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Papillary thyroid carcinoma (PTC), the most frequent neoplasia originating from the thyroid epithelium, accounts for about 80% of all thyroid cancers. Chimeric oncogenes, created by chromosomal rearrangements involving prevalently RET and, to a less extent, NTRK1 loci, are implicated in the development of papillary carcinoma. These are inappropriately expressed and stimulate constitutive signaling, bypassing the need for receptor activation by growth factors. Alternatively, mutant RAS directly stimulates BRAF, whereas mutant BRAF directly stimulates MEK.
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