Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2023 Mar 3;3(2):151-156.
doi: 10.21873/cdp.10194. eCollection 2023 Mar-Apr.

Anti-EGFR/BRAF-Tyrosine Kinase Inhibitors in Thyroid Carcinoma

Affiliations
Review

Anti-EGFR/BRAF-Tyrosine Kinase Inhibitors in Thyroid Carcinoma

Vasileios Papanikolaou et al. Cancer Diagn Progn. .

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.

PubMed Disclaimer

Conflict of interest statement

The Authors have no conflicts of interest to declare in relation to this study.

References

    1. Albertson RC, Cresko W, Detrich HW 3rd, Postlethwait JH. Evolutionary mutant models for human disease. Trends Genet. 2009;25(2):74–81. doi: 10.1016/j.tig.2008.11.006. - DOI - PMC - PubMed
    1. Albertson DG, Collins C, McCormick F, Gray JW. Chromosome aberrations in solid tumors. Nat Genet. 2003;34(4):369–376. doi: 10.1038/ng1215. - DOI - PubMed
    1. Chu YH, Sadow PM. Kinase fusion-related thyroid carcinomas: Towards predictive models for advanced actionable diagnostics. Endocr Pathol. 2022;33(4):421–435. doi: 10.1007/s12022-022-09739-9. - DOI - PMC - PubMed
    1. Kroll TG. Molecular events in follicular thyroid tumors. Cancer Treat Res. 2004;122:85–105. doi: 10.1007/1-4020-8107-3_4. - DOI - PubMed
    1. Ehlers M, Schmidt M, Mattes-Gyorgy K, Antke C, Enczmann J, Schlensog M, Japp A, Haase M, Allelein S, Dringenberg T, Giesel F, Esposito I, Schott M. BRAFV600E and BRAF-WT specific antitumor immunity in papillary thyroid cancer. Horm Metab Res. 2022;54(12):852–858. doi: 10.1055/a-1971-7019. - DOI - PubMed

LinkOut - more resources