Relationship of the oxidative damage biomarker 8-epi-prostaglandin F2α to risk of lung cancer development in the Shanghai Cohort Study. (3rd May 2018)

• Record Type: Journal Article
• Authors: Yuan, Jian-Min; Carmella, Steven G; Wang, Renwei; Tan, Yu-Ting; Adams-Haduch, Jennifer; Gao, Yu-Tang; Hecht, Stephen S
• Is Part Of: Carcinogenesis. Volume 39:Number 7(2018)
• Page Start: 948
• Page End: 954
• Publication Date: 2018-05-03
• Subjects: Carcinogenesis -- Periodicals; Cancer -- Genetic aspects -- Periodicals; Cancer -- Prevention -- Periodicals; Cancer -- Periodicals; 616.994071
• DOI: 10.1093/carcin/bgy060
• Languages: English
• ISSNs: 0143-3334

Abstract

Abstract : Oxidative damage by cigarette smoking-induced free radicals is thought to play an important role in the development of lung cancer. Using urine from a prospective cohort of more than 18, 000 men, we quantified 8-epi-prostaglandin F20 in baseline urine. Smokers with elevated levels 8-epi-prostaglandin F20doubled risk of lung cancer. A heightened state of oxidative stress in response to the insults of cigarette smoking contributes to lung carcinogenesis. Abstract: It has been hypothesized that the pathogenesis of lung cancer induced by cigarette smoking involves oxidative damage by free radicals. Epidemiological data on biomarkers of oxidative damage and risk of lung cancer development are sparse. A nested case–control study of 610 lung cancer cases and 610 matched controls was conducted within a prospective cohort of 18 244 Chinese men in Shanghai, China. The concentrations of 8- epi -prostaglandin F2α (8- epi PGF2α ), a biomarker of oxidative stress, were determined in baseline urine samples using a validated mass-spectrometry assay. Current smokers had significantly higher level of 8- epi PGF2α than former smokers or never smokers ( P < 0.001). 8- epi PGF2α levels were significantly higher in lung cancer cases than their smoking-matched controls in former and current smokers, but not different in never smokers ( P for interaction = 0.019). The relative risks of developing lung cancer for former and current smokers in the highest relative to the lowest quartile of 8- epi PGF2α were 5.25 ( P trend = 0.035) and 1.99 ( P trend =0.007), respectively. The effect of 8- epi PGF2α and biomarkers of cigarette smoke exposure on lung cancer risk was additive; the relative risk was 5.33 (95% confidence interval = 2.65–7.51) for current smokers with the highest thirds of 8- epi PGF2α and total cotinine compared with their lowest thirds. Smokers with a heightened state of oxidative stress in response to the insults of cigarette smoking may be more susceptible to smoking-induced lung carcinogenesis.