6616 POSTER Impact of Progression on Resource Utilization in the Treatment of NET

Abstract

restriction fragment size was identified by horizontal electrophoresis. The survival was determined using Kaplan–Meier method, and the log-rank test was used for evaluation of differences in survival. The association between genetic factors and cancer risk were analyzed by logistic regression, and the results were expressed as odds ratios (OR) and 95% confidence intervals (CI). Statistical analyses were performed using CRAN 2.4.0 statistical software, and the decision on significance was based on p < 0.05. Results: Comparison of allele distribution between PC patients and controls demonstrated that Val/Val genotype carriers in codon 432 CYP1B1 had lower PC risk of pancreatic cancer development compared wild type carriers (OR 0.59; 95%CI 0.36–0.96; p = 0.035). Heterozygotes also had lower risk (OR 0.69; 95%CI 0.49–0.97; p = 0.033). There was an even more signficant increase of risk in patients who had histologically verified PC. Variant allele in GSTP1 codone 105 was associated with a trend of higher PC risk (OR 1.38; 95%CI 0.96–1.97, p < 0.05). Increased PC risk was also observed for GSTT1deletion (OR 1.56; 95%CI 0.93–2.61, p < 0.05). The combination of GSTT1 mutation and GSTP1 deletion was associted with significantly increased PC risk (OR 2.5; 95%CI 1.20–5.20; p < 0.05). No significant association was observed between the polymorphism of other biotransforming genes and PC risk, and none of the gene polymorphisms investigated was associated with differences in PC survival. Conclusions: Gene polymorphism of biotransforming genes may be associated with the risk of PC.