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

尿 PGE-M，烟草烟雾肺损伤的生物标志物

• 批准号: 7378427
• 负责人: ANDREW Jess DANNENBERG
• 金额: $ 3.65万
• 依托单位: WEILL MEDICAL COLL OF CORNELL UNIV
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-04-01 至 2007-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7378427
• 关键词: URINARY; PGE; BIOMARKER; TOBACCO; SMOKE

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.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子弹和调查员（PI）可能已经从其他NIH来源获得了主要资金，因此可以在其他清晰的条目中代表。列出的机构适用于该中心，这不一定是调查员的机构。该提案的中心假设是选择性COX-2抑制剂Celecoxib的短期治疗将抑制尿液中PGE-M浓度冥想升高到与从未吸烟者中观察到的水平相当的水平。这项研究的主要目的是更好地定义TS暴露与PGE-M（PGE-M的主要代谢物）在吸烟者中的主要代谢物，而从不吸烟之间的关系，因为越来越多的证据表明，前列腺素的产生可能有助于癌变。其次，本研究旨在确定吸烟者和非吸烟者中尿PGE-M的相对贡献，PGE-M是前列腺素产生的潜在生物机构。我们还对TS与血管生成之间的关系感兴趣，因为TS已显示出像PGE2一样诱导VEGF。因此，与非吸烟者相比，吸烟者可能会增加血管生成的替代标志物，这是合理的，与一周的塞来昔布抑制了非吸烟者相比。