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. 2022 Feb 27;40(6):577–591. doi: 10.1093/stmcls/sxac009

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© The Author(s) 2022. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com.

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Figure 7. — Genetic changes are excluded as the cause of kidney organoid-derived tumor formation. (A). Global screening array (GSA) shows no major copy number variations or allelic changes in iPSCs and implanted organoids of line 4 (tumor organoid 1 and tumor organoid 2). (B) Heatmap representation of unsupervised hierarchical clustering based on differentially methylated regions (DMRs) between control organoids of line 4, tumor organoids of line 4, 3 unrelated iPSC (iPSC 1-3), tumorigenic iPSC line 4 (iPSC 4), and non-tumorigenic iPSC line 3 (iPSC 5) (fold change ≥ 2). A region that is hypomethylated in tumor organoids compared to control organoids that resemble the methylation status of iPSC is marked by an arrow. (C) GO enrichment analysis based on the selection of overlapping genes associated with the DMRs between control organoids and tumor organoids. Dot plot visualization shows the top 10 most significant processes. Dot size indicates the number of significant genes in the given pathway and color represents significance. (D) Table view of top 10 most significant processes identified including enrichment, P value, and affected genes.