中华结核和呼吸杂志
中華結覈和呼吸雜誌
중화결핵화호흡잡지
Chinese Journal of Tuberculosis and Respiratory Diseases
2010年
11期
817-822
,共6页
肺肿瘤%基因%多态性,单核苷酸%油烟
肺腫瘤%基因%多態性,單覈苷痠%油煙
폐종류%기인%다태성,단핵감산%유연
Lung neoplasms%Genes%Polymorphism,single nucleotide%Lampblack
目的 探讨细胞色素P4501 A1(CYP1A1)MspI位点多态性、谷胱甘肽硫转移酶(GSTM1)基因缺失及烹调油烟暴露与非吸烟女性肺癌易感性的关系.方法 2009年3一12月选择中南大学湘雅医院女性非吸烟的原发性肺癌患者及对照各160例,应用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)及聚合酶链反应(PCR)技术分别检测CYP1A1 MspI多态性及GSTM1基因型,分析基因的多态性、分型及烹调油烟暴露与肺癌遗传易感性的关系.结果 肺癌组及对照组烹调油烟暴露的频率分别为51.9%(83例)及33.7%(54例),差异有统计学意义(x2=10.734,P＜0.01);肺癌组MspI位点突变的等位基因频率为44.4%(71例),高于对照组(36.9%,59例),差异无统计学意义(X2=3.731,P＞0.05);携带突变型或杂合型基因同时又有油烟暴露个体患肺癌的风险明显增高,OR(odds ratio)值分别为3.032(95%CI为1.291～7.124)和2.769(95%CI为1.341～5.552);肺癌组GSTM1缺失型的频率为58.1%(93例),与对照组(45.0%,72例)比较,差异有统计学意义(X2=0.518,P＜0.05),GSTM1缺失型的个体患肺癌的风险明显增高,OR值为1.697(95%CI为1.090～2.640);携带GSTM1缺失型且有烹调油烟暴露的个体肺癌的易感性明显增加,其OR值为3.617(95%CI为1.899～6.891);GSTM1缺失型与CYP1A1 MspI杂合型或突变型联合作用时,个体患肺癌的风险亦增高,OR值分别为1.966(95%CI为1.007～3.836)和2.402(95%CI为1.023～5.640),差异明显.结论 烹调油烟暴露是非吸烟女性肺癌的危险因素;CYP1A1 MspI基因多态性与烹调油烟联合作用可增加肺癌发病的风险;GSTM1基因缺失可能是非吸烟女性肺癌的遗传易感因素,其与烹调油烟暴露联合作用可明显增加肺癌发病的风险,且GSTM1基因缺失与CYP1A1基因多态性存在交互作用.
目的 探討細胞色素P4501 A1(CYP1A1)MspI位點多態性、穀胱甘肽硫轉移酶(GSTM1)基因缺失及烹調油煙暴露與非吸煙女性肺癌易感性的關繫.方法 2009年3一12月選擇中南大學湘雅醫院女性非吸煙的原髮性肺癌患者及對照各160例,應用聚閤酶鏈反應-限製性片段長度多態性(PCR-RFLP)及聚閤酶鏈反應(PCR)技術分彆檢測CYP1A1 MspI多態性及GSTM1基因型,分析基因的多態性、分型及烹調油煙暴露與肺癌遺傳易感性的關繫.結果 肺癌組及對照組烹調油煙暴露的頻率分彆為51.9%(83例)及33.7%(54例),差異有統計學意義(x2=10.734,P＜0.01);肺癌組MspI位點突變的等位基因頻率為44.4%(71例),高于對照組(36.9%,59例),差異無統計學意義(X2=3.731,P＞0.05);攜帶突變型或雜閤型基因同時又有油煙暴露箇體患肺癌的風險明顯增高,OR(odds ratio)值分彆為3.032(95%CI為1.291～7.124)和2.769(95%CI為1.341～5.552);肺癌組GSTM1缺失型的頻率為58.1%(93例),與對照組(45.0%,72例)比較,差異有統計學意義(X2=0.518,P＜0.05),GSTM1缺失型的箇體患肺癌的風險明顯增高,OR值為1.697(95%CI為1.090～2.640);攜帶GSTM1缺失型且有烹調油煙暴露的箇體肺癌的易感性明顯增加,其OR值為3.617(95%CI為1.899～6.891);GSTM1缺失型與CYP1A1 MspI雜閤型或突變型聯閤作用時,箇體患肺癌的風險亦增高,OR值分彆為1.966(95%CI為1.007～3.836)和2.402(95%CI為1.023～5.640),差異明顯.結論 烹調油煙暴露是非吸煙女性肺癌的危險因素;CYP1A1 MspI基因多態性與烹調油煙聯閤作用可增加肺癌髮病的風險;GSTM1基因缺失可能是非吸煙女性肺癌的遺傳易感因素,其與烹調油煙暴露聯閤作用可明顯增加肺癌髮病的風險,且GSTM1基因缺失與CYP1A1基因多態性存在交互作用.
