BIOMARKERS OF BLACK-WHITE DIFFERENCES IN PROSTATE CANCER

前列腺癌黑白差异的生物标志物

• 批准号: 3204653
• 负责人: FANNY K ENNEVER
• 金额: $ 22.85万
• 依托单位: WAKE FOREST UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1993
• 资助国家: 美国
• 起止时间: 1993-08-20 至 1996-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3204653
• 关键词: African American; DNA damage; DNA repair; biomarker; cadmium; cancer risk; caucasian American; chemical carcinogen; environment related neoplasm /cancer; human subject; lifestyle; male; neoplasm /cancer epidemiology; nutrition related neoplasm /cancer; nutrition related tag; prostate neoplasms; racial /ethnic difference; toxin metabolism; urinalysis

The incidence of prostate cancer, the second leading of cancer deaths in men, appears to be rising, and occurs about 50% more often in Black men than in White men. Although environmental and genetic factors influence prostate cancer risk, little is currently known about specific environmental risk factors and how they interact with individual susceptibility. This application proposes to identify factors associated with prostate cancer in general and also how those factors may contribute to the significantly higher rate in Black men in particular. A case- control study is proposed, investigating 125 men with prostate cancer (50 Black and 75 White) and 250 age- and race-matched community controls. The research will take advantage of the ability of biomarkers to provide individual-specific information on exposure to, effect of, and/or susceptibility to prostate carcinogens. Three sets of biomarkers will be used, each investigating a specific hypothesis. The first hypothesis is that exposure to cadmium increases the risk of prostate cancer, and urinary cadmium concentration will be used as a biomarker of lifetime cadmium exposure. The second hypothesis is that the lower an individual's DNA capacity, the higher his risk of prostate cancer. Inherent DNA repair capacity will be estimated using biomarkers that reflect the net result of recent oxidative damage and inherent repair capacity and that reflect only recent oxidative damage. The third hypothesis is that increased activity of metabolic pathways may convert environmental chemicals and other xenobiotic compounds to carcinogens increase the risk of prostate cancer, using the ratio of parent compound to metabolites in urine as biomarkers of metabolic activity. The results of these biomarker measurements will be analyzed to determine case- control differences. In addition, associations with traditional prostate cancer risk factors will be analyzed for subsets of cases and controls, using the biomarkers of DNA repair capacity and metabolic activity to define men who may be more susceptible to risk factors than the cohort as a whole. This research has the potential to identify factors associated with prostate cancer risk, which would suggest further investigation of specific environmental causes of prostate cancer, which will lead to a better understanding of ways to prevent prostate cancer.

前列腺癌的发病率是癌症死亡的第二次领导 男人，似乎正在上升，黑人的发生大约50％ 比白人。 虽然环境和遗传因素影响 前列腺癌风险，目前对特定的了解知之甚少 环境风险因素以及他们如何与个人互动 敏感性。 该申请建议确定相关因素 总体上，前列腺癌以及这些因素如何贡献 尤其是黑人男性的比率明显更高。 案件 - 提出了对照研究，研究了125名前列腺癌男性（50 黑色和75个白色）和250年龄和赛车匹配的社区控制。 该研究将利用生物标志物提供的能力 有关暴露，影响和/或的个人特定信息 对前列腺致癌物的敏感性。 三套生物标志物将 使用，每个研究特定假设。 第一个假设 是否暴露于镉会增加前列腺癌的风险，并且 泌尿镉浓度将用作寿命的生物标志物 镉暴露。 第二个假设是较低 个体的DNA容量，他患前列腺癌的风险越高。 固有的DNA维修能力将使用生物标志物进行估算 反映最近氧化损伤和固有修复的净结果 容量，这仅反映了最近的氧化损伤。 第三 假设是，代谢途径的活动增加可能会转化 致癌物的环境化学品和其他异生物化合物 使用母体化合物的比率增加前列腺癌的风险 将尿液中的代谢物作为代谢活性的生物标志物。 结果 将分析这些生物标志物测量值以确定病例 - 控制差异。 此外，与传统前列腺的关联 将分析病例和对照组的癌症风险因素， 使用DNA修复能力和代谢活性的生物标志物 定义可能比同队员更容易受风险因素的男人 整体。 这项研究有可能确定因素 与前列腺癌风险有关，这将进一步 研究前列腺癌的特定环境原因，这 将会更好地理解预防前列腺癌的方法。