URINARY PGE-M, BIOMARKER OF TOBACCO-SMOKE LUNG INJURY

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The central hypothesis of this proposal is that short-term treatment with the selective COX-2 inhibitor celecoxib will suppress tobacco-smoke (TS) meditated elevation of urinary PGE-M concentration to levels comparable with those observed in never smokers. The primary purpose of this study is to better define the relationship between TS exposure and urinary PGE-M, the major metabolite of PGE2, in smokers and never smokers as there is increasing evidence to suggest that deregulated prostaglandin production may contribute to carcinogenesis. Secondarily, this study aims to determine the relative contribution of COX-2 activity to levels of urinary PGE-M, a potential biomaker of prostagladin production, in smokers and nonsmokers. We are also interested in the relationship between TS and angiogenesis since TS has been shown to induce VEGF as does PGE2. Therefore, it is reasonable to postulate that surrogate markers of angiogenesis may be increased in smokers compared to nonsmokers which may be suppressed by a week of celecoxib.