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BRAF Mutation and its effects on Radioiodine Uptake in Patients with Anaplastic Thyroid Cancer

Farzaneh Bozorg-Ghalati, Mehdi Hedayati


Context: Anaplastic thyroid carcinoma (ATC) is poorly differentiated subtype of thyroid cancer which either resistant to radioactive iodine (RAI) therapy or conventional chemotherapy. Each process of the biological characteristics in normal thyroid cells, including iodide uptake by sodium-iodide symporter (NIS), synthesis of thyroglobulin (Tg), expression of thyroid peroxidase (TPO) and receptor for thyrotropin (TSHR), can be an onset stage for emerging thyroid carcinoma. Decrease or absence of NIS mRNA in thyroid carcinomas has well described for resistant to RAI therapy in these patients.

Evidence Acquisition: The original articles related to the role of the BRAF mutations on the sodium-iodide symporter functions and radioiodine uptake in patients with anaplastic thyroid carcinoma were found by a search in Scopus, PubMed, Science direct, Springer and some else with an emphasis on literature published in the recent years.

Results: The related studies disclosed that mutations in the mitogen-activated protein kinase (MAPK) pathway happen in more than 90% of thyroid cancer. Also serine/threonine-protein kinase BRAF is an important component of the MAPK pathway. Its mutations cause reduction of NIS mRNA compared to tumors with other mutations.


BRAF mutation; Sodium-iodide symporter; Anaplastic thyroid cancer


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