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. Author manuscript; available in PMC: 2024 Jul 1.
Published in final edited form as: Lung Cancer. 2023 May 13;181:107250. doi: 10.1016/j.lungcan.2023.107250

Figure 1. EGFR exon 19 deletions in context of other genomic aberrations.

Figure 1.

(A) Frequency of common EGFR mutations and EGFR-K747_E746insIPVAIK and other variants in two separate cohorts. The larger cohort represents data from the commercial vendor Foundation Medicine20 and the smaller from our institutional cases from Beth Israel Deaconess Medical Center (BIDMC) between years 2004 to 2021. (B) Display of amino acid sequence of wild-type EGFR compared to the different variants of EGFR-K745_E746ins_XPVAIK mutations based on reference 19. Frequency of the different XPVAIK insertions curated from the COSMIC database is displayed. (C) Theoretical mechanism of the sensitivity of the EGFR-K747_E746insIPVAIK mutation that details the change that may allow for sensitivity to approved EGFR TKIs based on structural modeling from reference 19. There is no published crystal structure for this mutant. The proposed mechanism of activation depicted is similar to mechanisms described for EGFR-A763_Y764insFQEA and EGFR-L861Q.