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Because p53 and p73 are associated with critical cellular processes and can be inactivated or degraded by the human papillomavirus (HPV) E6 oncoprotein, we investigated the combined effects ofp53codon 72 andp73G4C14-to-A4T14 polymorphisms on the risk of HPV16-associated oral cancer. We analyzed genotype data from 326 patients with squamous cell carcinoma of the oral cavity or oropharynx and 349 cancer-free controls. We found that HPV16 seropositivity was associated with an increased risk of oral cancer [adjusted odds ratio (OR), 3.42; 95% confidence interval (CI), 2.28–5.13], especially among never-smokers (adjusted OR, 8.20; 95% CI, 3.66–18.4) and subjects with variant genotypes [adjusted OR forp53Arg/Pro + Pro/Pro (Pro carriers), 5.00; 95% CI, 2.72–9.21; adjusted OR forp73GC/AT + AT/AT (AT carriers), 3.83; 95% CI, 1.98–7.41]. HPV16 seropositivity was also associated with an significantly increased risk of oral cancer in all three risk groups with combined genotypes [adjusted ORs (95% CIs) were 2.28 (1.15–4.54) forp53Arg/Arg andp73GC/GC, the low-risk group; 3.97 (2.14–7.36) forp53Arg/Arg andp73AT carriers orp53Pro carriers andp73GC/GC, the medium-risk group and 5.11 (2.00–13.0) forp53Pro carriers andp73AT carriers, the high-risk group]. Moreover, HPV16-seropositive never-smokers in the high-risk group exhibited an ∼11-fold greater risk of oral cancer (adjusted OR, 11.3; 95% CI, 1.22–106.0) than did HPV16-seronegative never-smokers in the low-risk group. These findings suggest that the combined variants ofp53andp73significantly increase the risk of HPV16-associated oral cancer, especially among never-smokers.

carcinogenesis

Combined effects of the               p53               codon 72 and               p73               G4C14-to-A4T14 polymorphisms on the risk of HPV16-associated oral cancer in never-smokers