Oncogenic changes in a new transgenic model of BRAF^V600E in thyroid

Thyroid cancer is the most common endocrine cancer and its incidence has increased worldwide in the last two decades (1). Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer, representing up to 80% of all malignant thyroid tumors. The genetic background of PTC comprises the mutually exclusive activating mutations in effectors genes of MAPK signal transduction pathway such as RET, RAS, BRAF (2,3). Among them, the most frequent is the BRAF^V600E mutation (mutBRAF), resulting from a T→A transversion at nucleotide position 1799 in BRAF gene, which accounts for 45% of mutations in PTC and elicits a highly sustained activation of MAPK pathway (4).