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. 2022 Apr 5;13:1811. doi: 10.1038/s41467-022-29444-9

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — A, B Significantly altered genes associated with A LUAD and B LUSC proteotype are shown. Genes in bold are cancer drivers as defined by cBioportal. C EGFR protein expression, active pY sites, driver mutation and amplification status per LUAD cases. Blue diamonds show responders and yellow star cases show non-responders to EGFR TKI. D Tumor volume growth trend in response to Afatinib (n = 6) vs. Control (n = 5) in NSCLC PDX model 134 that has amplification and elevated protein expression of WT EGFR (mean ± SD) (linear mixed effects model, p-value = 2.3E-15). Source data are provided as a Source Data file.