© 1997 by European Society of Cardiology
Copyright © 1997, European Society of Cardiology
Interactive effect of the p53 gene and cigarette smoking on coronary artery disease
Department of Cardiovascular Medicine, University of New South Wales, Prince Henry/Prince of Wales Hospitals, Sydney, Australia
* Corresponding author. Department of Cardiovascular Medicine, Clinical Sciences Building, Prince Henry Hospital, Little Bay, NSW 2036, Australia. Tel.: +61 (2) 9382 5026; fax: +61 (2) 9382 5755; e-mail: x.l.wang@unsw.edu.au
Objective: p53 is a tumour suppressor protein involved in the control of cell growth and has an established role in carcinogenesis, particularly in relation to smoking. It may also be related to arteriosclerosis by affecting smooth muscle cell proliferation, a feature of atherogenesis. Methods: We explored a role for p53 in atherogenesis by assessing the association between two DNA polymorphisms of the p53 gene (MspI at intron 6 and HaeIII at intron 1) and angiographically documented coronary artery disease (CAD) in 654 Australian Caucasian patients. Results: There was a significant interactive effect of the two polymorphisms and cigarette smoking on CAD in a logistic regression analysis (P = 0.0039) but no association between CAD and either individual p53 polymorphic marker. CAD occurrence was more frequent in non-smoking patients with rare alleles at both sites (85.0%) compared to those homozygous for common alleles at both sites (70.4%). However, this was not seen in smokers (85.7 vs 82.8%). In all 654 patients cigarette smoking remained a significant predictor of CAD irrespective of p53 genotypes (P = 0.0065). Conclusions: Our findings identify an interactive effect of both p53 polymorphisms and cigarette smoking on the occurrence of coronary artery disease in that non-smoking patients with rare alleles at both sites had increased incidence of CAD. They illustrate the relevance of genotype-specific and environment-dependent enhanced cardiovascular risk and foreshadow a need for further studies to establish functional changes.
KEYWORDS p53 gene; DNA polymorphism; Cigarette smoking; Coronary artery disease; Gene–environment interaction
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