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. 2023 Nov 9;55(12):2189–2199. doi: 10.1038/s41588-023-01551-3

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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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Fig. 1 — a, Presence of ecDNA by molecular subgroup across 468 tumors from patients with medulloblastoma. b, A subset of recurrently (n ≥ 2) amplified genes on ecDNA in this patient cohort. p53 inhibitors: negative regulators of p53 pathway activity; COSMIC: genes listed as Tier 1 or Tier 2 of the COSMIC Cancer Gene Census⁶¹. c, Kaplan–Meier curve depicting five-year overall survival in the patient cohort stratified by the presence of ecDNA in tumors. P = 8.6 × 10^–6. d–f, Kaplan–Meier curves indicating overall survival for SHH (P = 4.8 × 10^–3) (d), Group 3 (P = 0.01) (e) and Group 4 (P = 0.01) (f) subgroups, stratified by ecDNA presence. P values for c–f were derived from two-sided log-rank test without correction for multiple hypotheses. g, Log hazard ratios for ecDNA status, medulloblastoma subgroup, age and sex estimated by Cox regression on overall survival. Sample size was n = 352 observations. Data are presented as maximum likelihood estimate (MLE) ±95% confidence intervals.