Abstract

Abstract Oxidative stress has been implicated in the development of prostate cancer (PCa); however, no study has comprehensively examined the associations between lipid, glucose and global oxidation with the development of prostate cancer. Using a prospective study design, we collected blood and urine samples among participants who are free of cancer in Ohio area. These participants were followed up 14 years. We selected 24 men who developed PCa during this period and matched them with 24 healthy controls by age and race among these participants (who did not develop prostate cancer) during this period. We measured the following biomarkers in these 48 samples (24 PCa cases and 24 health controls). Biomarkers included urine F2-isoprostanes (a marker of lipid oxidation), plasma advanced glycation end products (AGEs; a marker of advanced glycation and glucose oxidation), and plasma fluorescent oxidation products (FlOPs; markers of global oxidation). We have found that only AGEs were significantly higher in PCa cases than in health controls (182 vs. 152 μg/ml, P < 0.05). In the conditional logistic regression model, one standard deviation higher levels of AGEs were associated with increased risk of incident PCa (Relative risk = 1.79, 95% confidence interval = 1.00-3.21). In the model, one standard deviation higher levels of AGEs accounted for ∼8% variance of prostate cancer liability. Our results suggest that glycation and glucose oxidation but not lipid and global oxidation is an important etiology pathway for prostate cancer development. Lipid and global oxidation do not occur in parallel for the development of prostate cancer. If our results are confirmed by other studies, it may suggest a new pathway for prostate cancer prediction and treatment. Note: This abstract was not presented at the meeting. Citation Format: Tianying Wu. Lipid, glucose and global oxidation in relation to prostate cancer development. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 817. doi:10.1158/1538-7445.AM2015-817

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