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Updated: Aug 8, 2025

Spontaneous Murine Model of Anaplastic Thyroid Cancer
Published on: February 3, 2023
Anti-EGFR/BRAF-Tyrosine Kinase Inhibitors in Thyroid Carcinoma
Vasileios Papanikolaou1, Efthymios Kyrodimos1, Nicholas Mastronikolis2
11st Department of Otorhinolaryngology, Hippocration Hospital, University of Athens, Athens, Greece.
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.
Insights
Genetic alterations in EGFR and BRAF genes, crucial for cancer development, are explored in thyroid carcinoma. This review examines targeted therapies like tyrosine kinase inhibitors (TKIs) for patients with specific genetic signatures.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Genetic alterations in chromosome 7, including epidermal growth factor receptor (EGFR) and v-Raf murine sarcoma viral oncogene homolog B (BRAF) mutations, are key drivers in malignancy development.
- These genetic events, alongside chromosomal numerical imbalances (aneuploidy-polysomy), are critical for tumor progression.
- Identifying specific EGFR/BRAF mutations and deregulation mechanisms like amplification is essential for targeted therapy selection.
Purpose of the Study:
- To review the role of EGFR and BRAF alterations in various thyroid carcinoma subtypes.
- To explore novel therapeutic strategies, including tyrosine kinase inhibitors (TKIs) and monoclonal antibodies (mAbs), targeting these genetic alterations.
- To correlate specific genetic signatures with potential treatment responses in thyroid cancer patients.
Main Methods:
- Literature review of studies focusing on EGFR/BRAF alterations in thyroid carcinoma.
- Analysis of genetic mutations, including somatic mutations and gene amplification, within different thyroid cancer subtypes (FTC, PTC, MTC, ATC).
- Examination of targeted therapeutic approaches, such as TKIs and mAbs, based on identified genetic profiles.
Main Results:
- EGFR and BRAF alterations are significant in the pathogenesis of various thyroid carcinoma subtypes.
- Specific mutations and amplification events in EGFR and BRAF are identified as crucial biomarkers.
- The review highlights the potential of anti-EGFR/BRAF TKIs and mAbs for personalized treatment strategies.
Conclusions:
- EGFR/BRAF alterations play a critical role in thyroid carcinoma development and progression.
- Targeted therapies based on EGFR/BRAF mutational status offer promising treatment avenues for thyroid cancer patients.
- Personalized medicine approaches utilizing genetic profiling are essential for optimizing therapeutic outcomes in thyroid carcinoma.
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