癌变·畸变·突变
癌變·畸變·突變
암변·기변·돌변
CARCINOGENSES,TERATOGENSIS AND MUTAGENESIS
2014年
3期
171-174,179
,共5页
赵真真%石源源%刘颂%王笑峰%罗兵
趙真真%石源源%劉頌%王笑峰%囉兵
조진진%석원원%류송%왕소봉%라병
Tol样受体%胃癌%EB病毒%基因多态性
Tol樣受體%胃癌%EB病毒%基因多態性
Tol양수체%위암%EB병독%기인다태성
Toll-like receptor%gastric carcinoma%EBV%gene polymorphism
目的：探讨Toll样受体(TLR)家族成员TLR2基因启动子区-196~-174 del和TLR4基因Thr399Ile位点多态性与EBV相关胃癌(EBVaGC)及EBV阴性胃癌(EBVnGC)易感性的关系。方法：采用PCR技术检测52例EBVaGC，157例EBVnGC以及94例正常对照人群TLR2-196~-174 del基因多态性；PCR-限制性片段长度多态性(PCR-RELP)技术检测50例EBVaGC，67例EBVnGC以及71例正常对照TLR4 Thr399Ile位点基因型及等位基因分布；分析2种基因多态性与EBVaGC及EBVnGC易感性的关系。结果：胃癌组与对照组2比较TLR2(-196~-174 del)基因型分布无显著差异(=3.180，=0.075)，胃癌组del等位基因频率明显高于对照组(=4.875， P=0.027)，del等位基因携带者的罹患危险性明显高于非携带者(OR=1.491，95%CI=1.045~2.126)；EBVaGC组和EBVnGC组中，2TLR2(-196~-174 del)3种基因型以及del等位基因频率差异无统计学意义(=0.05，P=0.867)。EBVaGC组、EBVnGC组和正常对照组中均未发现TLR4基因Thr399Ile位点的多态，其基因型分布及等位基因频率差异均无统计学意义(P>0.05)。结论：TLR2(-196~-174 del)等位基因可能是胃癌发病危险因素，且在EBVaGC和EBVnGC两种胃癌发生中产生相同的影响。未发现TLR2(-196~-174 del)和TLR4基因Thr399Ile基因型分布与EBVaGC的易感性相关。()2Pχχχ
目的：探討Toll樣受體(TLR)傢族成員TLR2基因啟動子區-196~-174 del和TLR4基因Thr399Ile位點多態性與EBV相關胃癌(EBVaGC)及EBV陰性胃癌(EBVnGC)易感性的關繫。方法：採用PCR技術檢測52例EBVaGC，157例EBVnGC以及94例正常對照人群TLR2-196~-174 del基因多態性；PCR-限製性片段長度多態性(PCR-RELP)技術檢測50例EBVaGC，67例EBVnGC以及71例正常對照TLR4 Thr399Ile位點基因型及等位基因分佈；分析2種基因多態性與EBVaGC及EBVnGC易感性的關繫。結果：胃癌組與對照組2比較TLR2(-196~-174 del)基因型分佈無顯著差異(=3.180，=0.075)，胃癌組del等位基因頻率明顯高于對照組(=4.875， P=0.027)，del等位基因攜帶者的罹患危險性明顯高于非攜帶者(OR=1.491，95%CI=1.045~2.126)；EBVaGC組和EBVnGC組中，2TLR2(-196~-174 del)3種基因型以及del等位基因頻率差異無統計學意義(=0.05，P=0.867)。EBVaGC組、EBVnGC組和正常對照組中均未髮現TLR4基因Thr399Ile位點的多態，其基因型分佈及等位基因頻率差異均無統計學意義(P>0.05)。結論：TLR2(-196~-174 del)等位基因可能是胃癌髮病危險因素，且在EBVaGC和EBVnGC兩種胃癌髮生中產生相同的影響。未髮現TLR2(-196~-174 del)和TLR4基因Thr399Ile基因型分佈與EBVaGC的易感性相關。()2Pχχχ
목적：탐토Toll양수체(TLR)가족성원TLR2기인계동자구-196~-174 del화TLR4기인Thr399Ile위점다태성여EBV상관위암(EBVaGC)급EBV음성위암(EBVnGC)역감성적관계。방법：채용PCR기술검측52례EBVaGC，157례EBVnGC이급94례정상대조인군TLR2-196~-174 del기인다태성；PCR-한제성편단장도다태성(PCR-RELP)기술검측50례EBVaGC，67례EBVnGC이급71례정상대조TLR4 Thr399Ile위점기인형급등위기인분포；분석2충기인다태성여EBVaGC급EBVnGC역감성적관계。결과：위암조여대조조2비교TLR2(-196~-174 del)기인형분포무현저차이(=3.180，=0.075)，위암조del등위기인빈솔명현고우대조조(=4.875， P=0.027)，del등위기인휴대자적리환위험성명현고우비휴대자(OR=1.491，95%CI=1.045~2.126)；EBVaGC조화EBVnGC조중，2TLR2(-196~-174 del)3충기인형이급del등위기인빈솔차이무통계학의의(=0.05，P=0.867)。EBVaGC조、EBVnGC조화정상대조조중균미발현TLR4기인Thr399Ile위점적다태，기기인형분포급등위기인빈솔차이균무통계학의의(P>0.05)。결론：TLR2(-196~-174 del)등위기인가능시위암발병위험인소，차재EBVaGC화EBVnGC량충위암발생중산생상동적영향。미발현TLR2(-196~-174 del)화TLR4기인Thr399Ile기인형분포여EBVaGC적역감성상관。()2Pχχχ
OBJECTIVE: To explore the relationship of Toll-like receptors 2 (TLR2) and TLR4 Thr399Ile gene polymorphism and the susceptibility to EBV-associated gastric carcinoma (EBVaGC) and EBV-negative gastric carcinoma(EBVnGC). METHODS:TLR2 gene promoter region-196 to-174 del polymorphism was detected by using the allele-specific polymerase chain reaction in 52 EBVaGCs,157 EBVnGCs and 94 normal controls. TLR4 gene Thr399Ile genotype and allele distribution were evaluated by PCR and restriction fragment length polymorphism (PCR-RFLP) in 50 EBVaGCs,67 EBVnGCs and 71 normal controls. The relationship between gene polymorphism in TLR2 and TLR4 coding genes and the susceptibility to EBVaGC and EBVnGC was analysed. RESULTS:There was no significant 2difference ( =3.180,P=0.075) between gastric cancer group and control group in genotype distribution of TLR2(-196 to-174 del),but the del allele frequency of gastric cancer group was obviously higher than that of control group 2( =4.875,P=0.027),The risk of developing gastric carcinoma in del allele carriers was significantly higher than that in controls(OR=1.491,95%CI=1.045-2.126). TLR2 (-196 to-174 del) genotype and the frequency of del allele showed no 2significant difference in EBVaGC and EBVnGC group ( =0.05,P=0.867). TLR4 gene Thr399Ile locus mutation was not found in EBVaGC,EBVnGC or normal control groups. The genotype distribution and allele frequency also revealed no statistical differences . CONCLUSION:TLR2-196 to-174 del alleles could be risk factors for gastric carcinoma,butχχχits effects were not different in EBVaGC and EBVnGC. There was no obvious correlation in the genotype distribution of TLR2(-196 to-174 del) and TLR4 gene Thr399Ile and EBVaGC genetic susceptibility.
