MECHANISMS FOR PITUITARY TUMORIGENESIS

垂体肿瘤发生机制

• 批准号: 7376014
• 负责人: SHLOMO MELMED
• 金额: $ 0.22万
• 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: 2005
• 资助国家: 美国
• 起止时间: 2005-12-01 至 2006-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7376014
• 关键词: MECHANISMS; PITUITARY; TUMORIGENESIS

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Although pituitary tumors are common monoclonal neoplasms, they rarely metastasize outside the pituitary fossa, but cause considerable morbidity and mortality. Many molecular events underlying pituitary tumorigenesis have been elucidated in recent years, but no clear tumor marker has emerged which assists clinical decisions regarding appropriate therapy. We have recently described a novel estrogen-regulated activating oncogene, Pituitary Tumor Transforming Gene (PTTG), which is potently transforming in vitro and in vivo, regulates basic fibroblast growth factor (bFGF) secretion and inhibits chromatid separation. In experimental animal pituitary tumor models, increased PTTG expression occurs early in cell transformation (normal ? hyperplastic cell) and PTTG overexpression was observed in 99% of pituitary tumors. PTTG presents an attractive target for designing subcellular pituitary tumor therapy and increased understanding of its role and that of other genetic events in pituitary tumorigenesis may provide novel approaches to pituitary tumor management.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。虽然垂体瘤是常见的单克隆肿瘤，但很少转移到垂体窝外，但会引起相当大的发病率和死亡率。近年来，许多垂体肿瘤发生的分子基础已被阐明，但没有明确的肿瘤标志物已经出现，以协助临床决定适当的治疗。我们最近描述了一种新的雌激素调节的激活癌基因，PSTG肿瘤转化基因（PTTG），这是有力的转化在体外和体内，调节碱性成纤维细胞生长因子（bFGF）的分泌，抑制染色单体分离。在实验动物垂体瘤模型中，PTTG表达增加发生在细胞转化早期（正常？在99%的垂体瘤中观察到PTTG过度表达。PTTG为设计亚细胞垂体瘤治疗提供了一个有吸引力的靶点，并且对其作用的理解以及垂体瘤发生中的其他遗传事件可能为垂体瘤管理提供新的方法。