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. 2019 Dec;5(6):a004424. doi: 10.1101/mcs.a004424

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© 2019 Wrzeszczynski et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial License, which permits reuse and redistribution, except for commercial purposes, provided that the original author and source are credited.

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Figure 1. — (A) BRAF Chr 7:140477836 (c.1457_1471delATGTGACAGCACCTA_p.Asn486_Pro490del) as visualized in whole-genome sequencing (top track, WGS-Tumor), whole-exome sequencing (center track, WES-Tumor), and blood normal sample (lower track, Normal). (B) Sanger sequencing electropherogram confirming the BRAF ΔNVTAP variant. (C) Location of the deletion variant in BRAF protein (red) and residues involved in a potential salt bridge (green) (PDB:1UWH). (D) CA 19-9 marker serum levels (units/mL) over time. (E) Patient CT scan of pre- (left) and post- (right) dabrafenib treatment demonstrating decrease in the hepatic metastatic tumor burden posttreatment.