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. 2023 May 29;22:88. doi: 10.1186/s12943-023-01792-0

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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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Unbalanced Chromosome 17q upregulates MNA neuroblastoma essential genes and indicates adverse disease outcome. a Frequency (%) of DNA copy number gains (red) and losses (blue) for chromosome 1 to 22 in 100 primary human neuroblastoma samples. b, c Kaplan–Meier survival analyses by Chr 17q balance status (b, left), MYCN amplification status in Chr 17q unbalanced tumors (b, right) and MYCN amplification status (c). d Genomic distribution of 175 autosomal essential genes in MNA neuroblastoma. e Genomic location and percentage gain of essential (black and IGF2BP1 in blue) neuroblastoma genes on Chr 17 in primary neuroblastoma (non-essential TP53 on 17p is highlighted red). f Kaplan–Meier survival analyses by IGF2BP1 mRNA expression (best cut-off)