COBRE: RIH: THEME A: FETAL PROTEINS & PHENOTYPES IN CANCER: COLON CARCINOMA

COBRE：RIH：主题 A：胎儿蛋白质

• 批准号: 7381874
• 负责人: GYORGY BAFFY
• 金额: $ 7.25万
• 依托单位: RHODE ISLAND HOSPITAL
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-07-01 至 2007-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7381874
• 关键词: COBRE; RIH; THEME; FETAL; PROTEINS

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. Background and Aims Evidence is accumulating that obesity increases the risk of colon cancer but the underlying molecular mechanisms are not well known. Oxidative stress appears to be a major factor in this process. We hypothesize that colon carcinogenesis will be affected by uncoupling protein-2 (UCP2), a mitochondrial anion carrier involved in producing reactive oxygen species (ROS). To critically test this hypothesis, we are using in vitro and in vivo experimental paradigms. In addition, we are evaluating the correlation between UCP2 expression in human-derived colon cancer and various tumor markers and factors involved in colon carcinogenesis. Development and growth of sporadic colon cancer, a cause of significant mortality in the US, is greatly affected by intracellular levels of reactive oxygen species (ROS). Mitochondria are the primary source of ROS. Uncoupling protein-2 (UCP2) controls mitochondrial ROS production and reduces oxidative stress, but the relevance of this ability to the biology of cancer cells remains unclear. It is hypothesized that UCP2 modulates the initiation and progression of colon cancer. This project was terminated in Jan. 2006 after a competitive review of 12 RFAs. (see Program Evaluation Report section) Dr. Baffy received a "transition award" from Rhode Island Hospital to support 6 months of research.

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。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。背景和目的越来越多的证据表明肥胖增加了结肠癌的风险，但其潜在的分子机制尚不清楚。氧化应激似乎是这一过程中的一个主要因素。我们假设结肠癌的发生将受到解偶联蛋白-2（UCP 2）的影响，UCP 2是一种参与产生活性氧（ROS）的线粒体阴离子载体。为了严格检验这一假设，我们正在使用体外和体内实验范例。此外，我们正在评估UCP 2在人源性结肠癌中的表达与各种肿瘤标志物和结肠癌发生相关因素之间的相关性。散发性结肠癌的发展和生长是美国显著死亡率的原因，其受到细胞内活性氧（ROS）水平的极大影响。线粒体是ROS的主要来源。解偶联蛋白-2（UCP 2）控制线粒体ROS产生并减少氧化应激，但这种能力与癌细胞生物学的相关性仍不清楚。假设UCP 2调节结肠癌的发生和进展。在对12个区域渔业协定进行竞争性审查后，该项目于2006年1月终止。(see项目评估报告部分）Baffy博士获得了罗得岛医院的“过渡奖”，以支持6个月的研究。