<p class="first" id="d5965754e151">In the last decades, many studies conducted in
vitro, and in vivo, have shown that
thyroid autoimmunity and thyroid cancer (TC) (mainly papillary TC) can be concomitant,
even if the exact mechanisms at the basis of this association are still not clear.
Growing incidence of TC coincides with increased registration of autoimmune thyroid
disorders (AITD) suggesting an association between those pathologies. Elevated TSH
levels and thyroid autoimmunity were defined as independent risk factors for TC. However
a lot of evidence suggests that autoimmunity and inflammation, per se, are risk factors
for TC. The link between inflammation and TC involves multiple components of the immune
system, extracellular matrix, stroma, and adipose tissue, with pro-tumoral activity
of inflammation being opposed to anti-inflammatory effects, favoring protection against
cancer progression. Within the tumor microenvironment, inflammatory cells, belonging
both to innate (macrophages) and adaptive (lymphocytes) immune responses, are interconnected
with fibroblasts, endothelial cells, adipocytes, and extracellular matrix through
cytokines, chemokines and adipocytokines. Under the influence of transcriptional regulators
(such as Nuclear Factor-kappa B, mitogen-activated protein kinases, or Phosphoinositide-3
kinase/protein kinase-B), oncogenes connected to the different subtypes of TC promote
their farthermost proliferative effect on the tumor microenvironment. Future studies
will be necessary to understand the connections between thyroid autoimmunity and cancer,
also in order to design a tailored therapy for TC patients with AITD.
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