AIM

To investigate the contribution of polymorphisms in the , and genes on sporadic colorectal cancer (SCRC) risk.

METHODS

Six hundred forty-one individuals (227 patients with SCRC and 400 controls) were enrolled in the study. The variables analyzed were age, gender, tobacco and alcohol consumption, and clinical and histopathological tumor parameters. The *2A, *2C *5B and *6 polymorphisms were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The Tyr113His, His139Arg and *2C polymorphisms were detected by real-time PCR. Chi-squared test and binary logistic regression were used in the statistical analysis. Haplotype analysis was conducted using the Haploview program, version 2.05.

RESULTS

Age over 62 years was a risk factor for SCRC development (OR = 7.54, 95%CI: 4.94-11.50, < 0.01). Male individuals were less susceptible to SCRC (OR = 0.55, 95%CI: 0.35-0.85, < 0.01). The polymorphism was associated with SCRC in the codominant (heterozygous genotype: OR = 2.66, 95%CI: 1.64-4.32, < 0.01), dominant (OR = 2.82, 95%CI: 1.74-4.55, < 0.01), overdominant (OR = 2.58, 95%CI: 1.59-4.19, < 0.01), and log-additive models (OR = 2.84, 95%CI: 1.78-4.52, < 0.01). The polymorphism was associated with an increased SCRC risk in codominant (heterozygous genotype: OR = 2.81, 95%CI: 1.84-4.28, < 0.01; homozygous polymorphic: OR = 7.32, 95%CI: 1.85-28.96, < 0.01), dominant (OR = 2.97, 95%CI: 1.97-4.50, < 0.01), recessive (OR = 5.26, 95%CI: 1.35-20.50, = 0.016), overdominant (OR = 2.64, 95%CI: 1.74-4.01, < 0.01), and log-additive models (OR = 2.78, 95%CI: 1.91-4.06, < 0.01). The haplotype formed by the minor alleles of the CYP2E15B (C) and CYP2E16 (A) polymorphisms was associated with SCRC ( = 0.002). However, the *2A, *2C, and polymorphisms were not associated with SCRC.

CONCLUSION

In conclusion, the results demonstrated that and minor alleles play a role in the development of SCRC.