Anti-EGFR/BRAF-Tyrosine Kinase Inhibitors in Thyroid Carcinoma
- PMID: 36875315
- PMCID: PMC9949544
- DOI: 10.21873/cdp.10194
Anti-EGFR/BRAF-Tyrosine Kinase Inhibitors in Thyroid Carcinoma
Abstract
Alterations in significant genes located on chromosome 7 - including epidermal growth factor receptor (EGFR) and also v-Raf murine sarcoma viral oncogene homolog B (BRAF) as a mitogen-activated protein kinase (MAPK) - combined or not with numerical imbalances of the whole chromosome (aneuploidy-polysomy) are crucial genetic events involved in the development and progression of malignancies. Identification of EGFR/BRAF-dependent specific somatic mutations and other mechanisms of deregulation (i.e., amplification) is critical for applying targeted therapeutic approaches [tyrosine kinase inhibitors (TKIs] or monoclonal antibodies (mAbs). Thyroid carcinoma is a specific pathological entity characterized by a variety of histological sub-types. Follicular thyroid carcinoma (FTC), papillary thyroid carcinoma (PTC), medullary thyroid carcinoma (MTC), and anaplastic thyroid carcinoma (ATC) represent its main sub-types. In the current review, we explore the role of EGFR/BRAF alterations in thyroid carcinoma in conjunction with the corresponding anti-EGFR/BRAF TKI-based novel therapeutic strategies for patients with specific genetic signatures.
Keywords: Thyroid; carcinoma; epidermal growth factor; kinase; receptor; review; tyrosine.
Copyright 2023, International Institute of Anticancer Research.
Conflict of interest statement
The Authors have no conflicts of interest to declare in relation to this study.
References
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