AKT1 and thyroid gland undifferentiated (anaplastic) carcinoma: Corroborating EMT-associated chemotherapy resistance, when treated with the BRAF inhibitor Vemurafenib, the 8505c cell line, which is derived from anaplastic thyroid carcinoma and is resistant to the this inhibitor, presented a mesenchymal-like morphology, higher migration rates and higher levels of phosphorylated MET proto-oncogene, receptor tyrosine kinase (p-c-MET), phosphorylated AKT (p-AKT), vimentin, β-catenin and CD44 protein when compared to inhibitor-sensitive papillary thyroid cancer cells [40].