목적 탐토세포색소P4501 A1(CYP1A1)MspI위점다태성、곡광감태류전이매(GSTM1)기인결실급팽조유연폭로여비흡연녀성폐암역감성적관계.방법 2009년3일12월선택중남대학상아의원녀성비흡연적원발성폐암환자급대조각160례,응용취합매련반응-한제성편단장도다태성(PCR-RFLP)급취합매련반응(PCR)기술분별검측CYP1A1 MspI다태성급GSTM1기인형,분석기인적다태성、분형급팽조유연폭로여폐암유전역감성적관계.결과 폐암조급대조조팽조유연폭로적빈솔분별위51.9%(83례)급33.7%(54례),차이유통계학의의(x2=10.734,P＜0.01);폐암조MspI위점돌변적등위기인빈솔위44.4%(71례),고우대조조(36.9%,59례),차이무통계학의의(X2=3.731,P＞0.05);휴대돌변형혹잡합형기인동시우유유연폭로개체환폐암적풍험명현증고,OR(odds ratio)치분별위3.032(95%CI위1.291～7.124)화2.769(95%CI위1.341～5.552);폐암조GSTM1결실형적빈솔위58.1%(93례),여대조조(45.0%,72례)비교,차이유통계학의의(X2=0.518,P＜0.05),GSTM1결실형적개체환폐암적풍험명현증고,OR치위1.697(95%CI위1.090～2.640);휴대GSTM1결실형차유팽조유연폭로적개체폐암적역감성명현증가,기OR치위3.617(95%CI위1.899～6.891);GSTM1결실형여CYP1A1 MspI잡합형혹돌변형연합작용시,개체환폐암적풍험역증고,OR치분별위1.966(95%CI위1.007～3.836)화2.402(95%CI위1.023～5.640),차이명현.결론 팽조유연폭로시비흡연녀성폐암적위험인소;CYP1A1 MspI기인다태성여팽조유연연합작용가증가폐암발병적풍험;GSTM1기인결실가능시비흡연녀성폐암적유전역감인소,기여팽조유연폭로연합작용가명현증가폐암발병적풍험,차GSTM1기인결실여CYP1A1기인다태성존재교호작용.
Objective To study the correlation of polymorphisms of CYP1 A1 MspI,GSTM1 null genotype,cooking oil fumes independently and in combination with the risk of non-smoking lung cancer in females.Methods One hundred and sixty female non-smoking patients with primary lung cancer and 160controls were enrolled from Xiangya Hospital of Central South University.PCR-RELP and PCR were used to detect the distribution of CYP1A1 MspI and GSTM1 genotypes respectively.The correlation of these genes and cooking oil fumes with the susceptibility to lung cancer was analyzed.Results There was a significant difference in the frequencies of cooking oil fumes exposure between cancer cases and controls( x2 = 10.734,P ＜ 0.01 );but there was no statistical difference in CYP1A1 MspI polymorphisms between the 2 groups (x2= 3.731 ,P ＞ 0.05 ).The combination of CYP1A1 polymorphisms and cooking oil fumes significantly increased the risk of lung cancer.The frequencies of GSTM1 null genotype was significantly different between cancer cases and controls ( x2 = 0.518,P ＜ 0.05).The risk of lung cancer was higher in those with the GSTM1 null genotype and the OR was 1.697 ( 95% CI 1.090 - 2.640).Individuals with both GSTM1 null genotype and exposure to cooking fumes had a higher risk of cancer than those with only one of them,the OR being 3.617(95% CI 1.899 -6.891 ).The combination of the two genes significantly increased the risk of lung cancer.Conclusions Cooking oil fumes exposure was a risk factor for non-smoking lung cancer in females.The combination of CYP1 A1 with cooking oil fume increased the risk of female lung cancer.GSTM1 null genotype was associated with risk of lung cancer in non-smoking females.The combination of GSTM1 null genotype and cooking oil fumes significantly increased the risk of female lung cancer.The combination of CYP1 A1 and GSTM1 significantly increased the risk of lung cancer.
