Jin F et al. - In the current study it was shown that screening of smoke-associated metabolites and DNA adducts provides robust biomarkers and improve individual risk prediction in smokers for bladder cancer.

Methods
Liquid chromatography-mass spectrometry (LC-MS), and bioinformatic analysis were performed to determine the metabolome associated with bladder cancer in smokers.

Results
Smokers with bladder cancer had elevated levels of methylated metabolites, polycyclic aromatic hydrocarbons, DNA adducts, and DNA damage. DNA methyltransferase 1 expression was significantly higher in smokers than non-smokers with bladder cancer.
Strong associations existed between smokers and high-grade bladder cancer. In vitro exposure to the tobacco smoke carcinogens, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and benzo[a]pyrene was associated with increased levels of methylated metabolites, DNA adducts, and extensive DNA damage in bladder cancer cells.
Co-treatment of bladder cancer cells with these carcinogens and the methylation inhibitor, 5-aza-2'-deoxycytidine, rewired the methylated metabolites, DNA adducts, and DNA damage.