作者: Karl T. Kelsey , Karl T. Kelsey , Margaret R. Spitz , Zheng-Fa Zuo , John K. Wiencke
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摘要: The genes coding for separate isoforms of both the human glutathioneS-transferase class mu and theta enzymes (GSTM1and GSTT1) arepolymorphic with a variable ethnic distribution. These detoxifyreactive epoxides, including carcinogens produced by tobacco smoke. Becauseof this, null polymorphism in GSTM1 gene (coding enzyme) has been studied widely as possible sourceof inherited susceptibility to smoking-related lung cancer. more recentlydescribed GSTT1 also could contribute anincreased risk As incidence lungcancer is known differ ethnicity, we have conducted case-controlstudy United States 108 African-Americans (Blacks) 60Mexican-Americans (Hispanics) cancer 132 African-American(Black) 146 Mexican-American (Hispanic) controls investigate theassociation polymorphi sms inminority populations. In unadjusted data, there was borderlinesignificant association inMexican-Americans (odds ratio [OR] = 1.8, 95 percent confidence interval [CI]= 1.0-3.3 ) that not observed African-Americans. nullpolymorphism had higher prevalence cases than bothracial/ethnic groups, but this increase statistically significant.When data were analyzed using logistic regression controlling age,gender, race, smoking, no significant either trait withlung observed, ORs traits approximately 1.3.However, when individuals who bothpolymorphisms compared case status, interaction wasobserved. Logistic models showed OR oflung presence polymorphisms one(either or GSTM1) genotype be 2.9 (P < 0.04). Theseresults suggest may carcinogenic intermediates cigarettesmoke are substrates enzymes, increased additively bothGSTT1 polymorphisms.