PROSPECTIVE STUDY OF DIET AND PROSTATE CANCER

描述：（由申请人提供）本项目旨在确定饮食， 前列腺癌的病因有哪些？ 专业人士随访研究（HPFS）。尽管进展缓慢 在大多数前列腺癌中，一部分患者会经历更多的 侵略性和通常致命的过程。生物学中的异质性 肿瘤进展的可能性可能与获得性分子生物学相关。 特色因此，我们将尝试将饮食和荷尔蒙因素联系起来， 与前列腺癌的侵袭行为有关， 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改变的风险因素是否 在诊断后阶段，可以影响PSA复发的风险， 患有明显局限于器官的前列腺癌的男性因为我们的 最终目标是提供可行的预防方法， 许多旨在了解疾病的目标（激素，遗传因素， 总能量摄入），我们的许多目标的重点是可修改的因素 （阿司匹林，钙，欧米茄-3脂肪酸，番茄红素（西红柿）和维生素E）。 在1986年47，000名基线无癌症的HPFS男性中，我们预计有4，124人 到2004年，新的前列腺癌病例，包括573例转移病例。我们也 计划从1,732例乳腺切除术病例中获取肿瘤块。的来源 HPFS中的暴露数据为（1）问卷调查，包括饮食，（2） 血浆样品（胰岛素样生长因子，性激素，维生素D， 类胡萝卜素），和（3）血液和口腔细胞的MnSOD，维生素D和 雄激素受体CAG多态性。结局数据将基于（1） 病历和病理报告审查，用于首次诊断和复发 (PSA失败），和（2）用于微血管密度，VEGF，考克斯-2， PTEN丢失、增殖和凋亡。分层分析和多元 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， 了解前列腺癌发病率的可改变风险因素， 进展和复发。

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.