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. 2023 Sep 28;14:6066. doi: 10.1038/s41467-023-41559-1

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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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — a EGFR and NF1 somatic genetic alterations occurring in multiregional samples from IDH wild-type glioma. Samples are grouped by patient and clinical annotations are indicated in the bottom tracks. EGFR (red box) and NF1 (green box) alterations are mutually exclusive in 98.7% samples (152 out of 154, two-sided Fisher’s Exact test p = 1.72e−07). The mutual exclusivity between EGFR and NF1 alterations was also observed within the same patient (orange box). Co-occurring genetic alterations have been identified only in 2 samples from 2 patients (blue box). b Evolutionary model of glioblastoma from patient P065 that included 5 contrast-enhancing samples harboring mutual exclusive EGFR and NF1 alterations. NF1 truncating mutation specifically occurred in two samples with wild-type EGFR locus; conversely, EGFR was amplified in the other two NF1 wild-type samples. Tumor purity is indicated for each sample (percentages displayed). VAF, variant allele frequency. Number of truncal, shared, and private alterations are indicated.