钠碘同向转运体在分化型甲状腺癌中异常表达的研究进展  

Research Progress on Abnormal Expression of the Sodium-Iodide Symporter in Differentiated Thyroid Cancer

作　　者：刘汉卿 陈创[1] 涂毅[1] 孙圣荣[2] LIU Han-qing;CHEN Chuang;TU Yi;SUN Sheng-rong(Hubei General Hospital,Wuhan 430060,China)

机构地区：[1]武汉大学人民医院,湖北武汉430060 [2]武汉大学人民医院乳腺甲状腺中心,湖北省武汉市430060

出　　处：《肿瘤学杂志》2020年第12期1068-1074,共7页Journal of Chinese Oncology

基　　金：武汉市中青年医学骨干人才计划;武汉大学人民医院重点人才项目。

摘　　要：放射性核素碘内照射(131I治疗)是分化型甲状腺癌的重要治疗方式,钠碘同向转运体在131I的跨膜转运中起关键作用。而钠碘同向转运体在肿瘤细胞内均有不同程度的表达异常,这与驱动变异密切相关。全文就钠碘同向转运体的分子特征、调节机制及与BRAF突变、PI3K/AKT1通路变异、RAS突变和PTEN突变之间的关系和研究进展作一综述,并总结药物靶点设计与用药方案,为下一步研究提供新的思路。Radioiodine internal irritation(131I) is an important treatment for differentiated thyroid cancer and the sodium-iodide symporters play a key role in the transmembrane transport of 131I.The sodium-iodide symporters are abnormally expressed in tumor cells to varying degrees,which is closely related to driver mutations. This article reviews the molecular characteristics,regulatory mechanisms of sodium-iodide symporters,and their relationships with BRAF mutations,PI3K/AKT1 pathway mutations,RAS mutations,and PTEN mutations. The drug target designs and treatment regimens have been summarized to provide insights for future studies.

关 键 词：钠碘同向转运体 BRAF突变 PI3K/AKT1通路变异 RAS突变 PTEN突变 药物靶点 

分 类 号：R736.1[医药卫生—肿瘤]