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BRAF
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Interpretation 2240
Tier 2
BRAF
Variants
BRAF G466R
Primary Sites
Lung
Tumor Types
Adenocarcinoma
Interpretation

Somatic mutations in BRAF have been found in 1-4% of all NSCLC most of which are adenocarcinomas. The G466R mutation results in an amino acid substitution within the kinase domain of BRAF. Unlike other mutant BRAF proteins, G466R shows decreased kinase activity, however, it also causes paradoxically activation Erk signaling in cell culture Therapeutic implications of BRAF inhibitors in patients with this mutation need to be fully elucidated.

Citations
  1. Sen B, et al. Kinase-impaired BRAF mutations in lung cancer confer sensitivity to dasatinib. Sci Transl Med 2012;4(136):136ra70
  2. Davies H, et al. Mutations of the BRAF gene in human cancer. Nature 2002;417(6892):949-54
  3. https://www.mycancergenome.org/content/disease/lung-cancer/braf/70/
  4. Yao Z, et al. BRAF Mutants Evade ERK-Dependent Feedback by Different Mechanisms that Determine Their Sensitivity to Pharmacologic Inhibition. Cancer Cell 2015;28(3):370-83
  5. Heidorn SJ, et al. Kinase-dead BRAF and oncogenic RAS cooperate to drive tumor progression through CRAF. Cell 2010;140(2):209-21
  6. Houben R, et al. Constitutive activation of the Ras-Raf signaling pathway in metastatic melanoma is associated with poor prognosis. J Carcinog. 2004 Mar 26;3:6.
Last updated: 2018-04-18 18:23:55 UTC
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When using PMKB, please cite: Huang et al., JAMIA 2017


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