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. 2024 Nov 25;56(12):2790–2803. doi: 10.1038/s41588-024-01999-x

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© The Author(s) 2024

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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Extended Data Fig. 10 — a Karyotype heterogeneity between diagnosis and relapse cells in patient P5 based on structural variant (SV) burden (bottom) and its standard deviation (SD; top). Each grey dot represents a single cell. The structural variant burdens were compared using two-tailed Wilcoxon test (Diagnosis (n = 63), Relapse (n = 54)); Point ranges was defined by minima = mean - 2X standard deviation, maxima = mean + 2X standard deviation, point = mean. b Expression of the Ng et al. LSC Up transcriptomic stemness scores²⁷ in the single cells at diagnosis vs. relapse in patient P5 (n_Diagnosis = 3,444 and n_Relapse = 1,102). Stemness scores between disease stages were compared using two-tailed Wilcoxon test. Expression levels of the individual genes in the score were calculated from normalized and variance stabilized counts. Beeswarm plots show the 95% confidence interval for the mean. c Weighted nearest neighbor-based UMAP plots of diagnosis and relapse leukemic cells from patient P5 CITE-seq data. Cells are colored based on subclones identified using scTRIP and are shaped based on disease stage. d Enriched pathways at diagnosis and relapse in SC1-derived cells in patient P5. Genes with FDR < 0.05 and log-fold-change > 0.25 were included in the analysis. e Karyotype heterogeneity between diagnosis and refractory cells in patient P9 based on structural variant burden (bottom) and its standard deviation (top). Each grey dot represents a single cell. The structural variant burdens were compared using two-tailed Wilcoxon test (Diagnosis (n = 44), Refractory (n = 21)); Point ranges was defined by minima = mean - 2X standard deviation, maxima = mean + 2X standard deviation, point = mean. f Enriched pathways at diagnosis and refractory disease in SC1-derived cells in patient P9. Genes with FDR < 0.05 and log-fold-change > 0.25 were included in the analysis. g Enriched pathways at diagnosis and refractory disease in SC3-derived cells in patient P9. Genes with FDR < 0.05 and log-fold-change > 0.25 were included in the analysis. h Viabilities (fraction of viable cells compared to untreated control) of different populations after 24 h ex vivo exposure with indicated concentrations of venetoclax (VEN) in P9 diagnosis cells (P9D).