Utilization of bioinformatic tools designed to detect higher-order interactions even in the absence of main effects should become a standard practice within future prostate cancer epidemiology studies. This is a reasonable suggestion www.selleckchem.com/products/MDV3100.html especially since MDR has been reported in more than 90 genetic epidemiology studies based on a recent pubmed search. In summary, we did not observe strong main or gene combination effects of NAT1 and NAT2 polymorphisms in relation to PCa risk among men of African descent. However, confirmation is required in culturally diverse studies with more detailed exposure assessments using publically available data- mining tools. Consequently, our laboratory will consider whether other biotransformation related genes alone or in combination with environmental exposures predict PCa risk among men of African descent using data collected from a multi-center study.
Such findings will facilitate future studies focused on improving cancer prevention or detection strategies and ultimately reducing PCa health disparities. Supplementary Table Table SA Effect modification of NAT1 and NAT2 in relation to PCa susceptibility. #NAT1*10 alleles #Slow NAT2 alleles Cases (%)|| controls (%) Estimated OR (95% CI)a Estimated OR (95% CI)b P-value for Interaction 0 or 1 0 NAT2 Slow 12 (7.1) || 43 (9.4) 1.00 (Referent) 1.00 (Referent) 0.2897 0 or 1 1 NAT2 Slow 58 (34.3) || 158 (34.8) 1.32 (0.65�C2.67) 1.01 (0.46�C2.22) 0 or 1 2 NAT2 Slow 63 (37.3) || 132 (29.1) 1.71 (0.84�C3.47) 1.63 (0.74�C3.58) 2 0 NAT2 Slow 3 (1.8) || 18 (4.0) 0.60 (0.15�C2.37) 0.73 (0.17�C3.
13) 2 1 NAT2 Slow 22 (13.0) || 54 (11.9) 1.46 (0.65�C3.28) 1.18 (0.48�C2.90) 2 2 NAT2 Slow 11 (6.5) || 49 (10.8) 0.80 (0.32�C2.01) 0.75 (0.28�C2.04) 0 or 1 0 NAT2 Rapid 63 (37.3) || 132 (29.1) 1.00 (Referent) 1.00 (Referent) 0.2156 0 or 1 1 NAT2 Rapid 58 (34.3) || 158 (34.8) 0.77 (0.50�C1.18) 0.62 (0.38�C1.02) 0 or 1 2 NAT2 Rapid 12 (7.1) || 43 (9.4) 0.58 (0.29�C1.18) 0.61 (0.28�C1.34) 2 0 NAT2 Rapid 11 (6.5) || 49 (10.8) 0.47 (0.23�C0.97) 0.46 (0.21�C1.01) 2 1 NAT2 Rapid 22 (13.0) || 54 (11.9) 0.85 (0.48�C1.52) 0.72 (0.38�C1.40) 2 2 NAT2 Rapid 3 (1.8) || 18 (4.0) 0.35 (0.10�C1.23) 0.45 (0.12�C1.68) View it in a separate window Notes: aAssociations were determined using univariate logistic regression models to estimate the risk of developing PCa.
151 subjects had missing genotype data for NAT1 and/or NAT2; bRisk estimates adjusted for age (continuous variable) and West African Ancestry (WAA; continuous variable). Table SB Combined effects of N-acetyltransferase polymorphisms and cigarette smoking on PCa risk. N-acetyltransferase status Unadjusted OR (95% CI)a #Cases||#Ctrlsc Adjusted OR (95% CI)b Non-smokers Ever-smokers Non-smokers Ever-smokers NAT2 Rapid alleles 1.00 (Reference) 5||5 Dacomitinib 2.04 (0.54�C7.62) 57||28 1.