MOLECULAR MECHANISMS OF ESTROGEN INDUCED CARCINOGENESIS

雌激素致癌的分子机制

• 批准号: 2008783
• 负责人: HARI K BHAT
• 金额: $ 6.26万
• 依托单位: LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 1997
• 资助国家: 美国
• 起止时间: 1997-01-01 至 1997-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2008783
• 关键词: animal genetic material tag; carcinogenesis; catechols; clone cells; complementary DNA; estrogen receptors; estrogens; free radicals; gene expression; gene targeting; hamsters; hormone related neoplasm /cancer; immunocytochemistry; kidney neoplasms; molecular cloning; molecular oncology; northern blottings; protooncogene; receptor expression; transfection

DESCRIPTION (Adapted from the applicant's abstract): The foundation for the proposed hypothesis of this application assumes three critical steps to carcinogenesis as studied in the Syrian hamster kidney tumor model: 1) hormonal stimulation, 2) metabolic activation, 3) free radical generation. The specific aims are to: 1) clone and characterize Syrian hamster ER cDNA; 2) study the effect of metabolic activation/free radical generation of ER gene expression; 3) characterize the role of metabolic/estrogenic potential on cell specific expression of ER proteins on tumorigenesis in hamster kidneys; and 4) investigate the role of metabolic activation of estrogens and the interdependency of, if any, between overexpression and neu suppression.

描述（改编自申请人的摘要）： 本申请提出的假设假定了三个关键步骤， 在叙利亚仓鼠肾肿瘤模型中研究的致癌作用：1） 激素刺激，2）代谢活化，3）自由基生成。 具体目的是：1）克隆和鉴定叙利亚仓鼠ER cDNA; 2)研究ER代谢活化/自由基生成的作用 基因表达; 3）表征代谢/雌激素潜能的作用 雌激素受体蛋白的细胞特异性表达对金黄地鼠肿瘤发生的影响 肾脏;和4）研究雌激素代谢活化的作用 以及过度表达和neu之间的相互依赖性，如果有的话， 镇压