal of Public Health
基金 国家自然基金(30860247) 广西自然基金(桂科自0832017Z)
关键词 肝细胞癌 细胞因子 基因多态性 遗传易感性 hepatocellular carcinoma cytokine gene polymorphism hereditary susceptibility
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