CAJ | 학술논문

目的探讨吸烟与IL1B基因多态性、非小细胞肺癌(NSCLC)遗传易感性之间的关系.方法本文采用病例-对照研究,对889例肺癌患者和1005例性别、年龄与之相匹配的健康对照中IL1B rs1143623 G＞C和rs12621220 G＞A两个单核苷酸多态性位点(SNP)进行基因分型,并统计分析各基因型频率分布、吸烟与NSCLC患病的关系.结果 ①吸烟影响NSCLC易感性:有吸烟史的人群NSCLC患病风险较无吸烟史的人群高(校正性别、年龄、吸烟量等因素后,OR =3.744,95％ CI =2.885 ～4.858;P=2.980 ×10-23);对有吸烟史的人群分析后发现高吸烟量增加NSCLC的风险(P =4.350×10-29);进一步发现戒烟人群的吸烟量显著高于持续吸烟人群的吸烟量(P =0.016),持续吸烟但低吸烟量对NSCLC易感性有显著保护作用(校正性别、年龄、吸烟量等因素后,OR=0.219,95％ CI =0.164～0.291;P=2.233 × 10-25),即高吸烟量增加NSCLC风险;②吸烟因素影响IL1B rs1143623G＞C和rs12621220G＞A与NSCLC易感性的关联:在戒烟人群中,rs1143623G ＞C位点GC基因型对NSCLC发生具有较低限度的保护效应(校正性别、年龄、吸烟量等因素后,OR=0.543,95％ CI =0.291 ～1.011;P=0.054),该种保护作用相对稳固,表现为联合GC+CC基因型仍然对NSCLC有保护作用(校正OR=0.563,95％ CI =0.313 ～ 1.013;P=0.055),进一步亚组分析发现,此种保护效应主要体现在对腺癌(ADC)的保护(校正OR=0.491,95％ CI=0.241 ～1.001;P=0.050);rs12621220 G＞A位点GA基因型对NSCLC发生具有保护效应(校正OR =0.427,95％ CI=0.210～0.868;P=0.019),此种保护效应主要是与ADC相关.结论 IL1B基因多态性与NSCLC易感性和吸烟行为相关.
목적 탐토흡연여IL1B기인다태성、비소세포폐암(NSCLC)유전역감성지간적관계.방법 본문채용병례-대조연구,대889례폐암환자화1005례성별、년령여지상필배적건강대조중IL1B rs1143623 G＞C화rs12621220 G＞A량개단핵감산다태성위점(SNP)진행기인분형,병통계분석각기인형빈솔분포、흡연여NSCLC환병적관계.결과 ①흡연영향NSCLC역감성:유흡연사적인군NSCLC환병풍험교무흡연사적인군고(교정성별、년령、흡연량등인소후,OR =3.744,95％ CI =2.885 ～4.858;P=2.980 ×10-23);대유흡연사적인군분석후발현고흡연량증가NSCLC적풍험(P =4.350×10-29);진일보발현계연인군적흡연량현저고우지속흡연인군적흡연량(P =0.016),지속흡연단저흡연량대NSCLC역감성유현저보호작용(교정성별、년령、흡연량등인소후,OR=0.219,95％ CI =0.164～0.291;P=2.233 × 10-25),즉고흡연량증가NSCLC풍험;②흡연인소영향IL1B rs1143623G＞C화rs12621220G＞A여NSCLC역감성적관련:재계연인군중,rs1143623G ＞C위점GC기인형대NSCLC발생구유교저한도적보호효응(교정성별、년령、흡연량등인소후,OR=0.543,95％ CI =0.291 ～1.011;P=0.054),해충보호작용상대은고,표현위연합GC+CC기인형잉연대NSCLC유보호작용(교정OR=0.563,95％ CI =0.313 ～ 1.013;P=0.055),진일보아조분석발현,차충보호효응주요체현재대선암(ADC)적보호(교정OR=0.491,95％ CI=0.241 ～1.001;P=0.050);rs12621220 G＞A위점GA기인형대NSCLC발생구유보호효응(교정OR =0.427,95％ CI=0.210～0.868;P=0.019),차충보호효응주요시여ADC상관.결론 IL1B기인다태성여NSCLC역감성화흡연행위상관.
Objective The purpose of this study was to explore the association among IL1B polymorphisms,smoking and the risks of non-small cell lung cancer.Methods IL1B polymorphisms (rs1143623G ＞ A,rs12621220G ＞ C) were genotyped in 889 non-small cell lung cancer (NSCLC) cases and 1005 healthy controls.Results The results showed that smoking affected NSCLC susceptibility:People with smoking history have much higher risk of NSCLC than people without smoking history (after adjustment for factors,such as gender,age,pack-year,OR =3.744,95％ CI =2.885 ～ 4.858; P =2.980 × 10-23); Furthermore,people with higher smoking pack-years have much higher risk of NSCLC than those with lower smoking pack-years (P =4.350 × 10-29),and the persistent smokers who smoked lower pack-years,has significant protective effect on NSCLC susceptibility (aOR =0.219,95％ CI =0.164 ～ 0.291 ; P =2.233 × 10-25) than the people quitted smoking but smoked more pack-years (P =0.016).In addition,we found that the associations between NSCLC susceptibility and ILl B polymorphisms was influenced by smoking status.The logistic regression analysis results showed that:For rs 1143623,compared with the GG genotype,GC was significantly associated with decreased risk of NSCLC for the people of smoking cessation (aOR =0.543,95％ CI =0.291 ～ 1.011 ; P =0.054),and this protection was relatively stable when combined with CC genotype (aOR =0.563,95％ CI =0.313 ～ 1.013 ; P =0.055).In subgroups analysis we found that this protective effect was mainly existed in the subgroup of adenocarcinoma (ADC) (OR =0.491,95 ％ CI =0.241 ～ 1.001 ; P =0.050).For rs12621220,compared with the GG genotype,GA was significantly associated with decreased risk of NSCLC for the people of smoking cessation (OR =0.427,95％ CI =0.210 ～ 0.868 ; P =0.019),and this protective effect was mainly related to the ADC,combined with AA genotype,the protective effect did not disappear (OR =0.479,95％ CI =0.248 ～ 0.925 ; P =0.029).Conclusion Smoking status modified the associations between IL1 B polymorphisms and NSCLC susceptibility.