Abstract
The number of thyroid cancers is increasing. Standard treatment usually includes primary surgery, thyroid-stimulating hormone suppressive therapy, and ablation of the thyroid remnant with radioactive iodine (RAI). Despite the generally good prognosis of thyroid carcinoma, about 5% of patients will develop metastatic disease, which fails to respond to RAI, exhibiting a more aggressive behavior. The lack of specific, effective and well-tolerated drugs, the scarcity of data about the association of multi-targeting drugs, and the limited role of radioiodine for dedifferentiated thyroid cancer, call for further efforts in the field of new drugs development. Rearranged during transfection (RET)/papillary thyroid carcinoma gene rearrangements, BRAF (B-RAF proto-oncogene, serine/threonine kinase) gene mutations, RAS (rat sarcoma) mutations, and vascular endothelial growth factor receptor 2 angiogenesis pathways are some of the known pathways playing a crucial role in the development of thyroid cancer. Targeted novel compounds have been demonstrated to induce clinical responses and stabilization of disease. Sorafenib has been approved for differentiated thyroid cancer refractory to RAI.
Highlights
Thyroid cancer is the most common endocrine malignancy, causing approximately 1%–5% of all cancers in females and less than 2% in males [1,2].New risk factors have emerged in the last decade [3].Differentiated thyroid carcinomas (DTC), more than 90% of all thyroid tumors, arise from follicular cells, and are classified as papillary (PTC) or follicular (FTC) according to histopathological criteria [2].In the last decades, an increasing incidence of thyroid cancer (TC) has been reported, in particular for PTC [1]
The aim of this review is to evaluate the state of art of targeted therapies in the approach of dedifferentiated papillary thyroid cancer (DePTC)
Sunitinib (SU011248) is a small molecule, multitargeted Tyrosine Kinase Inhibitors (TKIs), acting as a selective inhibitor of VEGFR-1, 2, and 3, PDGF receptor (PDGFR), cKIT, and Rearranged during transfection (RET)/PTC subtypes 1 and 3, that are involved in signal transduction and growth and their inhibition is determinant in the development of solid tumors [67,68]
Summary
Thyroid cancer is the most common endocrine malignancy, causing approximately 1%–5% of all cancers in females and less than 2% in males [1,2]. Differentiated thyroid carcinomas (DTC), more than 90% of all thyroid tumors, arise from follicular cells, and are classified as papillary (PTC) or follicular (FTC) according to histopathological criteria [2]. If the tumor stage of the patients (pts) leads to suppose a significant risk of recurrence or disease-related mortality, subsequent radioiodine ablation is recommended [4]. Thyroid-stimulating hormone (TSH) suppressive therapy is undertaken and annual follow-up based on neck ultrasonography and serum thyroglobulin (Tg) determination are performed [5,6,7]. During the follow-up, 10%–15% of pts present recurrent disease (localized in the thyroid bed and lymph nodes), and show a reduction of survival (from 68% to 49% at 10-year); about one third of cancer-related deaths are associated with the presence of neck lesions alone [9]. The aim of this review is to evaluate the state of art of targeted therapies in the approach of dedifferentiated papillary thyroid cancer (DePTC)
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