Inhibiting BRAF Oncogene-Mediated Radioresistance Effectively Radiosensitizes BRAFV600E-Mutant Thyroid Cancer Cells by Constraining DNA Double-Strand Break Repair.

Affiliation

Arthur G. James Comprehensive Cancer Center and Richard J. Solove Research Institute, The Ohio State University Medical Center, Columbus, Ohio. [Email]

Abstract

Activating BRAF mutations, most commonly BRAFV600E, are a major oncogenic driver of many cancers. We explored whether BRAFV600E promotes radiation resistance and whether selectively targeting BRAFV600E with a BRAF inhibitor (vemurafenib, BRAFi) sensitizes BRAFV600E thyroid cancer cells to radiotherapy.