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. 2022 Jul 4;13:3833. doi: 10.1038/s41467-022-31155-0

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© The Author(s) 2022

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. 1 — a –log10 p-value (two-tailed Student’s t test) of each mRNA splicing factor expression in LSC-enriched vs LSC-depleted subsets from 78 AML patients (y axis) and their correlation (-log10 p-value) (log-rank test) with AML patients’ overall survival (x axis). b Kaplan–Meier curves showing outcomes of AML patients from the TCGA with above (n = 124) vs below (n = 155) median expression of RBM17. (P = 0.00568, log-rank test). c RBM17 transcript level in LSC-enriched (n = 138) vs LSC-depleted (n = 89) subsets from 78 AML patient samples (GSE76008). Average fold change of RBM17 expression in LSC-enriched over LSC-depleted subsets is indicated in the figure. Data are presented as mean ± SD, two-tailed Student’s t test. d Gene expression data (GSE35008) from sorted AML bone marrow samples were compared with data from healthy controls and revealed significantly increased RBM17 expression in AML LT-HSCs (Lin^–CD34 + CD38^–CD90 + , AML with normal karyotype, n = 3) compared with healthy control (n = 4). Data shown as mean ± SD, two-tailed Student’s t test. e Intracellular flow cytometric measurements of RBM17 protein level in the primitive CD34⁺ subset vs the committed CD34^- subsets from 8 primary AML samples. P = 0.0092, P value was calculated using paired t-test, two-tailed. f Expression of RBM17 in 152 AML specimens and each molecular genetic risk group from the TCGA-LAML cohort (Good: n = 38; Intermediate: n = 76; Poor: n = 38). Data are presented as mean ± SD, two-tailed Student’s t test, P(Good vs Intermediate) = 0.0196, P(Good vs Poor)=0.0051. g Expression of RBM17 in 236 AML specimens and each molecular genetic risk group from Beat AML cohort (Favorable: n = 85, Intermediate: n = 68, Adverse: n = 83). Data are presented as mean ± SD, two-tailed Student’s t test, P(Favorable vs Intermediate) = 0.0188, P(Favorable vs Adverse)=0.0041. h A heatmap showing the expression of differentially expressed transcripts identified from RBM17-high AML cases versus RBM17-low AML cases. i, j Gene set enrichment analysis (GESA) of the gene signature of high-RBM17 AML cases compared with previously published i LSC signatures and j ribonucleoprotein complex biogenesis and spliceosomal complex assembly pathways. The significance of NES was calculated using Kolmogorov–Smirnov statistics. *P < 0.05, **P < 0.01, ***P < 0.001. Source data are provided as a Source Data file.