Abstract

BackgroundOne of the most important factors leading to tumorigenesis is abnormality in the cells proliferation, because of the irregularity in cell cycle progression. CDKN2A (p16) and CDKN1B (p27) are tumor suppressors and regulators of cell cycle at G1 and G1-S transition. Any disorders in activity or expression of these two tumor suppressors can cause cancer. AimsIn this study, we appraised the relationship between 3 polymorphisms: p27 109VG (rs2066827) in exon1 and p16 [540CG (rs11515), 580CT (rs3088440)] in 3’UTR with the risk of colorectal cancer susceptibility in Iranian population. Subjects and methodsThis case-control study was carried out on 214 cases with CRC and 233 control subjects. For p27 109VG and p16 (540CG, 580CT) genotyping, PCR-RFLP technique was used. ResultsLogistic regression analysis revealed that G allele of p16 540CG significantly decreased the risk of CRC (OR = 0.63, CI = 0.42–0.95, P = 0.031), but subjects with TT genotype of 580CT are more likely to develop CRC (OR = 4.63, CI = 1.28–16.71, P = 0.019). There were no significant relationships with p27 109VG and haplotype of p16 (540CG, 580CT) with CRC risk in Iranian population. However, coincidence in VG genotype of p27 109VG and CC genotype of p16 540CG has significantly increased the susceptibility to colorectal cancer (OR = 2.02, CI = 1.02–3.98, P = 0.042). ConclusionThis study indicates that the p16 [540CG (rs11515), 580CT (rs3088440)] polymorphisms are associated with the risk of CRC in Iranian population.

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