本文選題：肺癌　切入點：非吸煙者　出處：《中華腫瘤防治雜志》2017年02期 　論文類型：期刊論文

【摘要】：目的位于染色體22q12.2區(qū)域的MTMR3(myotubularin related protein 3)基因是調控肌維管束蛋白表達的基因,MTMR3基因過度表達與腫瘤等疾病發(fā)生有關。本研究旨結合表達數(shù)量性狀(expression Quati tatire Trait Loci,eQTL)信息探討MTMR3基因多態(tài)性與非吸煙者肺癌易感性的關系,為探究肺癌的發(fā)病機制提供依據(jù)。方法對肺癌易感區(qū)域22q12.2進行連鎖不平衡和eQTL分析,篩選具有調控基因表達的致病位點并預測其調控的基因。本研究采用病例對照研究方法,病例為2013-03-05-2014-12-30遼寧省腫瘤醫(yī)院(96例)、中國醫(yī)科大學附屬第一醫(yī)院(92例)、中國醫(yī)科大學附屬第四醫(yī)院(90例)、沈陽軍區(qū)總醫(yī)院(95例)和人民解放軍沈陽二0二醫(yī)院(88例)5所三甲級醫(yī)院的原發(fā)性肺癌患者461例(病例組),同期社區(qū)中健康對照472名(對照組)。應用TaqMan基因分型技術對rs36605位點進行基因分型。采用t檢驗比較年齡在病例組與對照組間分布的差異,采用χ~2檢驗比較性別、各基因型以及各環(huán)境暴露因素在病例組與對照組間分布的差異,應用Logistic回歸計算OR值及其95%置信區(qū)間(CI)。結果經(jīng)eQTL分析得到rs36605位點是MTMR3基因的一個順式eQTL,rs36605位點可能與MTMR3基因的表達有關。以TT基因型為參照,AT基因型(OR=0.81,95%CI為0.60~1.10,P=0.178)和AA基因型(OR=1.85,95%CI為0.61~5.59,P=0.276)與肺癌的患病風險無統(tǒng)計學關聯(lián)。也未發(fā)現(xiàn)在顯性模型(OR=0.85,95%CI為0.63~1.15,P=0.291)以及隱形模型(OR=1.94,95%CI為0.64~5.86,P=0.238)中存在此關聯(lián)。試驗驗證了烹飪油煙暴露增加了肺癌的患病風險,調整OR=1.61,95%CI為1.06~2.45,P=0.025,但未發(fā)現(xiàn)烹飪油煙暴露與rs36605位點多態(tài)性之間存在交互作用,P0.05。結論試驗未發(fā)現(xiàn),22q12.2區(qū)域內的rs36605位點多態(tài)性與非吸煙者肺癌的易感性有關,尚不能得到MTMR3基因多態(tài)性與非吸煙者肺癌的易感性有關。
[Abstract]:Objective the MTMR3(myotubularin related protein 3 gene located on chromosome 22q12.2 is a gene that regulates the expression of muscle vascular bundle protein. The overexpression of MTMR3 gene is related to tumorigenesis and other diseases. The purpose of this study is to explore the expression of quantitative character expression Quati tatire Trait Locie QTL (QTL). The association between MTMR3 gene polymorphism and lung cancer susceptibility in non-smokers. Methods Linkage disequilibrium and eQTL analysis were carried out in 22q12.2 region of lung cancer susceptibility, and pathogenicity sites were screened for gene expression regulation and gene regulation was predicted. A case-control study was used in this study. The cases included 96 cases from Liaoning Provincial Oncology Hospital 2013-03-05-2014-12-30, 92 cases from the first affiliated Hospital of China Medical University, 90 cases from the 4th affiliated Hospital of China Medical University, 95 cases from the General Hospital of Shenyang military region) and 88 cases from Shenyang 202 Hospital of the people's Liberation Army. There were 461 patients with primary lung cancer (case group) and 472 healthy controls (control group) in the third grade A hospital. The rs36605 locus was genotyped by TaqMan genotyping technique. T test was used to compare age in the case group. The difference of distribution between the control group and the control group, 蠂 2 test was used to compare the distribution of sex, genotypes and environmental exposure factors between the case group and the control group. The OR value and its 95% confidence interval were calculated by Logistic regression. Results eQTL analysis showed that the rs36605 locus was a cis QTLL rs36605 locus of MTMR3 gene, which might be related to the expression of MTMR3 gene. There was no significant correlation between the risk of lung cancer and the risk of lung cancer. There was also no significant correlation between the overt model and the invisible model ORA (0.645.895 CI = 0.645.856 P0.238). The results showed that cooking oil smoke exposure increased the risk of lung cancer, and was not found in the dominant model (0.631.15P0.291) or in the invisible model (0.645.895 CI = 0.645.86P0.238), the results showed that cooking oil fume exposure increased the risk of lung cancer. The CI was 1.06 ~ 2.45% P0.025, but there was no interaction between cooking oil fume exposure and polymorphism of rs36605 locus. Conclusion the polymorphism of rs36605 locus in the 22q12.2 region was not associated with the susceptibility of non-smokers to lung cancer. No MTMR3 gene polymorphism has been found to be associated with the susceptibility of non-smokers to lung cancer.
【作者單位】： 中國醫(yī)科大學公共衛(wèi)生學院流行病學教研室;
【基金】：中華醫(yī)學會資助項目(CMB00726)
【分類號】：R734.2
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本文編號：1606421