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. 2025 Aug 21;16:7689. doi: 10.1038/s41467-025-62673-2

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© The Author(s) 2025

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 4 — A Principal component analysis (PCA) of top 5000 most variable genes, dots are colored based on tumor entity and shaped for tumoroid, tissue or PDX tissue. B Heatmap showing marker gene expression of the different tumor entities in tumor and tumoroid samples. C Heatmap showing the expression of the top 20 differentially expressed genes per tumor entity that have a CHIPseq binding peak of their characteristic (fusion-)protein in close proximity to the transcription start site. D Dot plot showing row-normalized mean expression values of genes that are targeted by our in-house drug library in the different tumor entities. Source data are provided as a Source Data file.