BACKGROUND: Deregulation of cell cycle plays an important role in tumorigenesis. Cyclin D1 gene (CCND1) is a key regulator of the G(1) 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% confidence 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.
BACKGROUND: Deregulation of cell cycle plays an important role in tumorigenesis. Cyclin D1 gene (CCND1) is a key regulator of the G(1) 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% confidence 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 CCND1G870A SNP may contribute to genetic susceptibility to OPLs and involve in oral cancer development.
Authors: Jonathan F Wilkey; Glenn Buchberger; Kirsten Saucier; Salony M Patel; Ellen Eisenberg; Hiroshi Nakagawa; Carmen Z Michaylira; Anil K Rustgi; Sanjay M Mallya Journal: Mol Carcinog Date: 2009-09 Impact factor: 4.784
Authors: Yuanqing Ye; Scott M Lippman; J Jack Lee; Meng Chen; Marsha L Frazier; Margaret R Spitz; Xifeng Wu Journal: Cancer Date: 2008-11-01 Impact factor: 6.860
Authors: Hushan Yang; Scott M Lippman; Maosheng Huang; J Jack Lee; Wei Wang; Margaret R Spitz; Xifeng Wu Journal: Eur J Cancer Date: 2008-06-23 Impact factor: 9.162
Authors: Vassiliki Papadimitrakopoulou; Julie G Izzo; Diane D Liu; Jeffrey Myers; Tania L Ceron; Jan Lewin; William N William; Anthea Atwell; J Jack Lee; Ann Gillenwater; Adel El-Naggar; Xifeng Wu; Scott M Lippman; Walter N Hittelman; Waun Ki Hong Journal: Cancer Prev Res (Phila) Date: 2009-01