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. 2023 Oct 18;146(6):849–852. doi: 10.1007/s00401-023-02640-7

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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. 1 — Characteristics of LTS patients. a Swimmer plot for 13 LTS patients demonstrates wide variety in timing and types of therapies. b Bar plot comparing oncogene mutation frequencies in LTS (n = 55) and molecular control (OS < 18 months, n = 208) cohorts highlights the higher frequency of MAPK pathway alterations in the LTS cohort. c Kaplan–Meier curve for combined LTS and molecular control cohort (n = 310) reveals that MAPK pathway genetic alterations are associated with improved OS at 36 months and shows differential survival among MAPK oncogenes. d Clonal map demonstrates molecular evolution of UM-607 from time of initial and subsequent biopsies, with thin lines for sub-clonal (< 10%) and thick lines for clonal branching events. e Histology stains demonstrate histologic evolution from low- to high-grade. f–g Clonal maps demonstrate the molecular evolution of UM-443 and UM-495 at various timepoints and tumor samples. h–i Joint analysis using t-SNE dimensionality reduction of LTS (23 patients, 27 tumors) and STS (20 patients; MNP2.0 cohort) H3K27M-DMGs reveals two clusters separating tumors from LTS/STS patients (h) and tumors with/without MAPK pathway alterations (i)