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Effects of interactions between common genetic variants and smoking on colorectal cancer.

ABSTRACT: Although genome-wide association studies (GWAS) have identified variants in approximately 40 susceptibility loci for colorectal cancer (CRC), there are few studies on the interactions between identified single-nucleotide polymorphisms (SNPs) and lifestyle risk factors. We evaluated whether smoking could modify associations between these genetic variants and CRC risk.A total of 703 CRC patients and 1406 healthy controls were included in this case-control study from the National Cancer Center in Korea. Thirty CRC susceptibility SNPs identified in previous GWAS were genotyped. A logistic regression model was used to examine associations between the SNPs and smoking behaviors by sex. The interaction was estimated by including an additional interaction term in the model.In men, an increased CRC risk was observed for longer durations (OR>28 vs. ?28years?=?1.49 (95% CI?=?1.11-1.98)), greater quantities (OR?20 vs. <20cigarettes/day?=?2.12 (1.61-2.79)), and longer pack-years of smoking (OR?21 vs. <21pack-years?=?1.78 (1.35-2.35)). In women, longer pack-years of smoking significantly increased CRC risk (OR?5 vs. <5pack-years?=?6.11 (1.10-34.00)). Moreover, there were significant interactions between smoking status and the polymorphisms rs1957636 at 14q22.3 (P interaction?=?5.5?×?10-4) and rs4813802 at 20p12.3 (P interaction?=?0.04) in men. Interactions between smoking status and the rs6687758 at 1q41 (P interaction?=?0.03), duration and the rs174537 at 11q12.2 (P interaction?=?0.05), and pack-years and the rs4813802 (P interaction?=?0.04) were also found in women.Associations between susceptibility SNPs and CRC risk may be modified by smoking behaviors, supporting the existence of gene-smoking interactions.

SUBMITTER: Song N

PROVIDER: S-EPMC5737484 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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Effects of interactions between common genetic variants and smoking on colorectal cancer.

Song Nan N Shin Aesun A Jung Hye Soo HS Oh Jae Hwan JH Kim Jeongseon J

BMC cancer 20171219 1

<h4>Background</h4>Although genome-wide association studies (GWAS) have identified variants in approximately 40 susceptibility loci for colorectal cancer (CRC), there are few studies on the interactions between identified single-nucleotide polymorphisms (SNPs) and lifestyle risk factors. We evaluated whether smoking could modify associations between these genetic variants and CRC risk.<h4>Methods</h4>A total of 703 CRC patients and 1406 healthy controls were included in this case-control study f ...[more]

PMID: 29258461

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Project description:BACKGROUND: Metabolic syndrome traits play an important role in the development of colorectal cancer. Adipokines, key metabolic syndrome cellular mediators, when abnormal, may induce carcinogenesis. METHODOLOGY/PRINCIPAL FINDINGS: To investigate whether polymorphisms of important adipokines, adiponectin (ADIPOQ) and its receptors, either alone or in combination with environmental factors, are implicated in colorectal cancer, a two-stage case-control study was conducted. In the first stage, we evaluated 24 tag single nucleotide polymorphisms (tag SNPs) across ADIPOQ ligand and two ADIPOQ receptors (ADIPOR1 and ADIPOR2) among 470 cases and 458 controls. One SNP with promising association was then analyzed in stage 2 among 314 cases and 355 controls. In our study, ADIPOQ rs1063538 was consistently associated with increased colorectal cancer risk, with an odds ratio (OR) of 1.94 (95%CI: 1.48-2.54) for CC genotype compared with TT genotype. In two-factor gene-environment interaction analyses, rs1063538 presented significant interactions with smoking status, family history of cancer and alcohol use, with ORs of 4.52 (95%CI: 2.78-7.34), 3.18 (95%CI: 1.73-5.82) and 1.97 (95%CI: 1.27-3.04) for smokers, individuals with family history of cancer or drinkers with CC genotype compared with non-smokers, individuals without family history of cancer or non-drinkers with TT genotype, respectively. Multifactor gene-environment interactions analysis revealed significant interactions between ADIPOQ rs1063538, ADIPOR1 rs1539355, smoking status and BMI. Individuals carrying one, two and at least three risk factors presented 1.18-fold (95%CI:0.89-fold to 1.58-fold), 1.87-fold (95%CI: 1.38-fold to 2.54-fold) and 4.39-fold (95%CI: 2.75-fold to 7.01-fold) increased colorectal cancer risk compared with those who without risk factor, respectively (P(trend) <0.0001). CONCLUSIONS/SIGNIFICANCE: Our results suggest that variants in ADIPOQ may contribute to increased colorectal cancer risk in Chinese and this contribution may be modified by environmental factors, such as smoking status, family history of cancer and BMI.

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Effects of interactions between common genetic variants and smoking on colorectal cancer.

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Effects of interactions between common genetic variants and smoking on colorectal cancer.

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