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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. 2 — (a) Significant drivers identified independently in the SU2C-MARK cohort (left) as compared to TCGA Lung Adenocarcinoma (LUAD; right upper) and TCGA Lung Squamous Cell Carcinoma (LUSC; right lower). Of note, the SU2C-MARK cohort includes a mixture of frequent drivers observed in LUAD and LUSC, consistent with it representing pan-NSCLC histologies. (b) Kaplan-Meier curves comparing checkpoint blockade treated ATM mutant patients and ATM wildtype patients in the Memorial Sloan Kettering Cancer Center (MSKCC) Impact cohort. ATM mutated patients demonstrated improved survival compared to unmutated patients (p = 0.03, logrank test).