NDLI: CYP2C9 variants increase risk of colorectal adenoma recurrence and modify associations with smoking but not aspirin treatment

Content Provider	Springer Nature Link
Author	Barry, Elizabeth L. Poole, Elizabeth M. Baron, John A. Makar, Karen W. Mott, Leila A. Sandler, Robert S. Ahnen, Dennis J. Bresalier, Robert S. McKeown Eyssen, Gail E. Ulrich, Cornelia M.
Copyright Year	2012
Abstract	The cytochrome P450 2C9 enzyme (CYP2C9) is involved in metabolism of endogenous compounds, drugs, and procarcinogens. Two common nonsynonymous polymorphisms in CYP2C9 are associated with reduced enzyme activity: CYP2C92 (rs1799853, R144C) and CYP2C93 (rs1057910, I359L).We investigated whether CYP2C9 genotype was associated with risk of colorectal adenoma and/or modified associations with aspirin treatment or cigarette smoking in a cohort of 928 participants in a randomized trial of aspirin chemoprevention. Generalized linear regression was used to compute relative risks (RRs) and 95 % confidence intervals (95 % CIs). Multiplicative interactions terms were used to assess effect modification. CYP2C9 genotype was associated with increased risks for adenoma recurrence of 29 % (RR = 1.29, 95 % CI 1.09–1.51) for ≥1 variant allele (CYP2C92 or 3) and 47 % (RR = 1.47, 95 % CI 1.19–1.83) for ≥1 CYP2C93 allele. The risk for advanced lesions or multiple (≥3) adenomas was increased by 64 % (RR = 1.64, 95 % CI 1.18–2.28) for ≥1 variant allele (CYP2C92 or 3) and 79 % (RR = 1.79, 95 % CI 1.16–2.75) for ≥1 CYP2C93 allele. Genotype modified associations with smoking, but not aspirin treatment. The adenoma risk was increased by 26 % (RR = 1.26, 95 % CI 0.99–1.58) for former smokers and 60 % (RR = 1.60, 95 % CI 1.19–2.15) for current smokers among wild-type individuals, but there was no increased risk among individuals with ≥1 variant allele (CYP2C92 or 3) (p interaction = 0.04).Carriers of CYP2C9 variants with lower enzyme activity have increased overall risk of colorectal adenoma but reduced adenoma risk associated with cigarette smoking. These results may be due to effects on the synthesis of endogenous eicosanoids and/or reduced activation of procarcinogens in smoke by CYP2C9 variants.
Starting Page	47
Ending Page	54
Page Count	8
File Format	PDF
ISSN	09575243
Journal	Cancer Causes & Control
Volume Number	24
Issue Number	1
e-ISSN	15737225
Language	English
Publisher	Springer Netherlands
Publisher Date	2012-10-19
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Colorectal neoplasia CYP2C9 Smoking Aspirin Polymorphism Cancer Research Biomedicine general Oncology Public Health Epidemiology Hematology
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology

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