Gisele Marques Alvarenga, Elane Barboza da Silva, Márcia Elaine Braga de Menezes, Rafael Perseguini Del Sarto and Aline Maria Araújo Martins
Since Dailey et al. first described the possible correlation between inflammation caused by autoimmune diseases and thyroid cancers in 1955, the majority of the events involving these two conditions have not been clearly elucidated, and this association is still very controversial in the literature. Chronic inflammation predisposes the organism to cell proliferation reactions, cytokines secretion and other phenomenas that influence rearrangements and mutations in thyroid follicular cells. Thus, is possible that in thyroid autoimmune phenotypes, the same mechanistic forces occur, mainly by the similarity of molecular events that affect both diseases. The large quantity of pro-inflammatory substances secreted within thyroid milieu in a chronic autoimmune condition, and the imbalance between anti and pro-apoptotic effectors, result in thyroid cells transformation, reducing thyroid hormones synthesis. Key important events regarding chronic inflammation momentum are those driving PTC carcinogenesis and its deregulation of the MAPK signaling pathway, causing rearrangements of RET/PTC, TRKA and mutation points in RAS and BRAF. In this review, we highlight the most relevant molecular events on thyroid disorders, giving an especial attention to mechanisms that drive molecular protagonists.