Metabolic gene polymorphisms have previously been suggested as risk factors for renal cell carcinoma (RCC). These polymorphisms are involved in activation or detoxiWcation of carcinogens in cigarette smoke which is another RCC risk factor. We evaluated gene-environment interactions between CYP1A1, GST 1 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 identiWed. DNA was collected for 245 cases. In a case-only analysis, interaction-odds ratios (OR) and 95% conWdence intervals (95% CI) were calculated using logistic regression. We observed a moderate, not statistically signiWcant, interaction between current smoking and CYP1A1*2C (OR 1.42; 95% CI 0.70-2.89) and GST 1 null (OR 1.35; 95% CI 0.65-2.79). For current smokers with both a variant (heterozygous or homozygous) in CYP1A1 and GST 1 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 GST 1. Our results show a modest trend towards a statistically signiWcant gene-environment interaction between CYP1A1, GST 1 and smoking in RCC. This could indicate that RCC risk among smokers might be more increased with the CYP1A1*2C genotype, GST 1 null, or both a CYP1A1 variant and GST 1 null.
AI at the prostate cancer susceptibility loci HPC1, PCaP, and HPC20 was seen more often in HPC compared with SPC. It appears that there are marked differences in the pattern of AI between sporadic and hereditary PCa.
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