Carcinogenesis Advance Access originally published online on April 25, 2006
Carcinogenesis 2006 27(10):2034-2037; doi:10.1093/carcin/bgl048
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Cyclin D1 gene polymorphism as a risk factor for oral premalignant lesions
Department of Epidemiology, The University of Texas M.D. Anderson Cancer Center Houston, TX 77030, USA
1 Department of Biostatistics, The University of Texas M.D. Anderson Cancer Center Houston, TX 77030, USA
2 Department of Thoracic/Head and Neck Oncology, The University of Texas M.D. Anderson Cancer Center Houston, TX 77030, USA
*To whom correspondence should be addressed at: Department of Epidemiology, Unit 1340, The University of Texas M.D. Anderson Cancer Center, 1155 Pressler Boulevard, Houston, TX 77030, USA. Tel: +1 713 745 2485; Fax: +1 713 792 4657; Email: xwu{at}mdanderson.org
Background: Deregulation of cell cycle plays an important role in tumorigenesis. Cyclin D1 gene (CCND1) is a key regulator of the G1 phase of the cell cycle. Methods: In this case–control study of 115 oral premalignant lesion (OPL) patients and 230 controls, we genotyped the CCND1 single nucleotide polymorphism (SNP) at the exon 4 splice site (G870A) and determined the association of this SNP with the risk of developing OPLs. Results: We found significant associations between the heterozygous variant allele (GA), the homozygous variant allele (AA) and OPL risk, with adjusted odds ratios (ORs) of 1.91 [95% confidenc interval (CI), 1.05–3.48] and 2.38 (95% CI, 1.16–4.87), respectively. The OR for individuals with at least one variant allele was 2.04 (95% CI, 1.15–3.60). When further stratified analyses were performed, the increased risk was more evident in younger individuals (OR = 2.82; 95% CI, 1.32–6.02), in men (OR = 2.97; 95%CI, 1.31–6.71) and in never smokers (OR = 2.92; 95% CI, 1.09–7.82). Finally, we found joint effects between the variant alleles and the smoking status. Using never smokers with the wild-type (GG) genotypes as the reference group, the ORs for never smokers with the variant genotypes (G/A + A/A), smokers with the G/G genotype and smokers with the G/A + A/A genotypes were 2.92 (1.09–7.82), 3.95 (1.36–11.5) and 7.01 (2.68–18.4), respectively. Conclusion: Our results suggest that the CCND1 G870A SNP may contribute to genetic susceptibility to OPLs and involve in oral cancer development.
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