胃肠病学
胃腸病學
위장병학
CHINESE JOURNAL OF GASTROENTEROLOGY
2014年
5期
270-274
,共5页
司君利%亓玉琴%纪丽莎%徐保华%崔京远
司君利%亓玉琴%紀麗莎%徐保華%崔京遠
사군리%기옥금%기려사%서보화%최경원
末端转移酶端粒%多态性,单核苷酸%胃肿瘤%幽门螺杆菌%多态性,限制性片段长度
末耑轉移酶耑粒%多態性,單覈苷痠%胃腫瘤%幽門螺桿菌%多態性,限製性片段長度
말단전이매단립%다태성,단핵감산%위종류%유문라간균%다태성,한제성편단장도
Telomerase%Polymorphism,Single Nucleotide%Stomach Neoplasms%Helicobacter pylori%Polymorphism,Restriction Fragment Length
背景：人端粒酶逆转录酶（hTERT）作为端粒酶的关键酶参与了包括胃癌在内的多种肿瘤的发生和发展，有研究发现该基因的多个单核苷酸多态性（SNP）位点与多种恶性肿瘤具有不同程度的相关性。目的：探讨 hTERT 基因rs2853676和 rs2853677位点 SNP 与胃癌遗传易感性的关系。方法：采用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）法检测297例胃癌、105例萎缩性胃炎和402例对照组患者 rs2853676和 rs2853677位点的基因多态性，采用病理学检查和13 C-尿素呼气试验检测幽门螺杆菌（Hp）感染。结果：胃癌组 rs2853676位点 AA 基因型频率显著高于对照组（15．2％对6．5％，P ＝0．01），AA 基因型携带者患胃癌的风险增加2．47倍（95％ CI：1．46～4．16）。三组 rs2853677位点 CC、TC、TT 基因型频率差异无统计学意义。与对照组相比，萎缩性胃炎组和胃癌组Hp 感染率显著升高（64．8％、56．9％对40．3％，P 均＜0．01），OR 值分别为2．73（95％ CI：1．74～4．26）、1．96（95％CI：1．44～2．67）。Logistic 回归分析发现，Hp 感染与基因突变无明显交互作用。结论：hTERT 基因 rs2853676基因多态性与胃癌遗传易感性有关，其增加胃癌的风险与 Hp 感染可能无关。
揹景：人耑粒酶逆轉錄酶（hTERT）作為耑粒酶的關鍵酶參與瞭包括胃癌在內的多種腫瘤的髮生和髮展，有研究髮現該基因的多箇單覈苷痠多態性（SNP）位點與多種噁性腫瘤具有不同程度的相關性。目的：探討 hTERT 基因rs2853676和 rs2853677位點 SNP 與胃癌遺傳易感性的關繫。方法：採用聚閤酶鏈反應-限製性片段長度多態性（PCR-RFLP）法檢測297例胃癌、105例萎縮性胃炎和402例對照組患者 rs2853676和 rs2853677位點的基因多態性，採用病理學檢查和13 C-尿素呼氣試驗檢測幽門螺桿菌（Hp）感染。結果：胃癌組 rs2853676位點 AA 基因型頻率顯著高于對照組（15．2％對6．5％，P ＝0．01），AA 基因型攜帶者患胃癌的風險增加2．47倍（95％ CI：1．46～4．16）。三組 rs2853677位點 CC、TC、TT 基因型頻率差異無統計學意義。與對照組相比，萎縮性胃炎組和胃癌組Hp 感染率顯著升高（64．8％、56．9％對40．3％，P 均＜0．01），OR 值分彆為2．73（95％ CI：1．74～4．26）、1．96（95％CI：1．44～2．67）。Logistic 迴歸分析髮現，Hp 感染與基因突變無明顯交互作用。結論：hTERT 基因 rs2853676基因多態性與胃癌遺傳易感性有關，其增加胃癌的風險與 Hp 感染可能無關。
배경：인단립매역전록매（hTERT）작위단립매적관건매삼여료포괄위암재내적다충종류적발생화발전，유연구발현해기인적다개단핵감산다태성（SNP）위점여다충악성종류구유불동정도적상관성。목적：탐토 hTERT 기인rs2853676화 rs2853677위점 SNP 여위암유전역감성적관계。방법：채용취합매련반응-한제성편단장도다태성（PCR-RFLP）법검측297례위암、105례위축성위염화402례대조조환자 rs2853676화 rs2853677위점적기인다태성，채용병이학검사화13 C-뇨소호기시험검측유문라간균（Hp）감염。결과：위암조 rs2853676위점 AA 기인형빈솔현저고우대조조（15．2％대6．5％，P ＝0．01），AA 기인형휴대자환위암적풍험증가2．47배（95％ CI：1．46～4．16）。삼조 rs2853677위점 CC、TC、TT 기인형빈솔차이무통계학의의。여대조조상비，위축성위염조화위암조Hp 감염솔현저승고（64．8％、56．9％대40．3％，P 균＜0．01），OR 치분별위2．73（95％ CI：1．74～4．26）、1．96（95％CI：1．44～2．67）。Logistic 회귀분석발현，Hp 감염여기인돌변무명현교호작용。결론：hTERT 기인 rs2853676기인다태성여위암유전역감성유관，기증가위암적풍험여 Hp 감염가능무관。
Background:As an important catalytic subunit of telomerase,human telomerase reverse transcriptase (hTERT)plays an important role in the development and progression of many cancers including gastric cancer.It has been reported that several single nucleotide polymorphisms (SNPs)of hTERT had varying degrees of association with risk of neoplasms. Aims:To study the correlation between SNPs of hTERT rs2853676 and rs2853677 and susceptibility to gastric cancer. Methods:Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to detect the genotypes of rs2853676 and rs2853677 of hTERT in 297 gastric cancer patients,105 atrophic gastritis and 402 controls. Helicobacter pylori (Hp)infection was detected by pathological examination and 13 C-urea breath test.Results:Frequency of AA genotype of rs2853676 was significantly higher in gastric cancer group when compared with control group (15.2%vs.6.5%,P =0.01).The risk of gastric cancer in AA genotype carriers increased 2.47-fold (95% CI:1.46-4.16) when compared with GG carriers.No significant differences in the frequencies of CC,TC and TT genotypes of rs2853677 were found among gastric cancer patients,atrophic gastritis patients and controls.Hp infection rates in atrophic gastritis group and gastric cancer group were significantly increased than those in controls (64.8%,56.9% vs.40.3%,P all <0.01),OR were 2.73 (95% CI:1.74-4.26),1.96 (95% CI:1.44-2.67),respectively.Logistic regression analysis showed that there was no significant interaction between Hp infection and gene mutation.Conclusions:Polymorphism of hTERT gene rs2853676 may play a role in susceptibility to gastric cancer,and Hp infection may not be involved in the increase of risk of gastric cancer caused by hTERT gene polymorphism.
