What is the pathophysiology of papillary thyroid carcinoma (PTC)?

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@omni Several chromosomal rearrangements have been identified in papillary thyroid carcinoma. The first oncogenic events identified in papillary thyroid carcinoma were chromosomal rearrangements involving the rearranged during transfection (RET) proto-oncogene, which arises from a paracentric inversion of chromosome 10. [9] RET fusion proteins (the RET/PTC family) appear to play an oncogenic role in approximately 20% of papillary thyroid carcinomas, with RET/PTC1, RET/PTC2, and RET/PTC3 accounting for most cases. [10, 9] In addition, the NTRK1 and the MET proto-oncogene may be overexpressed and/or amplified.
Evidence also suggests that some molecules that physiologically regulate the growth of the thyrocytes, such as interleukin-1 and interleukin-8, or other cytokines (eg, insulinlike growth factor 1, transforming growth factor beta, epidermal growth factor) could play a role in the pathogenesis of this cancer. There is also a clear association between radiation exposure (from radiotherapy or fallout) and incidence of papillary thyroid carcinoma. Port et al reported that papillary thyroid cancers in patients exposed to radiation from the Chernobyl accident could be completely distinguished from sporadic papillary thyroid cancers in patients with no history of radiation exposure, on the basis of gene expression patterns involving seven genes (ie, SFRP1, MMP1, ESM1, KRTAP2-1, COL13A1, BAALC, PAGE1).