Symposium on Mechanisms of estrogen carcinogenesis

雌激素致癌机制研讨会

• 批准号: 6415051
• 负责人: Judy L Bolton
• 金额: $ 1.29万
• 依托单位: UNIVERSITY OF ILLINOIS AT CHICAGO
• 依托单位国家: 美国
• 财政年份: 2001
• 资助国家: 美国
• 起止时间: 2001-08-01 至 2002-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6415051
• 关键词: breast neoplasms; chemical carcinogenesis; estrogens; hormone regulation /control mechanism; hormone related neoplasm /cancer; kidney neoplasms; liver neoplasms; meeting /conference /symposium; uterus neoplasms

DESCRIPTION (Provided by Applicant): This proposal is a request for financial support for a one day symposium on Mechanisms of Estrogen Carcinogenesis to be presented at the American Chemical Society national Meeting, Chicago, IL, Aug. 26-31. There is a clear association between excessive exposure to synthetic and endogenous estrogens and the development of cancer in several tissues including breast, endometrium, liver, and kidney. Besides heredity, the known risk factors for women developing these cancers are all associated with longer estrogen exposure: early menses, late menopause, and long term estrogen replacement therapy. The mechanism(s) of estrogen carcinogenesis is not known. The central theme of this symposium is that excessive binding of estrogens to the estrogen receptor and/or the formation of quinoids is an important mechanism of carcinogenesis for endogenous estrogens and certain estrogens present in estrogen replacement prescriptions. The speakers chosen for this symposium are all supported by R01 grants funded by the National Cancer Institute. In addition, the speakers have published peer-reviewed publications in several highly respected journals including those supported by the American Chemical Society. This symposium will explore three potential mechanisms of estrogen carcinogenesis, including 1) excessive binding of estrogens to the estrogen receptor leading to enhanced cell proliferation and/or 2) the metabolism of estrogens to 0-quinones causing either oxidative damage to DNA and/or 3) alkylation of DNA resulting in initiation and promotion of the carcinogenic process. Given the direct link between excessive exposure to estrogens, metabolism of estrogens, and increased risk of breast and endometrial cancer, it is crucial that factors which affect the formation, reactivity, and cellular targets of estrogens and their metabolites be throughly explored. This symposium will address all of these issues and establish key research areas for the future.

描述（由申请人提供）： 本提案请求为为期一天的研讨会提供财政支持 雌激素致癌机制将在美国化学展上发表 协会全国会议，伊利诺伊州芝加哥，8 月 26 日至 31 日。 有一个明确的 过度接触合成雌激素和内源雌激素之间的关联 以及包括乳腺癌在内的多种组织中癌症的发展， 子宫内膜、肝脏和肾脏。 除了遗传之外，已知的危险因素 女性患这些癌症都与较长的雌激素有关 暴露：月经提前、绝经晚期和长期雌激素替代 治疗。 雌激素致癌的机制尚不清楚。 这 本次研讨会的中心主题是雌激素与机体的过度结合 雌激素受体和/或醌类化合物的形成是一个重要机制 内源性雌激素和某些雌激素的致癌作用 雌激素替代处方。 本次研讨会选定的演讲嘉宾 全部由国家癌症研究所资助的 R01 赠款支持。 在 此外，演讲者还在多个出版物上发表了同行评审的出版物 备受推崇的期刊，包括美国化学会支持的期刊 社会。 本次研讨会将探讨雌激素的三种潜在机制 致癌作用，包括1）雌激素与雌激素过度结合 受体导致细胞增殖增强和/或 2) 代谢 雌激素转化为 0-醌，导致 DNA 氧化损伤和/或 3) DNA 烷基化导致致癌物质的启动和促进 过程。 鉴于过度接触雌激素之间存在直接联系， 雌激素代谢，增加患乳腺癌和子宫内膜癌的风险， 影响形成、反应性和反应性的因素至关重要 雌激素及其代谢物的细胞靶标得到彻底探索。 本次研讨会将解决所有这些问题并建立重点研究 未来的领域。