中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2008年
28期
1961-1965
,共5页
许东奎%张雪梅%赵平%蔡建春%赵丹%谭文%郭永丽%林东昕
許東奎%張雪梅%趙平%蔡建春%趙丹%譚文%郭永麗%林東昕
허동규%장설매%조평%채건춘%조단%담문%곽영려%림동흔
胰腺肿瘤%环氧化酶2%多态性,单核苷酸
胰腺腫瘤%環氧化酶2%多態性,單覈苷痠
이선종류%배양화매2%다태성,단핵감산
Pancreatic neoplasms%Cyclooxygenase 2%Polymorphism,single nucleotide
目的 探讨环氧化酶(COX)-2基因启动子区的-1290A>G,-1195G>A和-765G>C单核苷酸多态与胰腺癌发生风险的关系.方法 对象包括283例胰腺癌患者和566名正常对照组.采用PCR-限制性片段长度多态方法进行COX-2基因启动子区-1290A>G,-1195G>A和-765G>C多态的基因型分析,不同基因型与单体型携带者发生胰腺癌相对风险度的评估使用比值比(OR)及95%可信区间(CI).结果 多变量Logistic回归分析显示-1195AA和-765GC基因型与胰腺癌发生的风险升高相关,OR值分别为1.75(95% CI=1.16～2.64)和2.53(95% CI=1.43～4.47).单体型分析显示:与A－1290-G-1195-G-765相比较,含有-1195A等位基因的A-1290A-1195G-765和G-1290-A-1195-C-765两种单体型携带者发生胰腺癌的相对风险升高,OR值分别为1.26(95%CI=1.02～1.56)和5.54(95%c,=1.79～17.16).-765CG和-1195AA基因型与吸烟具有交互作用,共同增加胰腺癌发生的风险.结论 COX-2基因启动子区的-1195G>A和-765G>C单核苷酸多态与胰腺癌遗传易感性相关.
目的 探討環氧化酶(COX)-2基因啟動子區的-1290A>G,-1195G>A和-765G>C單覈苷痠多態與胰腺癌髮生風險的關繫.方法 對象包括283例胰腺癌患者和566名正常對照組.採用PCR-限製性片段長度多態方法進行COX-2基因啟動子區-1290A>G,-1195G>A和-765G>C多態的基因型分析,不同基因型與單體型攜帶者髮生胰腺癌相對風險度的評估使用比值比(OR)及95%可信區間(CI).結果 多變量Logistic迴歸分析顯示-1195AA和-765GC基因型與胰腺癌髮生的風險升高相關,OR值分彆為1.75(95% CI=1.16～2.64)和2.53(95% CI=1.43～4.47).單體型分析顯示:與A－1290-G-1195-G-765相比較,含有-1195A等位基因的A-1290A-1195G-765和G-1290-A-1195-C-765兩種單體型攜帶者髮生胰腺癌的相對風險升高,OR值分彆為1.26(95%CI=1.02～1.56)和5.54(95%c,=1.79～17.16).-765CG和-1195AA基因型與吸煙具有交互作用,共同增加胰腺癌髮生的風險.結論 COX-2基因啟動子區的-1195G>A和-765G>C單覈苷痠多態與胰腺癌遺傳易感性相關.
목적 탐토배양화매(COX)-2기인계동자구적-1290A>G,-1195G>A화-765G>C단핵감산다태여이선암발생풍험적관계.방법 대상포괄283례이선암환자화566명정상대조조.채용PCR-한제성편단장도다태방법진행COX-2기인계동자구-1290A>G,-1195G>A화-765G>C다태적기인형분석,불동기인형여단체형휴대자발생이선암상대풍험도적평고사용비치비(OR)급95%가신구간(CI).결과 다변량Logistic회귀분석현시-1195AA화-765GC기인형여이선암발생적풍험승고상관,OR치분별위1.75(95% CI=1.16～2.64)화2.53(95% CI=1.43～4.47).단체형분석현시:여A－1290-G-1195-G-765상비교,함유-1195A등위기인적A-1290A-1195G-765화G-1290-A-1195-C-765량충단체형휴대자발생이선암적상대풍험승고,OR치분별위1.26(95%CI=1.02～1.56)화5.54(95%c,=1.79～17.16).-765CG화-1195AA기인형여흡연구유교호작용,공동증가이선암발생적풍험.결론 COX-2기인계동자구적-1195G>A화-765G>C단핵감산다태여이선암유전역감성상관.
objective To evaluate the effects of -1290A>G,-1195G>A and-765G>Csingle nucleotide polymorphisms(SNPs)in the promoter of cyelooxygenase(COX)-2 gene on the risk of pathogenesis of pancreatic cancer.Methods Peripheral blood samples were collected from 283 patients with pancreatic cancer and 566 nomud controls. Questionnaire survey was conducted to understand the demographic data and status of smoking and smoking cessation of the subjects.Polymerase chain reaction based restriction fragment length polymorphism(PCR-RFIP)was used to detect the genotypes of the gene fragments containing the 3 SNP sites in the promoter regions of the COX-2 gene.Statistical tests were performed to analyze the relations among different factors and the risk of pancreatic cancer.Results Three SNPs,-1290A>G,-1195G>A,and-765G>C were identified.A case-control analysis revealed 1.75-fold(95%CI=1.16-2.64)and 2.53－fold (95%CI=1.43-4.47)excesses of risks of developing pancreatic cancer for the -1195AA and -765CG genotype carlqerg respectively compared with the non-carriers.Compared with A-1290-G-1195-G-765 containing haplotype.greater risks of developing pancreatic cancer were observed for A-1290-A-1195-G-765(OR=1.26,95%,CI=1.02-1.56)and G-1290 A-1195-C-765(OR=5.54,95%CI=1.79-17.16)containing haplotypes.There were interactions between the-765CG or-1195AA genotype and smoking in the risk of developing pancreatic cancer.Conclusion The SNP of -1195A>G and -765G>C in the COX-2 promoter may play an important role in mediating hereditary susceptibility to developing pancreatic cancer.
