Lung

, Volume 187, Issue 2, pp 110–115

Association Between p53 codon 72 Genetic Polymorphism and Tobacco Use and Lung Cancer Risk

Authors

    • Epidemiology Division, School of Public Health, Faculty of MedicineUniversity of Chile
  • Luis A. Quiñones
    • Molecular and Clinical Pharmacology Program, IFT, Institute of Biomedical Sciences, Faculty of MedicineUniversity of Chile
  • Jane C. Schroeder
    • Department of Epidemiology, Gillings School of Public HealthNorth Carolina University at Chapel Hill
  • Leonel D. Gil
    • Laboratory of Environmental Toxicology, ICBM, Faculty of MedicineUniversity of Chile
  • Carlos E. Irarrázabal
    • Department of Molecular and Integrative Physiology, Faculty of MedicineLos Andes University
Article

DOI: 10.1007/s00408-008-9133-3

Cite this article as:
Cáceres, D.D., Quiñones, L.A., Schroeder, J.C. et al. Lung (2009) 187: 110. doi:10.1007/s00408-008-9133-3

Abstract

Lung cancer (LCa) is the leading cause of death by cancer in men. Genetic and environmental factors play a synergistic role in its etiology. We explore in 111 lung cancer cases and 133 unrelated noncancer controls the gene-environment interaction (G × E) between p53cd72 polymorphism variants and smoking and the effect on LCa risk in two kinds of case-control designs. We assessed the interaction odds ratio (IOR) using an adjusted unconditional logistic model. We found a significant and positive interaction association between Pro* allele carriers and smoking habits in both case-control and case-only designs: IOR = 3.90 (95% confidence interval [CI] = 1.10–13.81) and 3.05 (95% CI = 1.63–5.72), respectively. These exploratory results suggest a synergistic effect of the smoking habit and the susceptibility of the Pro allele on lung cancer risk compared with each risk factor alone.

Keywords

Lung cancer Case control Case only Gene-environment interaction Genetic polymorphisms Risk effect modification Synergistic effect

Copyright information

© Springer Science+Business Media, LLC 2008