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. 2017 Mar 13;7:44206. doi: 10.1038/srep44206

Figure 1. Concurrent genetic alterations drive rapid resistance to EGFR TKI treatment in EGFR-mutant lung adenocarcinoma.

Figure 1

(A) Computed tomography indicates the clinical course and timeline of disease in the patient with rapid progression on EGFR TKI therapy and shows the EGFR-mutant lung adenocarcinoma (red arrows) analyzed both prior to erlotinib treatment and upon resistance at 4 months. (B) Key somatic mutations identified by exon-capture and deep sequencing of the pre- and post-treatment tumor in (A) demonstrating concurrent alterations in EGFR and BRAF and the frequency of each mutation in pre- and post- treatment tumor samples. P-values indicated as determined by a two-tailed Fischer’s exact test. (C) DNA copy number alterations inferred from exon-capture and sequencing data indicate the focal amplification of the EGFRL858R-mutant allele was lost upon acquired resistance while the patient’s resistant tumor gained a focal amplification of MET, with no change in BRAF (relative positions indicated, chromosome 7).