RESUMEN
Thyroid cancer represents the most frequent endocrine neoplasm and is epidemiologically linked to a growing incidence worldwide, which is only in part explained by the increased detection of small cancers in a preclinical stage. Understanding the molecular pathogenesis of well-differentiated thyroid cancers and poorly-differentiated thyroid cancers has prompted interest into the identification of crucial signaling pathways and molecular derangements related to genetic and epigenetic alterations. Increasing attention has been recently focused on inflammation and immunity as major culprit mechanisms involved in thyroid tumourigenesis, through the detection of activated immune cells, pro-inflammatory cytokines, as well as signal integrations between inflammatory and proliferative pathways within the thyroid tumour micro-environment. In addition to playing important roles in tumour surveillance and rejection, the presence of tumour-associated macrophages and the activation of NF-κB signaling pathway are now reckoned as hallmarks and crucial mediator of inflammation-induced growth and progression of thyroid cancer. Thorough understanding of this immunological link and identification of novel molecular targets could provide unprecedented opportunities for research and development of diagnostic, prognostic and treatment strategies for thyroid cancer.