IMR Press / FBL / Volume 20 / Issue 7 / DOI: 10.2741/4359

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

The role of BRAF in the pathogenesis of thyroid carcinoma
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1 Department of Medical Ultrasound, Shanghai Tenth People’s Hospital, Tenth People’s Hospital of Tongji University, 200072, Shanghai, China
2 Institute of Medical Intervention Engineering, Tongji University, North Zhongshan Road, Shanghai, China
Front. Biosci. (Landmark Ed) 2015, 20(7), 1068–1078;
Published: 1 June 2015
(This article belongs to the Special Issue Pathogenesis and diagnostic modalities in cancer)

BRAF is a cytoplasmic serine-threonine protein kinasethat plays a critical role in the MAPK signaling pathway. BRAF is the only member of the RAF family activated by mutation in human cancers. A single amino acid substitution (V600E) accounts for a multitude of human cancers, which causes constitutive kinase activity. In papillary thyroid cancer (PTC) and papillary-derived anaplastic thyroid cancer (ATC), the BRAFV600E mutation promotes follicular cell transformation. The BRAFV600E mutation could provide valuable prognostic information for thyroid cancer, because this mutation has been correlated with more aggressive and iodine-resistant phenotypes. Evidence has also shown that the detection of the BRAFV600E mutation in cancer is crucial in order to identify novel avenues for thyroid cancer treatment. Based on the BRAF kinase structure, novel drugs can potentially be designed to target oncogenic BRAF in cancer therapeutics. This review will focus on the recent progress in understandingthe functions of BRAF, the role of the BRAF mutations in thyroid carcinoma, and the correlation between BRAF mutations and cancer microenvironment.

Thyroid Carcinoma
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