Somatic mutations in BRAF have been found in 1-4% of all NSCLC most of which are adenocarcinomas and may be a potential therapeutic target in some settings. The BRAF V590I variant lies within the protein kinase domain of the Braf protein, has not been biochemically characterized, but results in similar cell proliferation and viability levels to wild-type Braf in culture (PMID: 29533785), and therefore is predicted to have no effect on Braf protein function, but its oncogenic potential has not been characterized. Clinical correlation is recommended.
Robinson SD et al . BRAF V600E-mutated lung adenocarcinoma with metastases to the brain responding to treatment with vemurafenib. Lung Cancer. 2014 Aug;85(2):326-30.
Paik PK et al.. Clinical characteristics of patients with lung adenocarcinomas harboring BRAF mutations. J Clin Oncology, 2011 May 20;29(15):2046-51.
Planchard D, et al. Dabrafenib in patients with BRAF(V600E)-positive advanced non-small-cell lung cancer: a single-arm, multicentre, open-label, phase 2 trial. Lancet Oncol 2016;17(5):642-50
Flaherty KT, et al. Improved survival with MEK inhibition in BRAF-mutated melanoma. N Engl J Med 2012;367(2):107-14
Ng PK, et al. Systematic Functional Annotation of Somatic Mutations in Cancer. Cancer Cell. 2018 Mar 12;33(3):450-462.
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