Purpose: The present study clarified the sensitivity of the BRAF tyrosine kinase inhibitor mechanism in patients with BRAF compound mutation and predicted the sensitivity using molecular dynamics simulation.
Methods: We examined 16 BRAF tumors with p.V600E-positive non-small-cell lung cancer.
Results: One patient (6.2%) had a BRAF p.V600E and p.K601_W604 compound mutation with a good clinical response to dabrafenib and trametinib. Molecular dynamics simulation also complemented the effect.
Conclusions: The combination of a genetic analysis and computational simulation model may help predict the sensitivity for dabrafenib in cases with a rare BRAF compound mutation. The construction of a genomic and simulation fused database is important for the development of personalized medicine in this field.
Keywords: BRAF; MD simulation; Non-small-cell lung cancer.
Copyright © 2022. Published by Elsevier Inc.