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. 2021 Dec 14;41(7):1011–1023. doi: 10.1038/s41388-021-02141-5

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© The Author(s) 2021

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. 7 — A–C, Representative IHC images of spleen samples stained for A BrdU as proliferation marker, B p53 protein, and C cleaved caspase 3 (CC3) as apoptosis marker. D Quantification of CC3 in 10 fields of view per mouse sample. Shown are mean ± SD; datapoints represent individual mice; 2way ANOVA with Dunnett’s multiple comparisons test. E, F Leukemia samples were collected from control and treated mice at 2 and 6 hours after therapy and analyzed by RNAseq and GSEA. E Graphs depict GSEA results for the indicated gene sets in pairwise comparisons between control and treated leukemias. Bars, false discovery rate (FDRq); dots, enrichment score. F Violin plots illustrate distribution of FDRq values from GSEA with multiple p53-related gene sets (Table S1). Each data point represents one gene set. G mRNA expression (RT–qPCR) of p53 target genes Cdkn1a and Bbc3 normalized to Actb (β-actin). Shown is the mean ± SD log2-fold change in treated leukemia samples relative to untreated; 2way ANOVA with Dunnett’s multiple comparisons test; datapoints represent individual mice.