Research progress in thyroid cancer: dedifferentiation mechanisms and differentiation therapies

VernacularTitle:甲状腺癌失分化机制与分化治疗的研究进展
Author: Junyao WANG ¹ ; Ziyan HE ; Xian QIU ; Ri SA ; Yuchen JIN ; Libo CHEN
Author Information

1. 上海交通大学附属第六人民医院核医学科，上海　200233
Keywords: Thyroid neoplasms; Cell dedifferentiation; Radiotherapy; Iodine radioisotopes; Trends
From: Chinese Journal of Nuclear Medicine and Molecular Imaging 2022;42(11):686-691
CountryChina
Language:Chinese
Abstract: 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.