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（申请人提供）： 该提案是为一个为期一天的研讨会提供财政支持的请求， 雌激素致癌机制将在美国化学学会上发表 学会全国会议，芝加哥，IL，8月26日至31日。 有明确 合成雌激素与内源性雌激素过度接触之间的关系 以及包括乳腺在内的多种组织中的癌症的发展， 子宫内膜肝脏和肾脏 除了遗传，已知的风险因素 患上这些癌症的女性都与较长时间的雌激素有关， 暴露：月经早，绝经晚，长期雌激素替代 疗法 雌激素致癌的机制尚不清楚。 的 这次研讨会的中心主题是，雌激素过度结合到 雌激素受体和/或醌类化合物的形成是一个重要的机制 致癌作用的内源性雌激素和某些雌激素存在于 雌激素替代处方。 本次研讨会的发言人 都由国家癌症研究所资助的R 01赠款支持。 在 此外，演讲者还在几个国家出版了同行评审的出版物， 备受推崇的期刊，包括由美国化学学会支持的期刊， 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，导致增强的细胞增殖和/或2）代谢 雌激素对O-醌类的作用，导致DNA氧化损伤和/或3） DNA的烷基化导致致癌物质的启动和促进 过程 考虑到过量暴露于雌激素之间的直接联系， 雌激素代谢，增加乳腺癌和子宫内膜癌的风险， 关键的是，影响形成、反应性和 雌激素及其代谢产物的细胞靶点有待深入研究。 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。