Inflammation and Chronic Prostatic Diseases: Evidence for a Link? Alessandro Sciarra, Franco Di Silverio, Stefano Salciccia, Ana Maria Autran Gomez, Alessandro Gentilucci, Vincenzo Gentile  European Urology  Volume 52, Issue 4, Pages 964-972 (October 2007) DOI: 10.1016/j.eururo.2007.06.038 Copyright © 2007 European Association of Urology Terms and Conditions

Fig. 1 Increased apoptotic activity in human benign prostatic hyperplasia tissue using a cyclooxygenase-2 inhibitor. Immunohistochemical analysis [25]. Arrows indicate increased apoptotic activity at epithelial cells level (TdT-mediated dUTP nick-end labeling method). European Urology 2007 52, 964-972DOI: (10.1016/j.eururo.2007.06.038) Copyright © 2007 European Association of Urology Terms and Conditions

Fig. 2 Inflammation and prostate growth: a possible pathogenetic mechanism. Role of oxidative stress by oxidant electrophiles, nitric oxide and cyclooxygenase activity; protective role of glutathione-S-transferase. European Urology 2007 52, 964-972DOI: (10.1016/j.eururo.2007.06.038) Copyright © 2007 European Association of Urology Terms and Conditions

Fig. 3 Possible event cascade for prostate cancer: inflammation as early event, proliferative inflammatory atrophy (PIA), prostatic intraepithelial neoplasia (PIN), and prostate cancer. Role of oxidants, nitric oxide, and cyclooxygenase-2 activities in the transition from inflammation and PIA. Role of glutathione-S-transferase–P1 methylation and inactivation in the transition from PIA to high-grade PIN and therefore to prostate cancer. European Urology 2007 52, 964-972DOI: (10.1016/j.eururo.2007.06.038) Copyright © 2007 European Association of Urology Terms and Conditions