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. 2023 Apr 6;55(5):807–819. doi: 10.1038/s41588-023-01355-5

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© The Author(s) 2023

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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Extended Data Fig. 3 — (a) Somatic copy number alterations were analyzed using GISTIC2.0 (ref. ⁸⁷) to identify significantly recurrent focal amplifications and deletions. Strong overlap between the events identified in the SU2C-MARK cohort and those previously described in TCGA LUAD and LUSC was observed. A subset of validated lung cancer drivers within regions of focal copy number alteration are annotated. (b) Volcano plot of logistic regression results for focal amplifications. Focal amplification of cytoband 5p15.33 (which contains TERT) is associated with resistance to checkpoint blockade. CR = Complete Response, PR = Partial Response, SD = Stable Disease, PD = Progressive Disease. (c) Kaplan-Meier curves comparing checkpoint blockade treated patients with and without TERT amplifications (AMP) in the Memorial Sloan Kettering Cancer Center (MSKCC) Impact cohort (p = 0.7, logrank test).