Symposium on Mechanisms of estrogen carcinogenesis

描述(由申请人提供)： 这项建议是为一个为期一天的研讨会申请财政支持。 雌激素致癌机制将在美国化学学会上发表 协会全国会议，伊利诺伊州芝加哥，8月26日至31日。有一种明确的 过量暴露于合成雌激素和内源性雌激素之间的关系 以及包括乳腺癌在内的几种组织中癌症的发展， 子宫内膜、肝脏和肾脏。除了遗传，已知的风险因素 罹患这些癌症的女性都与雌激素过长有关。 暴露：月经早、绝经晚和长期雌激素替代 心理治疗。雌激素致癌的机制(S)尚不清楚。这个 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/或藜麦类化合物的形成是一个重要的机制 内源性雌激素和某些雌激素的致癌作用 雌激素替代处方。为这次研讨会选定的演讲者 都是由国家癌症研究所资助的R01赠款支持的。在……里面 此外，发言者还出版了几份同行评议的出版物。 备受推崇的期刊，包括那些由美国化学协会支持的期刊 社会。本次研讨会将探讨雌激素的三种潜在作用机制。 致癌，包括1)雌激素与雌激素的过度结合 受体促进细胞增殖和/或2)新陈代谢 雌激素对0-苯二酚造成DNA氧化损伤和/或3) DNA的烷基化导致致癌物的启动和促进 进程。鉴于过度接触雌激素之间的直接联系， 雌激素的代谢，以及乳腺癌和子宫内膜癌风险的增加， 至关重要的是，影响形成、反应性和 彻底探索雌激素及其代谢物的细胞靶点。 本次研讨会将讨论所有这些问题，并建立关键研究 面向未来的领域。

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.