Inflammation in thyroid oncogenesis

Abstract

It is commonly accepted that cancer is linked to inflammation. The possible mechanisms by which inflammation can contribute to carcinogenesis include induction of genomic instability, alterations in epigenetic events and subsequent inappropriate gene expression, enhanced proliferation of initiated cells, resistance to apoptosis, aggressive tumor neovascularization, invasion through tumor-associated basement membrane and metastasis. Inflammation also affects immune surveillance and responses to therapy. In this review, we overview the current understanding of different aspects of thyroid cancer and inflammation. Several studies have strongly suggested an increased risk of PTC in patients with Hashimoto's thyroiditis (HT), the most common autoimmune disease in thyroid cancer. Furthermore, an intense immune infiltrate is often associated with papillary thyroid carcinoma (PTC), and might play a critical role in the regulation of carcinogenesis and in carcinoma progression. The characterization of the most relevant inflammatory pathways of cancer-related inflammation (CRI) is instrumental for the identification of new target molecules that could lead to improved diagnosis and treatment.

Keywords: Cancer-related inflammation; chemokine; inflammatory cell; thyroid cancer.

Figure 1

The complex relationship between mast cell and thyroid cancer cell. Mast cells exert a protumorigenic effect in thyroid cancer. They are recruited in tumor site by tumor-derived VEGF-A (and possibly by other chemoattractants), and are activated by cancer cell-secreted unknown factors. Activated mast cells secrete histamine, and the chemokines CXCL1 and CXCL10, that induce thyroid cancer cell proliferation, survival and invasion.