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Cyclooxygenase-2 gene polymorphisms reduce the risk of oral premalignant lesions

  1. Xia Pu MS1,
  2. Scott M. Lippman MD2,
  3. Hushan Yang PhD1,
  4. J. Jack Lee PhD3,
  5. Xifeng Wu MD, PhD1,†,*

Article first published online: 5 FEB 2009

DOI: 10.1002/cncr.24157

Issue

Cancer

Cancer

Volume 115, Issue 7, pages 1498–1506, 1 April 2009

Additional Information

How to Cite

Pu, X., Lippman, S. M., Yang, H., Lee, J. J. and Wu, X. (2009), Cyclooxygenase-2 gene polymorphisms reduce the risk of oral premalignant lesions. Cancer, 115: 1498–1506. doi: 10.1002/cncr.24157

Author Information

  1. 1

    Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas

  2. 2

    Department of Thoracic/Head and Neck Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas

  3. 3

    Department of Biostatistics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas

  1. †

    Fax: (713) 792-4657

*Department of Epidemiology, Unit 1340, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030

Publication History

  1. Issue published online: 19 MAR 2009
  2. Article first published online: 5 FEB 2009
  3. Manuscript Accepted: 2 OCT 2008
  4. Manuscript Received: 25 AUG 2008

Funded by

  • National Cancer Institute. Grant Numbers: CA 106,451, CA 097007

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Keywords:

  • COX-2;
  • polymorphism;
  • haplotype;
  • diplotype;
  • oral premalignant lesion

Abstract

BACKGROUND:

Oral premalignant lesions (OPLs) have the potential to transform into malignant oral cancers. Overexpression of the cyclooxygenase-2 gene (COX-2) is observed frequently in OPLs and oral cancers, suggesting that this gene may play an important role in the progression of oral cancer. Single-nucleotide polymorphisms of COX-2 have been associated with the risk of multiple cancers; however, to date, their effects on OPL susceptibility have not been evaluated sufficiently.

METHODS:

The authors conducted a case-control study that included 147 patients with OPL and a group of 147 healthy, matched controls. The effects of 3 potentially functional COX-2 polymorphisms on the risk of OPL were evaluated: the −765 G→C polymorphism (rs20417), the exon 10 +837 T→C polymorphism (rs5275), and the exon 10 −90 C→T polymorphism (rs689470).

RESULTS:

The variant-containing genotypes of COX-2 exon 10 +837T→C variant were associated with a significantly reduced risk of OPL (odds ratio [OR], 0.48; 95% confidence interval [95% CI], 0.28-0.80). This protective effect also was significant in men, younger individuals, ever smokers, and ever drinkers. Consistently, a common halotype WMW (in the following order: −765G→C, exon 10 +837T→C, and exon 10 −90C→T; w, widetype; M, variable allele) and a common diplotype (WWW/WMW) that contained the variant allele of exon 10 +837T→C, both were associated with a reduced risk of OPL (WMW: OR, 0.55; 95% CI, 0.33-0.93; WWW/WMW: OR, 0.44; 95% CI, 0.22-0.89). In addition, using never smokers with the variant-containing genotypes as the reference group, interaction effects were observed between specific COX-2 variants and tobacco smoking in the modulation of OPL risk.

CONCLUSIONS:

Overall, the current results provided the first epidemiologic evidence indicating that potentially functional polymorphisms of the COX-2 gene may have an impact on individual susceptibility to OPLs. Cancer 2009. © 2009 American Cancer Society.

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