72 (GSTP1), p = 0 8 (GSTT1) and p = 0 43 (GSTM1)] Because the pu

72 (GSTP1), p = 0.8 (GSTT1) and p = 0.43 (GSTM1)]. Because the published data about the association of GST polymorphism and susceptibility QNZ to prostate cancer are not conclusive, and because it was suggested that the incidence of prostate cancer varies with geography,

the second purpose of the study was to analyze the strength of these associations in our selected population. Calculated chi-square for equality of mean column scores and Cramér’s V yielded 0.506 and 0.023, respectively, which did not account for significant differences in the GST frequencies between healthy subjects and those diagnosed with prostate cancer. The absence of any association between null genotypes or polymorphism in GST and prostate cancer was confirmed also by analyzing case-control groups. Table 4 shows the distribution of the GST genotypes among PI3K inhibitor controls and prostate cancer patients. The patients did not have significantly different frequencies in genotypes and alleles in comparison to controls. Table 4 Distribution of GSTP1, GSTT1 and GSTM1 genotypes in controls and patients with prostate cancer. Polymorphism Controls Number (%) of subjects Cases Number (%) of subjects 95% selleck kinase inhibitor CI for proportion difference Cramér’s V OR (95% CI)

p-value GSTP1             No. 228 129         Ile/Ile 110 (48.2) 56 (43.4)     1.0   Ile/Val+Val/Val 118 (51.8) 73 (56.6) -0.15 to 0,06 0.047 0.72 (0.45 to 1.13) 0.38 Val/Val 5 (2.2) 6 (4.7) -0,08 Coproporphyrinogen III oxidase to 0,01 0.068 2.17 (0.54 to 9.18) 0.22 GSTT1             No. 228 129         positive 183 (80.3) 105 (81.4)     1.0   null 45 (19.7) 24 (18.6) -0.08 to 0.09 -0.014 0.93 (0.51 to 1.66) 0.80 GSTM1             No. 228 129         positive 98 (43.0) 60 (46.5)     1.0   null 130 (57.0) 69 (53.5) -0,07 to 0,14 0.034 0.87 (0.55 to 1.37) 0.52 In addition, we have found no clear association between smoking habits and prostate cancer, and between smoking habits and single or combined genotypes in relation to prostate cancer. Neither did the comprehensive score, a pooled value indicating the presence of at least one variant allele,

show a significantly reduced or unchanged risk of prostate cancer (data not shown). Discussion and evaluation To assess possible association between GST gene polymorphisms and occurrence of prostate cancer in Slovakia, we had to infer from population estimates acquired in the first part of the study on a sample of 228 consecutive men who scheduled appointments in the Department of Urology. It is known that the allele frequencies of metabolic genes are not equally distributed throughout the human population but follow diverse ethnic and/or geographic-specific patterns. Our results on GSTM1 – and GSTT1 -null frequencies, 57% and 19.7%, respectively, did not differ significantly either from the values obtained previously by a Slovakian group of researchers (51.2% and 18%, respectively) or from those published by other authors [1].

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