Polymorphisms in genes related to activation or detoxification of carcinogens might interact with smoking to increase renal cancer risk: results from The Netherlands Cohort Study on diet and cancer.
until further notice
SourceWorld Journal of Urology, 26, 1, (2008), pp. 103-110
Article / Letter to editor
Display more detailsDisplay less details
Blood Transfusion and Transplantation Immunology
Epidemiology, Biostatistics & HTA
Radboud University Nijmegen Medical Centre
World Journal of Urology
SubjectNCEBP 1: Molecular epidemiology; NCMLS 2: Immune Regulation; ONCOL 1: Hereditary cancer and cancer-related syndromes; ONCOL 3: Translational research; ONCOL 5: Aetiology, screening and detection; UMCN 1.2: Molecular diagnosis, prognosis and monitoring
Metabolic gene polymorphisms have previously been suggested as risk factors for renal cell carcinoma (RCC). These polymorphisms are involved in activation or detoxification of carcinogens in cigarette smoke which is another RCC risk factor. We evaluated gene-environment interactions between CYP1A1, GSTmicro1 and smoking in a large population-based RCC case group. The Netherlands Cohort Study on diet and cancer (NLCS) comprises 120,852 persons who completed a questionnaire on smoking and other risk factors at baseline. After 11.3 years of follow-up, 337 incident RCC cases were identified. DNA was collected for 245 cases. In a case-only analysis, interaction-odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using logistic regression. We observed a moderate, not statistically significant, interaction between current smoking and CYP1A1*2C (OR 1.42; 95% CI 0.70-2.89) and GSTmicro1 null (OR 1.35; 95% CI 0.65-2.79). For current smokers with both a variant (heterozygous or homozygous) in CYP1A1 and GSTmicro1 null, risk was also increased (OR 1.63; 95% CI 0.63-4.24). No interaction was observed between ever smokers, smoking duration (increments of 10 smoking years) or amount (increments of 5 cigarettes/day) and CYP1A or GSTmicro1. Our results show a modest trend towards a statistically significant gene-environment interaction between CYP1A1, GSTmicro1 and smoking in RCC. This could indicate that RCC risk among smokers might be more increased with the CYP1A1*2C genotype, GSTmicro1 null, or both a CYP1A1 variant and GSTmicro1 null.
Upload full text
Use your RU credentials (u/z-number and password) to log in with SURFconext to upload a file for processing by the repository team.