Statistical analysis Age is presented as median and interquartile range (IQR) because the data showed departures from normality (according to Shapiro-Wilk’s

test). The χ2 method was used to test frequencies of genotypes/allele in prostate cancer patients and controls. buy GS-1101 The strength of the nominal association in the contingency tables is reflected by Cramér’s (V) coefficient of contingency. The odds ratios (OR), estimates of the relative risk, with 95% confidence intervals (CI) were computed to assess strengths of association of the genotypes with prostate cancer. All p values cited are two-sided alternatives; differences resulting in a p value of less or equal to 0.05 were declared statistically significant [16]. The Hardy Weinberg equilibrium was tested for the genotype proportions in the control group, as a measure for quality control. Results Since previous reports suggested that there are no differences in GSTM1, GSTT1 and GSTP1 allele frequencies in relation to age and sex [17], we conducted a retrospective study on a selected population of men in order to examine whether the gene frequencies were https://www.selleckchem.com/products/Temsirolimus.html consistent with research findings Roscovitine cell line across Europe. Statistical analysis of data collected from a survey of community sample in the north-western part of Slovakia showed

that our estimates were not significantly different from either those found in the Caucasian population of Garte and co-workers [1] (Table 2) or those found previously by a research group in Slovakia [1] (Table 3). Table 2 Distribution of GSTP1, GSTT1 and GSTM1 genotypes in our control group

and in Caucasian population (GSEC project-Genetic Susceptibility to Environmental Carcinogens) published by Garte and co-workers [1]. Polymorphism Our control group Number (%) of subjects Caucasians-GSEC Number (%) of subjects 95% CI for proportion difference Cramér’s V p-value GSTP1           No. 228 1137       Ile/Ile 110 (48.2) 498 (43.8) -0.03 to 0.12 0.033 0.22 Ile/Val+Val/Val 118 (51.8) 561 (49.3) -0.05 to 0.09 0.018 0.51 GSTT1           No. 228 5577       positive 183 (80.3) 4774 (80.2)       null 45 (19.7) 1103 (19.8) -0.05 to 0.06 0.005 0.99 GSTM1           No. 228 10514       positive 98 (43.0) 4931 (46.9) IMP dehydrogenase       null 130 (57.0) 5583 (53.1) -0.03 to 0.10 0.011 0.24 Table 3 Distribution of GSTT1 and GSTM1 genotypes in our control group and in Slovak population (GSEC project-Genetic Susceptibility to Environmental Carcinogens) published by Garte and co-workers [1]. Polymorphism Our control group Number (%) of subjects Slovak population-GSEC Number (%) of subjects 95% CI for proportion difference Cramér’s V p-value GSTT1           No. 228 332       positive 183 (80.3) 272 (82.0)       null 45 (19.7) 60 (18.0) -0.05 to 0.09 0.021 0.62 GSTM1           No. 228 332       positive 98 (43.0) 162 (48.8)       null 130 (57.0) 170 (51.2) -0.03 to 0.14 -0.057 0.