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Mishra, V.C., Allen, D.J., Nicolaou, C., Sharif, H., Hudd, C., Karim, O.M.A., Motiwala, H.G. and Laniado, M.E. (2007) Does Intraprostatic Inflammation Have a Role in the Pathogenesis and Progression of Benign Prostatic Hyperplasia? BJU International, 100, 327-331.
http://dx.doi.org/10.1111/j.1464-410X.2007.06910.x

has been cited by the following article:

• TITLE: Non Selective Inhibition of COX Activity Reversed Inflammation and Reactive Oxygen Radicals Mediated Prostate Cancer Risk and Decreased Disease Progression in Preclinical Model

  AUTHORS: Maxwell Omabe, Kenneth Nwobini Omabe, Clement Ademola Famurewa, Alberta Egwu Okorocha, Grace Maxwell Omabe

  KEYWORDS: Inflammation, Prostate Cancer, Reactive Oxygen Species

  JOURNAL NAME: Journal of Cancer Therapy, Vol.7 No.1, January 28, 2016

  ABSTRACT: Prostate cancer (PCa) represents the most frequent urologic diagnosis in elderly males. We have previously shown that exposure of prostate to lipopolysaccharide (LPS) promotes cancer risk. We investigated the effect of non-selective cyclooxygenase (COX) inhibition on prostate inflammation-mediated cancer risk in vivo. The prostates of male rats were inoculated with E. coli as sources of inflammatory molecules (LPS) and were treated with COX inhibitor, aspirin 2 mg/Kg orally for 14 days or PBS. Oxidative stress was induced with two 2 mls of hydrogen peroxide orally twice daily or PBS for 14 days; they were either treated with COX inhibitor or PBS for another 14 days. Blood was collected and analyzed for acid phosphatase and PSA. Data showed presences of LPS in the prostate of the rats resulted in gradual increase in PSA when compared to control (P P 2O2 had 2.5 fold increase in acid phosphatase (ACP) compared control (P P ity in rats.