Extended Data Fig 1. Patients with atypical EGFR mutations have worse clinical outcomes than those with classical EGFR mutations.
a, Diagram of patient sample sources and types across databases. b, Lollipop plot of frequency of all EGFR mutations observed in patients with NSCLC (N=24,934 mutations). EGFR mutations associated with acquired drug resistance, as described by the literature, are highlighted in red. c–f, Kaplan-Meier plot of TTF of patients with NSCLC tumors harboring classical (N=264 patients) or atypical EGFR mutations stratified by (c) exon after treatment with an EGFR TKI (Exon 18 N= 40, Exon 19 N=19, Exon 20 N=15, Exon 21 N=26), or EGFR TKI class including 1st- (d), 2nd- (e), or 3rd- (f) gen TKIs in MD Anderson GEMINI and Moffitt Cancer center databases. Patients that received prior chemotherapy or immunotherapy were included, but TTF was calculated for first EGFR TKI received. g, h, Kaplan-Meier plot of PFI (g) and OS (h) of patients with NSCLC tumors harboring classical (N=50 for PFI and N=52 for OS) or atypical (N=35 for PFI and N=39 for OS) EGFR mutations from cBioPortal. Atypical EGFR mutations were limited to mutations in the tyrosine kinase domain, and treatment and stage were unknown. c–h, HRs and p-values were calculated using two-sided Mantel-Cox, Log-Rank tests