GORDON RESEARCH CONFERENCE ON HORMONAL CARCINOGENESIS

该提案要求提供资金，以协助支持第二个 两年一度的戈登激素研究会议 致癌作用将在新汉普顿学校举行，新 汉普郡，1987年8月2日至7日。 这次会议是为了汇集一个 一系列相关的多学科实验系统 通过共同的目标，了解细胞增殖和 激素在细胞和器官中的致癌活性 内分泌器官和靶组织中的水平。 这将提供一个 一个机会，一个不同的基础科学家群体分享他们的 会议期间非正式讨论和询问中的新想法和数据 本周的会议。 最令人不安的财产的一些 类固醇和非类固醇激素，特别是雌激素， 其致癌活性。 为了解决这个问题， 这是日益关注的，以下会议主题将 在我们即将举行的会议上提出：（1）激素相关 人类癌症-处理癌症的致癌方面 子宫内暴露于DES和激素、致癌物和 子宫内膜细胞;（2）分化和经胎盘 致癌作用-处理经胎盘暴露于DES， 乳腺发育和癌变的特异性 致癌物诱导的肿瘤中的癌基因激活与 （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 系统，雌激素和抗雌激素调节生长分泌 人乳腺癌中的因子和催乳素生长因子，以及 乳腺癌;（4）生长因子和癌基因处理 雌激素诱导细胞凋亡的细胞分子机制 类固醇激素受体与基因调控 乳腺癌中的表达;（5）激素 致癌作用-处理雌激素诱导的 仓鼠肾癌与雌激素促进 （6）生物激活和不可逆性 结合-处理调节雌激素生物活化和 雌激素的代谢和生物活化以及DNA损伤 叙利亚仓鼠肾;（7）P-450在类固醇羟基化中的作用 - 处理儿茶酚雌激素的形成： 现象，肝细胞色素P-450：调节内源性 类固醇代谢和共价雌激素结合特异性 仓鼠细胞色素P-450：可能的后果;（8）雄激素 致癌作用-处理雄激素和雌激素的结合- 诱导大鼠背侧前列腺增生和发育不良 和类固醇诱导的雄性叙利亚仓鼠肿瘤 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.