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Radioactive Iodine-Refractory Differentiated Thyroid Cancer and Redifferentiation Therapy.

Authors
  • Liu, Jierui1, 2, 3
  • Liu, Yanqing1, 2
  • Lin, Yansong1, 2, 4
  • Liang, Jun5
  • 1 Department of Nuclear Medicine, Peking Union Medical College Hospital, Beijing, China. , (China)
  • 2 Beijing Key Laboratory of Molecular Targeted Diagnosis and Therapy in Nuclear Medicine, Beijing, China. , (China)
  • 3 Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, China. , (China)
  • 4 Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, China. [email protected] , (China)
  • 5 Department of Oncology, Peking University International Hospital, Beijing, China. [email protected] , (China)
Type
Published Article
Journal
Endocrinology and metabolism (Seoul, Korea)
Publication Date
Sep 01, 2019
Volume
34
Issue
3
Pages
215–225
Identifiers
DOI: 10.3803/EnM.2019.34.3.215
PMID: 31565873
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The retained functionality of the sodium iodide symporter (NIS) expressed in differentiated thyroid cancer (DTC) cells allows the further utilization of post-surgical radioactive iodine (RAI) therapy, which is an effective treatment for reducing the risk of recurrence, and even the mortality, of DTC. Whereas, the dedifferentiation of DTC could influence the expression of functional NIS, thereby reducing the efficacy of RAI therapy in advanced DTC. Genetic alternations (such as BRAF and the rearranged during transfection [RET]/papillary thyroid cancer [PTC] rearrangement) have been widely reported to be prominently responsible for the onset, progression, and dedifferentiation of PTC, mainly through activating the mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K) signaling cascades. These genetic alternations have been suggested to associate with the reduced expression of iodide-handling genes in thyroid cancer, especially the NIS gene, disabling iodine uptake and causing resistance to RAI therapy. Recently, novel and promising approaches aiming at various targets have been attempted to restore the expression of these iodine-metabolizing genes and enhance iodine uptake through in vitro studies and studies of RAI-refractory (RAIR)-DTC patients. In this review, we discuss the regulation of NIS, known mechanisms of dedifferentiation including the MAPK and PI3K pathways, and the current status of redifferentiation therapy for RAIR-DTC patients. Copyright © 2019 Korean Endocrine Society.

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