甲状腺癌失分化机制与分化治疗的研究进展  

Research progress in thyroid cancer:dedifferentiation mechanisms and differentiation therapies

作　　者：汪君瑶 何紫燕 邱娴 萨日 靳雨辰 陈立波[1] Wang Junyao;He Ziyan;Qiu Xian;Sa Ri;Jin Yuchen;Chen Libo(Department of Nuclear Medicine,Shanghai Jiao Tong University Affiliated Sixth People′s Hospital,Shanghai 200233,China)

机构地区：[1]上海交通大学附属第六人民医院核医学科,上海200233

出　　处：《中华核医学与分子影像杂志》2022年第11期686-691,共6页Chinese Journal of Nuclear Medicine and Molecular Imaging

基　　金：国家自然科学基金(82171981)。

摘　　要：摄碘是甲状腺癌(TC)分化水平的标志和患者131I治疗获益的基石。然而,B-Raf原癌基因丝/苏氨酸蛋白激酶(BRAF)、端粒酶反转录酶(TERT)启动子和肿瘤蛋白p53(TP53)等的致癌突变可导致近70%的复发或转移性TC出现失分化表型。除遗传学改变外,表观遗传学、自噬、肿瘤微环境等途径也参与了TC失分化和对131I治疗的抵抗。靶向上述途径有可能改善TC恶性表型并恢复131I治疗的敏感性,具有重要临床意义。该文基于TC失分化的相关机制,阐述了TC分化治疗相关的临床前实验和临床研究进展。Iodine accumulation represents a differentiation marker of thyroid cancer(TC)and a cornerstone of benefits from 131I therapy.However,dedifferentiation phenotypes occur in nearly 70%of recurrent or metastatic TCs driven by oncogenic mutations such as B-Raf proto-oncogene,serine/threonine kinase(BRAF),telomerase reverse transcriptase(TERT)promoters,and tumor proten p53(TP53).Beyond genetic alterations,epigenetics,autophagy,tumor microenvironment and other pathways are also involved in the dedifferentiation of TC and the tolerance to 131I therapy.Targeting the above-mentioned pathways has potential to improve the malignant phenotype of TC and restore sensitivity to 131I therapy,which is of great clinical significance.Based on the relevant mechanisms of dedifferentiation,this paper elaborates on the progress of preclinical experiments and clinical studies related to differentiation therapies of TC.

关 键 词：甲状腺肿瘤 细胞去分化 放射疗法 碘放射性同位素 发展趋势 

分 类 号：R736.1[医药卫生—肿瘤]