Abstract
Many studies have examined the association between the CYP1A1 Ile462Val gene polymorphisms and lung cancer risk in various populations, but their results have been inconsistent. To assess this relationship more precisely, a meta-analysis was performed. Ultimately, 43 case-control studies, comprising 19,228 subjects were included. A significantly elevated lung cancer risk was associated with 2 Ile462Val genotype variants (for Val/Val vs Ile/Ile: OR = 1.22, 95% CI = 1.08–1.40; for (Ile/Val +Val/Val) vs Ile/Ile: OR = 1.15, 95% CI = 1.07–1.23) in overall population. In the stratified analysis, a significant association was found in Asians, Caucasians and lung SCC, not lung AC and lung SCLC. Additionally, a significant association was found in smoker population and not found in non-smoker populations. This meta-analysis suggests that the Ile462Val polymorphisms of CYP1A1 correlate with increased lung cancer susceptibility in Asian and Caucasian populations and there is an interaction with smoking status, but these associations vary in different histological types of lung caner.
Highlights
Lung cancer remains the most lethal cancer worldwide, despite improvements in diagnostic and therapeutic techniques [1]
This meta-analysis suggests that the Ile462Val polymorphisms of CYP1A1 correlate with increased lung cancer susceptibility in Asian and Caucasian populations and there is an interaction with smoking status, but these associations vary in different histological types of lung caner
CYP1A1 is a phase I enzyme that regulates the metabolic activation of major classes of tobacco procarcinogens, such as aromatic amines and
Summary
Lung cancer remains the most lethal cancer worldwide, despite improvements in diagnostic and therapeutic techniques [1]. The mechanism of lung carcinogenesis is not understood. Cigarette smoking is the major cause of lung cancer, not all smokers develop lung cancer [3], which suggests that other causes such as genetic susceptibility might contribute to the variation in individual lung cancer risk [4,5]. Cytochrome P450 1A1 (CYP1A1) metabolizes several suspected procarcinogens, polycyclic aromatic hydrocarbons (PAHs), into highly reactive intermediates [6]. These compounds bind to DNA to form adducts, which, if unrepaired, can initiate or accelerate carcinogenesis. The ethnicity source, histological types of lung caner and smoking status of case
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