BETA 2 ADRENERGIC RECEPTORS AND PROSTATE CANCER RISK

Beta 2 肾上腺素能受体和前列腺癌风险

• 批准号: 6378158
• 负责人: Sara S. Strom
• 金额: $ 7.55万
• 依托单位: UNIVERSITY OF TX MD ANDERSON CAN CTR
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-07-17 至 2003-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6378158
• 关键词: adipose tissue; alleles; beta adrenergic receptor; cancer risk; cardiovascular disorder; clinical research; comorbidity; diabetes mellitus; dietary fiber; gene frequency; genetic markers; human subject; hypertension; male; neoplasm /cancer epidemiology; neoplasm /cancer genetics; prostate neoplasms; questionnaires; racial /ethnic difference; smoking; tobacco abuse

DESCRIPTION (Applicant's Description) This proposal is designed to build upon ongoing studies evaluating epidemiologic and molecular determinants of clinical prostate cancer (PC) susceptibility being conducted at the UT MD Anderson Cancer Center (CA 68578 M. Spitz, M.D., Principal Investigator, DAMD 17-98-1-8471 S.Strom, Ph.D., Principal Investigator. A role for individual variability in androgen biosynthesis as a modifier of PC risk is under intensive investigation. Based on the fact that catecholamines act synergistically with androgens through beta-adrenergic receptors as important regulators of prostate growth and differentiation, we present a novel hypothesis that individual genetic differences in the beta-adrenergic receptor may be associated with PC risk. Specifically, we will determine whether common allelic variants in beta-adrenergic gene modify the risk of developing prostate cancer. By integrating these genotypic data with information on diet, body composition, co-morbid conditions, and other lifestyle characteristics known to alter testosterone levels, we will gain insight into the role that individual variability in the neuroendocrine control of prostate growth plays in PC risk. The proposed pilot epidemiologic study will be the first of which we are aware to examine the contribution of gene-based variability in the beta-adrenergic response and risk of developing prostate cancer. Correlation of markers with PC risk in this pilot or hypothesis generating study would provide the impetus to pursue further the role of neuroendocrine factors in the etiology and progression of PC.

描述（申请人的描述）本提案旨在建立在 正在进行的研究，评估流行病学和分子决定因素， 在UT MD进行的临床前列腺癌（PC）易感性 安德森癌症中心（CA 68578 M。斯皮茨医学博士，主要研究者，DAMD 17-98-1-8471 S.Strom，Ph.D.，首席研究员。 个人角色 雄激素生物合成的变异性作为PC风险的修饰因子， 深入调查。 基于儿茶酚胺 通过β-肾上腺素能受体与雄激素协同作用， 调节前列腺生长和分化，我们提出了一种新的 β-肾上腺素能受体的个体遗传差异 可能与PC风险有关。 具体来说，我们将确定 β-肾上腺素能基因中常见的等位基因变异改变了发生 前列腺癌 通过整合这些基因型数据与信息， 饮食、身体成分、共病状况和其他生活方式 已知改变睾丸激素水平的特征，我们将深入了解 个体差异在前列腺神经内分泌调控中作用 增长在PC风险中发挥作用。 拟议的试点流行病学研究将是 首先我们知道要检查基于基因的贡献 β-肾上腺素能反应的变异性和前列腺增生的风险 癌 在该试验或假设中标志物与PC风险的相关性 开展研究将推动进一步发挥 神经内分泌因素在PC的病因和进展中的作用。