Etiology
Approximately 75% of thyroid cancer cases are papillary thyroid carcinomas (PTC), while approximately 10% are follicular thyroid carcinomas (FTC). Both of these epithelial-derived cancers are considered to be differentiated thyroid carcinomas (DTC). Radiation therapy and ionizing radiation are well-documented risk factors for the development of PTC.⁴ Several studies have shown an increased risk for PTC in individuals who have Hashimotos’ thyroiditis, and recently a link with activation of the PI3k/Akt pathway has been suggested.⁵ Interestingly, despite increased incidence, prognosis may be better in individuals with underlying autoimmune thyroiditis.⁶ There also appears to be a familial component to the susceptibility to PTC.⁷ Many gene mutations associated with PTC, such as rearrangements of RET and NTRK1 tyrosine kinases and activating mutations of BRAF and RAS, ultimately activate the mitogen-activated protein kinase (MAPK) signaling cascade a d thus promote cell division. BRAF mutations appear to be quite common in PTC, and were found in approximately 40% of cases in one study.⁸ The finding of different BRAF mutations within the various foci of multifocal PTC suggests that some foci arise independently from unrelated neoplastic clones.⁹ RAS mutations or PAX8-PPAR gamma 1 rearrangements are frequently seen in FTC.¹⁰ The prevalence of FTC may be increased in iodine-deficient areas compared with iodinesufficient regions.¹¹ Higher serum thyroid-stimulating hormone (TSH) concentrations, even within the normal range, appear to be a risk factor for the development of DTC.^12–14

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