GORDON RESEARCH CONFERENCE ON HORMONAL CARCINOGENESIS

这项提议要求提供资金，以协助支持第二个 两年一度的戈登激素研究会议 致癌将在纽约新汉普顿学校举行 汉普郡，1987年8月2日至7日。这次会议是为了召集一位 一系列相关的多学科实验体系 共同的目标是了解细胞的增殖和 激素在细胞和组织中的致癌活性 在内分泌器官和靶组织中的水平。这将提供一个 一群不同的基础科学家有机会分享他们的 在非正式讨论和询问中的新想法和新数据 这次会议的一周。其中一些最令人不安的属性 类固醇和非类固醇激素，特别是雌激素，是 它们的致癌活性。为了解决这个问题， 这是越来越令人关注的，以下会议主题将 在我们即将到来的会议上介绍：(1)与激素相关的 人类癌症.处理致癌方面的问题 宫内暴露于DES和激素、致癌物和 子宫内膜细胞；(2)分化和经胎盘 致癌-处理经胎盘暴露于DES和 乳腺发育与癌的发生及特异性 致癌物诱导的肿瘤中癌基因的激活与 宿主发育；(3)细胞增殖的培养模型- 转化生长因子在上皮细胞中的作用 雌激素和抗雌激素调节的生长分泌系统 人类乳腺癌中的因子和催乳素生长因子，以及 乳腺癌；(4)生长因子与癌基因交易 雌激素诱导细胞的细胞分子机制研究 转化与类固醇激素受体与基因调控 乳腺癌的表达；(5)激素分期 致癌--雌激素诱导的组织发生 仓鼠肾癌与雌激素的促进作用 大鼠肝细胞癌变；(6)生物活化和不可逆性 结合-处理雌激素生物激活和调节的调节 雌激素的代谢和生物激活与DNA损伤 叙利亚地鼠肾；(7)P-450在类固醇羟化中的作用 -处理邻苯二酚雌激素的形成：过多 现象，肝细胞色素P-450：内源性调节 类固醇代谢和共价雌激素与特异性结合 仓鼠细胞色素P-450‘S：可能的后果；(8)雄激素 致癌-处理组合雄激素-雌激素- 大鼠平卧背侧诱发的增生和异型增生 和类固醇诱发的肿瘤在雄性叙利亚仓鼠中出现 生殖道：自分泌调节肿瘤生长 机制。

This proposal requests funds to assist in the support of the second biennial Gordon Research Conference on Hormonal Carcinogenesis to be held in the New Hampton School, New Hampshire, August 2-7, 1987. This meeting is to bring together a series of multidisciplinary experimental systems that are related by the common goal of understanding the cell proliferative and carcinogenic activities of hormones at the cellular and organismal levels in endocrine organs and target tissues. This will provide an opportunity for a diverse group of basic scientists to share their new ideas and data in informal discussion and enquiry during the week of this conference. The most disturbing property of some steroidal and nonsteroidal hormones, particularly estrogens, is their carcinogenic activity. In an effort to address this problem, which is of increasing concern, the following session topics will presented in our upcoming Conference: (1) Hormone Associated Human Cancers - dealing with carcinogenic aspects of intrauterine exposure to DES and hormones, carcinogens and endometrial cells; (2) Differentiation and Transplacental carcinogenesis - dealing with transplacental exposure to DES and mammary development and carcinogenesis and specificity of oncogene activation in carcinogen-induced tumors is related to host development; (3) Culture Models for Cell Proliferation - dealing with role of transforming growth factors in epithelial cell systems, estrogen and antiestrogen regulated secretion of growth factors in human breast cancers and prolactin growth factors, and mammary cancers; (4) Growth Factors and Oncogenes - dealing with cellular and molecular mechanisms of estrogen induced cell transformation and steroid hormone receptors and control of gene expression in breast cancer; (5) Stages in Hormonal Carcinogenesis - dealing with histogenesis of estrogen-induced renal carcinomas in the hamster and estrogen promotion of hepactcarcinogenesis in rats; (6) Bioactivation and Irreversible Binding - dealing with regulation of estrogen bioactivation and metabolism and bioactivation of estrogens and DNA damage in Syrian hamster kidney; (7) Role of P-450 in Steroid Hydroxylation - dealing with catechol estrogen formation: a plethora of phenomena, hepatic cytochromes P-450: regulation of endogenous steroid metabolism and covalent estrogen binding to specific hamster cytochrome P-450's: possible consequences; (8) Androgen Carcinogenesis - dealing with combined androgen-estrogen- induced hyperplasia and dysplasia in the rat dorslateral prostrate and steroid induced tumors arising in the male Syrian hamster reproductive tract: regulation of tumor growth by autocrine mechanism.