Abstract
ABSTRACT Well-differentiated thyroid cancers are typically managed with surgery followed by radioiodine ablation. These cancers often retain the ability to concentrate intracellular iodine. However, cancer cell dedifferentiation frequently confers radioiodine resistance, termed thyroglobulin-elevated negative iodine scintigraphy (TENIS) syndrome. Elucidation of the sodium/iodide symporter (NIS) mechanism that mediates active iodide transport has enabled advances in the pathophysiologic understanding and clinical management of TENIS syndrome. This review summarizes molecular cloning of the NIS gene and implications for thyroid biology. It highlights studies of NIS gene regulation across tissues and utilization of NIS as a reporter gene to restore radioiodine uptake in advanced thyroid cancers. Quantitative NIS expression analyses and correlations with radioiodine uptake are also discussed. Overall, this review underscores the vital role of NIS-mediated iodide transport in thyroid pathophysiology and modern radioiodine therapeutic paradigms for advanced thyroid cancers, including TENIS syndrome. Further research into mechanisms underlying differential NIS expression and therapeutic modulation of NIS activity is warranted.
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