A review on the mechanism of iodide metabolic dysfunction in differentiated thyroid cancer. (5th January 2019)

• Record Type: Journal Article
• Authors: Zhao, Yinlong; Zhong, Lili; Yi, Heqing
• Is Part Of: Molecular and cellular endocrinology. Volume 479(2019)
• Page Start: 71
• Page End: 77
• Publication Date: 2019-01-05
• Subjects: Differentiated thyroid cancer -- 131iodide -- Iodide metabolism; Endocrinology -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Endocrinology -- Periodicals; Hormones -- Periodicals; Endocrinologie -- Périodiques; Cytology; Endocrinology; Molecular biology; Periodicals; 573.4
• DOI: 10.1016/j.mce.2018.09.002
• Languages: English
• ISSNs: 0303-7207

Abstract

Abstract: The incidence of differentiated thyroid cancer (DTC) has been increasing rapidly worldwide, and the risk factors remain unclear. With the growing number of patients with DTC, the related issues have been gradually highlighted. 131 Iodide ( 131 I) is an important treatment for DTC and has the potential to reduce the risk of recurrence. 131 I is also an effective treatment for distant metastases of thyroid carcinoma. However, iodide metabolism dysfunction in metastatic foci causes patients to lose the opportunity of 131 I treatment. This article reviews the related mechanisms of iodide metabolism dysfunction in DTC cells and summarizes the clinical transformation progression. Highlights: A comprehensive analysis of the main mechanism of iodide metabolic dysfunction in differentiated thyroid cancer (DTC). The basic research and clinical transformation progression in the restoration of iodide metabolic function in DTC. Targeted oncogenes and epigenetic regulation are expected to restore the 131 iodide metabolic function. Targeting kinase drugs is a practical way to restore the 131 iodide metabolic function in DTC patients.