The incidence of thyroid cancer worldwide is increasing. Thyroid carcinomas derived from follicular epithelial cells include a broad spectrum of histotypes ranging from well-differentiated thyroid carcinoma, including papillary thyroid carcinoma (PTC) and follicular thyroid carcinoma (FTC), to poorly differentiated thyroid carcinoma and the rare anaplastic thyroid carcinoma (ATC). Whereas the prognosis of differentiated thyroid cancer is good, ATC is one of the most lethal human malignancies, 90% of patients die within six months of diagnosis. The sudden onset and explosive course of ATC necessitate immediate involvement by surgeons, radiation and medical oncologists, and palliative care teams. Target therapies for ATC are currently being evaluated in clinical trials. However, ATC is still resistant to all types of therapy, and disease prognosis has remained unchanged.

ATC may derive de novo or from preexisting papillary thyroid carcinoma or follicular thyroid carcinoma. Many patients do indeed have a history of preexisting well-differentiated thyroid carcinoma or nodular goiters. A small number of gene mutations have been identified in ATC, and there appears to be a progression in mutations acquired during dedifferentiation (e.g., RAS and BRAF). Other mutations found in ATC are in the TP53, -catenin, and PIK3CA genes. Thus, still little is known about the molecular events that lead from the highly curable differentiated tumors to ATCs.

Under this frame, we invite investigators to contribute with original articles and review articles addressing advances in molecular tools and therapy of ATC. Potential topics include, but are not limited to:

• Molecular profiling of ATC
• Predictive biomarkers of progression to ATC
• Risk factors for ATC
• Animal models of ATC
• Histopathological tools for improved diagnosis of ATC
• Genetic lesions in ATC
• Epigenetics/methylome of ATC
• Role of cancer stem cells in ATC
• microRNAs in ATC
• Targeted therapies of ATC

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