, Volume 187, Issue 2, pp 110–115

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


    • 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

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


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.


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

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© Springer Science+Business Media, LLC 2008