Association between p53 codon 72 genetic polymorphism and tobacco use and lung cancer risk

Dante D. Cáceres, Luis A. Quiñones, Jane C. Schroeder, Leonel D. Gil, Carlos E. Irarrázabal

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


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 Proallele 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.

Original languageEnglish
Pages (from-to)110-115
Number of pages6
Issue number2
StatePublished - Apr 2009

Bibliographical note

Funding Information:
The National Fund of Scientific Development and Technology (FONDECYT) (Grant No. 2990019) supported this work. Dr. Dante Cáceres thanks Dr. Nevin Schrimshaw and the Ellison Medical Foundation-International Nutrition Foundation.


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


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