Abstract 2790: Prospective study of urinary prostaglandin E2 metabolite and lung cancer risk

Abstract

Abstract Cumulative evidence from both in vitro and animal studies suggests that cyclooxygenase-2 (COX-2) may be involved in the development and progression of lung cancer. Overproduction of prostaglandin E synthase and prostaglandin E2 (PGE2), one of the end products of the COX-2 pathway, has been implicated in the pathogenesis of non-small cell lung cancer. It is believed that the pro-inflammation effects of COX-2 pathway are largely mediated through PGE2. PGE2 is quickly converted to 11α-hydroxy-9,15-dioxo-2,3,4,5-tetranor-prostane-1,20-dioic acid (PGE-M), a major PGE2 metabolite and excreted from urine. In this study, we evaluated the association of urinary PGE-M levels and lung cancer risk. A nested case-control study was conducted within the Shanghai Women's Health Study, in which 74,942 Chinese women aged 40-70 years were recruited from 1997 to 2000 and followed up for up to 10 years. Urinary PGE-M in 192 incident lung cancer patients were compared to 192 matched controls. The baseline level of urinary PGE-M was comparable between cases and controls. Excluding 20 case-control pairs who were diagnosed with lung cancer within one year of follow-up or excluding 22 case-control pairs who ever smoked did not change the null association. No interaction was found between PGE-M and smoking or passive smoking in relation to lung cancer risk. Our data suggest that the PGE2 pathway may not play a major role in lung cancer development in non-smoking women. Further studies are being conducted to evaluate whether genetic variations in the PGE2 pathway will modify the urinary PGE-M and lung cancer association. Given the substantial laboratory evidence, further evaluation of the COX-2 pathway in lung cancer pathogenesis, including other urinary biomarkers and genetic variations, may be warranted. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2790.