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PROSPECTIVE STUDY OF DIET AND PROSTATE CANCER

PROSPECTIVE STUDY OF DIET AND PROSTATE CANCER
饮食与前列腺癌的前瞻性研究
批准号:
6597571
负责人:
EDWARD GIOVANNUCCI
金额:
$27.95万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2002
资助国家:
美国
项目状态:
已结题
起止时间:
2002-04-01 至 2003-03-31

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中文摘要
翻译
描述:(申请者提供)该项目旨在确定饮食, 健康人群中与前列腺癌相关的激素和遗传因素 专业人员跟踪研究(HPFS)。尽管进展速度很慢 在大多数前列腺癌中,一部分患者将经历更多的 攻击性很强,通常是致命的。生物中的异质性 肿瘤进展的可能性可能与获得性分子有关 特点。因此,我们将尝试将饮食和荷尔蒙因素联系起来 与前列腺癌侵袭性行为相关的特定分子 决定生物潜能的特征,包括细胞 增殖、分化、凋亡、炎症和血管生成。我们 还将检查已确定的饮食和其他可修改的风险因素 在诊断后阶段,是否会影响以下人群的PSA复发风险 接受明显器官受限前列腺癌治疗的男性。因为我们的 最终目标是提供可行的预防方法,此外 许多目标都是为了了解这种疾病(激素、遗传因素、 总能量摄入量),我们的许多目标的重点是可改变的因素 (阿司匹林、钙、欧米茄-3脂肪酸、番茄红素和维生素E)。 1986年,在47,000名未患癌症的HPFS男性中,我们预计有4,124人 到2004年新增前列腺癌病例,包括573例转移性病例。我们也 计划从1,732例前列腺切除术病例中获取肿瘤块。的来源 HPFS中的暴露数据是(1)问卷,包括饮食,(2) 血浆样本(胰岛素样生长因子、性激素、维生素D、 类胡萝卜素),以及(3)血液和口腔细胞DNA中的MnSOD,维生素D和 雄激素受体CAG基因多态性。结果数据将基于(1) 初诊和复发的病历和病理报告审查 (2)微血管密度、血管内皮生长因子、环氧合酶-2、 PTEN缺失、增殖和凋亡。分层分析与多元分析 分析将用于控制潜在的混杂因素。这 该项目可能会产生重要的新发现,这可能有助于我们的 了解前列腺癌发病率的可改变的危险因素, 进展和复发。
英文摘要
DESCRIPTION: (provided by Applicant) This project aims to identify dietary, hormonal, and genetic factors related to prostate cancer in the Health Professionals Follow-Up Study (HPFS). In spite of the slow progression rates of most prostate cancers, a subset of patients will experience a more aggressive and generally fatal course. The heterogeneity in biologic potential for progression among tumors is likely related to acquired molecular characteristics. Thus, we will try to link dietary and hormonal factors that are related to aggressive behavior in prostate cancer to specific molecular characteristics that determine biologic potential, including cell proliferation, differentiation, apoptosis, inflammation, and angiogenesis. We will also examine whether identified dietary and other modifiable risk factors can, in the post-diagnostic period, influence the risk for PSA relapse among men treated with apparently organ-confined prostate cancer. Because our ultimate goal is to provide feasible approaches for prevention, in addition to many aims geared towards understanding the disease (hormones, genetic factors, total energy intake), the focus of many of our aims is on modifiable factors (aspirin, calcium, omega-3 fatty acids, lycopene (tomatoes), and vitamin E). Among 47,000 HPFS men free of cancer at baseline in 1986, we anticipate 4,124 new cases of prostate cancer by 2004, including 573 metastatic cases. We also plan to acquire tumor blocks from 1,732 prostatectomy cases. The sources of the exposure data in the HPFS are (1) questionnaire, including diet, (2) plasma samples (insulin-like growth factors, sex hormones, vitamin D, carotenoids), and (3) blood and buccal cell DNA for MnSOD, vitamin D and androgen receptor CAG polymorphisms. The outcome data will be based on (1) medical record and pathology report review for initial diagnosis and relapse (PSA failure), and (2) tissue blocks for microvessel density, VEGF, COX-2, PTEN loss, proliferation, and apoptosis. Stratified analysis and multivariate analysis will be used to control for potential confounding factors. This project is likely to yield important new findings that may help our understanding of modifiable risk factors for prostate cancer incidence, progression, and relapse.
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