MOLECULAR EPIDEMIOLOGY AND PREVENTION OF BREAST CANCER

乳腺癌的分子流行病学和预防

• 批准号: 7376658
• 负责人: STEVEN A AKMAN
• 金额: $ 0.05万
• 依托单位: WAKE FOREST UNIVERSITY HEALTH SCIENCES
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-04-17 至 2007-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7376658
• 关键词: DNA; DNA repair; breast neoplasms; cancer risk; epidemiology; genotype; human; lipids; neoplasm /cancer; peroxidation; prevention

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. This study will use a cancer case-control study design to evaluate two hypotheses. The study subjects will include 800 incident breast cancer cases (recruited from the Departments of Surgery and Hematology/Oncology) and 800 controls (frequency-matched by age and race). A self-administered questionnaire will be used to collect data on other known breast cancer risk factors - such as demographic factors, family history of cancer, medication, ionizing radiation exposure, smoking, and ethanol consumption. The first study is to evaluate the role of DNA repair in human breast cancer risk. The working hypothesis is that breast cancer risk is associated with defective/deficient DNA repair. Mitogen-activated peripheral T-lymphocytes will be used for DNA repair functional measurements. Genomic DNA will be used for the determination of genetic variants of DNA repair genes (i.e., XRCC1, XRCC3, XPD, APE, and PARP). The second study is to evaluate the interaction between drug metabolism enzymes, GSTT1/M1 and dietary fat in human breast cancer risk. The working hypothesis is that women with null GSTM1/T1 genotypes cannot effectively detoxify reactive free radicals, which may lead to lipid peroxidation, oxidative DNA damage. Genomic DNA will be used for the GSTT1/M1 genotyping. Plasma samples will be used to measure fatty acid profile and lipid peroxidation levels.

该子项目是利用 NIH/NCRR 资助的中心拨款提供的资源的众多研究子项目之一。子项目和研究者 (PI) 可能已从另一个 NIH 来源获得主要资金，因此可以在其他 CRISP 条目中出现。列出的机构是中心的机构，不一定是研究者的机构。本研究将使用癌症病例对照研究设计来评估两个假设。研究对象将包括 800 例乳腺癌病例（从外科和血液学/肿瘤科招募）和 800 例对照（按年龄和种族进行频率匹配）。自填问卷将用于收集其他已知乳腺癌风险因素的数据，例如人口因素、癌症家族史、药物、电离辐射暴露、吸烟和乙醇消耗。第一项研究是评估 DNA 修复在人类乳腺癌风险中的作用。目前的假设是乳腺癌风险与 DNA 修复缺陷/缺陷有关。丝裂原激活的外周 T 淋巴细胞将用于 DNA 修复功能测量。基因组 DNA 将用于确定 DNA 修复基因的遗传变异（即 XRCC1、XRCC3、XPD、APE 和 PARP）。第二项研究是评估药物代谢酶、GSTT1/M1 和膳食脂肪之间的相互作用在人类乳腺癌风险中的作用。工作假设是，GSTM1/T1 基因型无效的女性无法有效解毒反应性自由基，这可能导致脂质过氧化、氧化性 DNA 损伤。基因组 DNA 将用于 GSTT1/M1 基因分型。血浆样本将用于测量脂肪酸谱和脂质过氧化水平。