These methodological differences in NAT SNPs assayed across studies, makes it impossible to make comparisons Veliparib price and draw any firm conclusions about the role of polymorphic NATs in prostate cancer risk. In the current study, genotype misclassification was minimized due to the determination of the fifteen SNPs in NAT1 and NAT2 pertinent to classifying genotypes accurately. In addition, the quality of the genotype data is strengthened by lack of departures from Hardy-Weinberg equilibrium, stringent quality control standards, and the observation of NAT1 and NAT2 genotype frequencies commensurate with published reports involving men of African descent. Cigarette smoking may increase a man��s risk for developing and dying from PCa, based on pooled data from 24 studies involving 21,600 men with the disease indicates.

6 This meta-analysis, conducted by Huncharek and colleagues (2010) pooled findings from numerous studies to better illuminate risks not clearly shown in previous individual studies. Pooled analysis revealed consistent evidence that both the chance of developing PCa and dying from PCa increases with smoking, even though many of the studies analyzed used crude smoking classifications (i.e., ever versus never smoking). In eight studies that provided more in-depth number of cigarettes smoked per day in nearly 8,700 men, Huncharek��s team revealed a 1.3 fold increase in the risk of dying from PCa in the heaviest smokers versus nonsmokers. They also observed a 1.22 fold increase in PCa risk among the heaviest smokers, based on pooled information from four studies of about 2,100 men.

In an exploratory analysis, we assessed whether a crude smoking classification (i.e., ever versus never smoking) combined with inheritance of slow NAT2 (linked with a reduced capacity to detoxify cigarette-derived procarcinogens (i.e., aromatic amines) would increase one��s chances of developing PCa. However, we were unable to observe significant gene-environment interactions. Nevertheless, we cannot ignore the possibility that the lack of available data on duration of smoking, tobacco smoking preferences (cigarette, pipe, cigars), and the extent of inhalation may lead to under-estimation of both exposure to cigarette-smoke derived agents as well as observed risk estimates. In addition, subsequent studies with adequate statistical power are necessary to effectively evaluate gene- environment interactions.

Emphasis needs to be placed on studies that quantify the number of cigarette packs and smoking duration that influence PCa risk and progression. Drug_discovery We considered the strengths and challenges of the current study. Like many genetic epidemiology studies, the current study did not adjust risk estimates for potential cofounders such as family history of prostate cancer, body mass index, and socio-economic status.