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p53 codon 72 polymorphism associated with risk of human papillomavirus-associated squamous cell carcinoma of the oropharynx in never-smokers.

Publication ,  Journal Article
Ji, X; Neumann, AS; Sturgis, EM; Adler-Storthz, K; Dahlstrom, KR; Schiller, JT; Wei, Q; Li, G
Published in: Carcinogenesis
April 2008

The tumor suppressor p53 protein can be bound, degraded and inactivated by the human papillomavirus (HPV) E6 oncoprotein. The p53 protein's susceptibility to this oncoprotein may be influenced by the p53 codon 72 polymorphism, but the role of such a polymorphism in the development of HPV16-associated squamous cell carcinoma of the oropharynx (SCCOP) has not been established. To investigate the role of the p53 codon 72 polymorphism in the risk of HPV16-associated SCCOP, we conducted a hospital-based case-control study of 188 non-Hispanic white patients with newly diagnosed SCCOP and 342 cancer-free control subjects frequency matched by age (+/-5 years), sex, tobacco smoking status and alcohol drinking status. We found that HPV16 seropositivity was associated with an increased risk of SCCOP [adjusted odds ratio (OR), 5.7; 95% confidence interval (CI), 3.7-8.7], especially among never-smokers (adjusted OR, 14.1; 95% CI, 6.0-32.9) and among subjects with the p53 codon 72 variant genotypes [Arginine (Arg)/Proline (Pro) and Pro/Pro] (adjusted OR, 9.2; 95% CI, 4.7-17.7). A significant multiplicative interaction on the risk of SCCOP was also found between the p53 codon 72 polymorphism and HPV16 seropositivity (P = 0.05). Among never-smokers, the risk of SCCOP for those who had both HPV16 seropositivity and p53 codon 72 variant genotypes (Arg/Pro + Pro/Pro) was particularly high (adjusted OR, 22.5; 95% CI, 4.8-106.2). These findings suggest that p53 codon 72 variant genotypes modify the risk of HPV16-associated SCCOP and may be markers of genetic susceptibility to HPV16-associated SCCOP, especially among never-smokers.

Duke Scholars

Published In

Carcinogenesis

DOI

EISSN

1460-2180

Publication Date

April 2008

Volume

29

Issue

4

Start / End Page

875 / 879

Location

England

Related Subject Headings

  • Tumor Suppressor Protein p53
  • Smoking Cessation
  • Reference Values
  • Polymorphism, Genetic
  • Polymerase Chain Reaction
  • Pharyngeal Neoplasms
  • Patient Selection
  • Papillomavirus Infections
  • Oncology & Carcinogenesis
  • Mouth Neoplasms
 

Citation

APA
Chicago
ICMJE
MLA
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Ji, X., Neumann, A. S., Sturgis, E. M., Adler-Storthz, K., Dahlstrom, K. R., Schiller, J. T., … Li, G. (2008). p53 codon 72 polymorphism associated with risk of human papillomavirus-associated squamous cell carcinoma of the oropharynx in never-smokers. Carcinogenesis, 29(4), 875–879. https://doi.org/10.1093/carcin/bgn039
Ji, Xuemei, Ana S. Neumann, Erich M. Sturgis, Karen Adler-Storthz, Kristina R. Dahlstrom, John T. Schiller, Qingyi Wei, and Guojun Li. “p53 codon 72 polymorphism associated with risk of human papillomavirus-associated squamous cell carcinoma of the oropharynx in never-smokers.Carcinogenesis 29, no. 4 (April 2008): 875–79. https://doi.org/10.1093/carcin/bgn039.
Ji X, Neumann AS, Sturgis EM, Adler-Storthz K, Dahlstrom KR, Schiller JT, et al. p53 codon 72 polymorphism associated with risk of human papillomavirus-associated squamous cell carcinoma of the oropharynx in never-smokers. Carcinogenesis. 2008 Apr;29(4):875–9.
Ji, Xuemei, et al. “p53 codon 72 polymorphism associated with risk of human papillomavirus-associated squamous cell carcinoma of the oropharynx in never-smokers.Carcinogenesis, vol. 29, no. 4, Apr. 2008, pp. 875–79. Pubmed, doi:10.1093/carcin/bgn039.
Ji X, Neumann AS, Sturgis EM, Adler-Storthz K, Dahlstrom KR, Schiller JT, Wei Q, Li G. p53 codon 72 polymorphism associated with risk of human papillomavirus-associated squamous cell carcinoma of the oropharynx in never-smokers. Carcinogenesis. 2008 Apr;29(4):875–879.
Journal cover image

Published In

Carcinogenesis

DOI

EISSN

1460-2180

Publication Date

April 2008

Volume

29

Issue

4

Start / End Page

875 / 879

Location

England

Related Subject Headings

  • Tumor Suppressor Protein p53
  • Smoking Cessation
  • Reference Values
  • Polymorphism, Genetic
  • Polymerase Chain Reaction
  • Pharyngeal Neoplasms
  • Patient Selection
  • Papillomavirus Infections
  • Oncology & Carcinogenesis
  • Mouth Neoplasms