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. Author manuscript; available in PMC: 2020 Feb 15.
Published in final edited form as: Clin Cancer Res. 2018 Oct 23;25(4):1248–1260. doi: 10.1158/1078-0432.CCR-18-1640

Figure 1: A patient with lung adenocarcinoma harboring MET exon14 alteration and acquired KRAS G12S.

Figure 1:

A. The clinical course and treatment history of PT-5 with a MET exon 14 alteration (KRAS wild type) at the time of progression on cytotoxic chemotherapy. The next biopsy took place after progression on MET bivalent antibody and showed a newly acquired KRAS G12S mutation. B. Computed tomography scans of the patient before and after progression during crizotinib treatment. C. MSK-IMPACT sequence analysis of paired samples before and after crizotinib resistance. D. The copy number plots for paired samples before and after crizotinib resistance. E. The top and bottom 20 genes differentially expressed in METex14 (n=3) vs MET wildtype amplified (n=5) lung adenocarcinomas from BCCA. F. The same analysis but for TCGA tumors with 7 METex14 and 7 MET wildtype amplified tumors. G. The top GSEA Oncogenic Signatures upregulated in METex14 vs MET wildtype amplified tumors. Gene sets related to KRAS signaling are indicated in bold. H. Representative GSEA enrichment plots for the top KRAS-related signatures in BCCA (top) and TCGA (bottom).