TRANSGENIC ANALYSIS OF LH HYPERSECRETION

LH 分泌过多的转基因分析

• 批准号: 6497462
• 负责人: JOHN H. NILSON
• 金额: $ 30.98万
• 依托单位: CASE WESTERN RESERVE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2001
• 资助国家: 美国
• 起止时间: 2001-02-15 至 2006-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6497462
• 关键词: carcinogenesis; cyclins; female; follicle stimulating hormone; gene induction /repression; genetic polymorphism; genetically modified animals; granulosa cell; hormone receptor; hormone regulation /control mechanism; hormone related neoplasm /cancer; laboratory mouse; luteinizing hormone; microarray technology; molecular cloning; neoplasm /cancer genetics; ovary neoplasms; receptor expression; secretion

DESCRIPTION: (Adapted from the Investigator's Abstract): Studies in this grant period will focus on the hypothesis that chronic hypersecretion of LH, with a significant contribution from FSH, causes tumor formation by altering expression of a complex network of genes including a progressive down-regulation of the LH receptors and an increase in cyclin D2. The investigators will also map and clone the three non-allelic variants in the CF-1 genome necessary for GC tumorigenesis and contribute to its complete penetrance. In identifying gene expression profiles unique to the formation of granulosa cell tumors, these studies should contribute to a better understanding of permissive and causative events that underlie tumor formation.

描述：（根据调查员的摘要改编）：该赠款中的研究 时期将集中于以下假设：慢性LH的长期分泌 FSH的显着贡献，通过改变会导致肿瘤形成 复杂基因网络的表达，包括渐进式 LH受体的下调和细胞周期蛋白D2的增加。这 研究人员还将在该中绘制并克隆三个非平行性变体 CF-1基因组是GC肿瘤发生的必要条件，并有助于其完整 外观。在识别基因表达的谱图中 颗粒细胞肿瘤，这些研究应有助于更好 了解肿瘤形成构成的允许性和因果事件。