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Thyroid cancer is the most prevalent endocrine cancer worldwide. Angiogenesis, the formation of new blood vessels, plays a pivotal role in the development and progression of tumors. Over the past years, cancer research has focused on the ability of tumors to induce newly formed blood vessel, because tumor growth and the process of cancer metastasis mainly depends on angiogenesis. Tumor neovascularization occurs following the imbalance between pro-angiogenic and antiangiogenic factors until the tumor switches to an angiogenic phenotype. A number of signaling factors and receptors that are implicated in the regulation of angiogenesis have been identified and characterized; most notably, the vascular endothelial growth factors (VEGFs) family and their receptors, which are the main pro-angiogenic molecules during early development and in pathological conditions such as cancer. Although thyroid is a highly vascularized organ, angiogenic switch in tumors of this organ leads to the formation of a vast network of blood vessels that favors the dissemination of tumor cells to distant organs and results in deterioration of patient conditions. Accordingly, the identification of key angiogenic biomarkers for thyroid cancer can facilitate diagnosis, prognosis and clinical decision-making and also may help to discover targeting factors for effective cancer therapy as well as monitoring response to therapy. Hence, the main purposes of this review are to summarize the types and mechanisms of angiogenesis emphasizing the prominent factors implicated in thyroid cancer angiogenesis.

Killer immunoglobulin-like receptors (KIR) play a pivotal role in commencement of both innate and adaptive immunity. Dysregulation of KIRs is associated with an increased risk of autoimmune disorders. This study was designed to assess whether polymorphisms in KIR gene family and their respective HLA class I ligands confer protection or susceptibly to Graves' disease (GD). Eighty patients with confirmed GD (cases) and 176 healthy unrelated subjects (controls) were recruited. Using a polymerase chain reaction sequence-specific primer directed method (PCR-SSP), presence or absence of KIR genes and their HLA ligands were determined. No significant differences were observed between case and control groups regarding individual KIR gene frequencies (p > 0.05 in all cases). The frequency of group A haplotype (the most common KIR haplotype, encompassing 2DL1/2DL3/3DL1/2DS4/2DP1/3DP1/2DL4/3DL2/3DL3), was not different between individuals with and without GD. Moreover, among all other haplotypes (group Bx), no significant differences regarding distribution of centromeric and telomeric gene clusters were identifiable. Inhibitory/activatory gene contents were also comparable between the two groups. Four models of KIR-HLA interaction (inhibition, activation, unrestrained inhibition, and unrestrained activation) were constructed. No combination proved to confer susceptibility to, or offer protection against GD. It seems that the contribution of KIR gene polymorphism to natural killer cell dysfunction and other autoimmune abnormalities observed in GD is limited.

Thyroid cancer, as the most prevalent endocrine malignancy, comprises nearly 1% of all cancers in the world. The metastatic propagation of thyroid cancer is under the control of a number of modulating processes and factors such as signaling pathways and their components, cell division regulators, metabolic reprogramming factors, extracellular matrix remodelers, epithelial to mesenchymal transition modulators, epigenetic mechanisms, hypoxia and cytokines. Identifying the exact molecular mechanisms of these dysregulated processes could help to discover the key targets for therapeutic purposes and utilizing them as diagnostic, prognostic and predictors of the clinical course of patients. In this review article, we describe different aspects of thyroid cancer metastasis by focusing on defective genes and pathways involved in its metastatic spread.

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