New Biomarkers in Thyroid Cancer and Autoimmune Diseases

Dear Colleagues,

Thyroid cancer is a complex disease with multiple subtypes, each with a distinct set of driver mutations such as BRAF, TERT, p53, RET, and RAS. Identifying these mutations is crucial for accurate diagnosis, prognosis, and targeted therapy. Thyroid cancer exhibits intra-tumor heterogeneity, which can complicate genetic analysis and the interpretation of results. In addition to genetic mutations, epigenetic changes such as DNA methylation and histone modification can contribute to thyroid cancer development and progression. These changes can be challenging to detect and quantify but may provide valuable diagnostic and prognostic information. Despite significant progress in understanding the genetic basis of thyroid cancer, translating this knowledge into clinical practice remains a challenge. More research is needed to develop effective targeted therapies and improve patient outcomes.

Autoimmune thyroid diseases, such as Hashimoto's thyroiditis and Graves' disease, have been associated with a slightly increased risk of developing thyroid cancer. On the other hand, several studies have reported a prevalence of autoimmune thyroid disease in patients with PTC ranging from 22% to 53%. One of the main ways that inflammation can contribute to thyroid cancer is by activating inflammatory signaling pathways such as NF-κB and STAT3. These pathways can induce the expression of pro-inflammatory molecules stimulating cell growth and survival, promoting angiogenesis, and suppressing the immune response, as well as cause oxidative stress, leading to DNA damage and mutations. This chronic inflammatory environment can create an ideal setting for cancer development by facilitating the accumulation of genetic mutations and epigenetic changes, causing alterations in DNA methylation patterns and changes in gene expression. This may result in the activation of oncogenes or the inactivation of tumor suppressor genes (TSGs), which can contribute to cancer development.  Another mechanism contributing to thyroid cancer development is genetic instability, including a loss of heterozygosity (LOH), which can contribute to the accumulation of genetic changes in a cell, leading to more aggressive cancer phenotypes. Importantly, genetic instability can occur in non-cancerous thyroid cells during an inflammatory process (i.e., thyroiditis) in response to the release of inflammatory cytokines and chemokines, which can ultimately lead to the development of thyroid cancer.

Investigating the genetics underlying thyroid cancer is fundamental for understanding the clinical course of the disease and the contribution of autoimmune diseases to carcinogenesis, as well as remaining essential for accurate diagnosis.

We invite research papers that will consolidate our understanding of the biology of thyroid cancer and how prolonged inflammation can impact cancerogenesis. The Special Issue will publish full research articles and comprehensive reviews on all aspects related to the theme of thyroid cancer and autoimmune diseases, including new biomarkers.

Dr. Karolina H. Czarnecka-Chrebelska
Guest Editor

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• thyroid cancer
• papillary thyroid cancer
• follicular thyroid cancer
• autoimmune diseases of the thyroid thyroiditis
• prolonged inflammation
• genetic instability
• epimutations
• oxidative stress
• driver mutations