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作 者:许小英[1] 令亚琴(综述)[1] 刘昕(审校)[1]
机构地区:[1]兰州大学基础医学院病理生理研究所,730000
出 处:《国际肿瘤学杂志》2009年第12期902-905,共4页Journal of International Oncology
摘 要:研究表明,甲状腺激素受体(TR)在许多肿瘤的发生过程中伴有染色体杂合子丢失、基因启动子区甲基化及基因突变等,出现TR mRNA或蛋白质表达异常,且TR异常与某些神经系统肿瘤如星形细胞瘤和垂体瘤的分化程度相关。目前,关于TR的作用途径及机制主要包括:垂体瘤转化-1、β-连环蛋白等肿瘤相关因子和细胞外信号调节激酶、磷脂酰肌醇-3激酶信号传导通路等。Many studies demonstrate alterations in the level of mRNA or protein expression of thyroid hormone receptor(TR) which result from chromosomal loss of heterozygosity, methylation status of promoter region and mutation in different types of human cancers. Moreover, abnoImity of TR has connection with differentiation of some neural tumors, such as astrocytomas and pituitary tumor. Pituitary tumor-transforming 1 and β- catenin have a great impact on the ways and the mechanism of the TR function as well as signal transduction pathways of extracellular signal-regulated kinase and phosphatidylinositol 3-kinase.
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