Abstract
Radioiodine (RAI) is the mainstay of treatment for differentiated thyroid carcinoma (DTC) following total thyroidectomy. Nevertheless, about 5% of patients with DTC are RAI-refractory (RAI-R). Understanding the molecular mechanisms associated with DTC during progression towards RAI-R DTC, including thyroid-stimulating hormone levels, may help to explain the pathophysiology of challenging RAI-R DTC clinical cases.Graphical
Highlights
Thyroid cancer is the most frequent endocrine malignancy and has the highest growing incidence rate between the other kinds of solid tumors in the United States [1]
Radioiodine (RAI) ablation followed by long-term suppression of thyroid-stimulating hormone (TSH) through thyroid hormone supplementation is the treatment plan for patients with Differentiated thyroid carcinoma (DTC) [3]
RAI is the mainstay of treatment for patients with DTC following total thyroidectomy
Summary
Thyroid cancer is the most frequent endocrine malignancy and has the highest growing incidence rate between the other kinds of solid tumors in the United States [1]. Differentiated thyroid carcinoma (DTC) accounts for 85–95% of all thyroid cancers [2]. Radioiodine (RAI) ablation followed by long-term suppression of thyroid-stimulating hormone (TSH) through thyroid hormone supplementation is the treatment plan for patients with DTC [3]. RAI is the mainstay of treatment for patients with DTC following total thyroidectomy. A small percentage of patients with recurrent DTC have tumors that do not concentrate 131I, resulting in RAI resistance, poor prognosis, and a clinical challenge for physicians and patients [4]. Understanding the biological mechanisms associated with DTC progression towards radioiodine-refractory (RAI-R) DTC may be beneficial in providing an effective and appropriate plan for these cases
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