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A ) Uniform manifold approximation and projection (UMAP) representing the healthy donors, malignant cells and microenvironment cells from AML BM,, AML+MS BM and myeloid sarcoma, colored by the <t>cell</t> type. B. Principal component analysis of BayesPrism deconvoluted malignant cell <t>expression</t> profiles of myeloid sarcoma (MS), associated BM (AML+MS BM), and AML BM without myeloid sarcoma (AML BM) from bulk RNA-seq data. C. Differential expression analysis comparing myeloid sarcoma (MS) to HD counterpart, AML BM with myeloid sarcoma (AML+MS) and AML BM without myeloid sarcoma (AML) hematopoietic stem and progenitor cells (HSPC) or myeloid cells in the <t>single</t> cell data, or MS to AML or AML+MS in bulk deconvoluted malignant cells. Dotplot summarizes the Hallmark pathway enrichment analysis in up-regulated genes in myeloid sarcoma. Only pathways enriched in at least two comparisons are shown. EMT: epithelial to mesenchymal transition. D. Violin plot showing enrichment of “KRAS activity up” Hallmark pathway in myeloid sarcoma (MS) compared to AML and AML+MS BM. Wilcoxon and Kruskal-Wallis tests were used to evaluate statistical significance. E. Average single-cell data group expression of differentially expressed genes in more than four comparisons from the “allograft rejection” (allo. rej.), “epithelial-mesenchymal transition” (EMT), “interferon alpha response” (IFNα), “interferon gamma response” (IFNγ), “KRAS signaling up” (KRAS) Hallmark pathways. The bottom rows annotate the pathway(s) to which each <t>gene</t> belongs; grey indicates the gene does not belong to the pathway. F. Differentially expressed genes between AML BMs with (AML+MS BM) and without (AML BM) myeloid sarcoma in bulk RNA-seq data. G. Differentially expressed genes comparing deconvoluted myeloid sarcoma and AML BM malignant cells of patients with myeloid sarcoma (AML+MS BM). H. UMAP representation of T cells from AML BM, AML+MS BM and MS. I. Quantification of CD8 + cytotoxic T cells in AML BM, AML+MS BM and myeloid sarcoma (MS). J. Quantification of T Reg in AML BM, AML+MS BM and myeloid sarcoma (MS). K. Effector T cell scores in paired bulk RNA-Seq data of AML+MS BM and MS.
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A ) Uniform manifold approximation and projection (UMAP) representing the healthy donors, malignant cells and microenvironment cells from AML BM,, AML+MS BM and myeloid sarcoma, colored by the <t>cell</t> type. B. Principal component analysis of BayesPrism deconvoluted malignant cell <t>expression</t> profiles of myeloid sarcoma (MS), associated BM (AML+MS BM), and AML BM without myeloid sarcoma (AML BM) from bulk RNA-seq data. C. Differential expression analysis comparing myeloid sarcoma (MS) to HD counterpart, AML BM with myeloid sarcoma (AML+MS) and AML BM without myeloid sarcoma (AML) hematopoietic stem and progenitor cells (HSPC) or myeloid cells in the <t>single</t> cell data, or MS to AML or AML+MS in bulk deconvoluted malignant cells. Dotplot summarizes the Hallmark pathway enrichment analysis in up-regulated genes in myeloid sarcoma. Only pathways enriched in at least two comparisons are shown. EMT: epithelial to mesenchymal transition. D. Violin plot showing enrichment of “KRAS activity up” Hallmark pathway in myeloid sarcoma (MS) compared to AML and AML+MS BM. Wilcoxon and Kruskal-Wallis tests were used to evaluate statistical significance. E. Average single-cell data group expression of differentially expressed genes in more than four comparisons from the “allograft rejection” (allo. rej.), “epithelial-mesenchymal transition” (EMT), “interferon alpha response” (IFNα), “interferon gamma response” (IFNγ), “KRAS signaling up” (KRAS) Hallmark pathways. The bottom rows annotate the pathway(s) to which each <t>gene</t> belongs; grey indicates the gene does not belong to the pathway. F. Differentially expressed genes between AML BMs with (AML+MS BM) and without (AML BM) myeloid sarcoma in bulk RNA-seq data. G. Differentially expressed genes comparing deconvoluted myeloid sarcoma and AML BM malignant cells of patients with myeloid sarcoma (AML+MS BM). H. UMAP representation of T cells from AML BM, AML+MS BM and MS. I. Quantification of CD8 + cytotoxic T cells in AML BM, AML+MS BM and myeloid sarcoma (MS). J. Quantification of T Reg in AML BM, AML+MS BM and myeloid sarcoma (MS). K. Effector T cell scores in paired bulk RNA-Seq data of AML+MS BM and MS.
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A ) Uniform manifold approximation and projection (UMAP) representing the healthy donors, malignant cells and microenvironment cells from AML BM,, AML+MS BM and myeloid sarcoma, colored by the <t>cell</t> type. B. Principal component analysis of BayesPrism deconvoluted malignant cell <t>expression</t> profiles of myeloid sarcoma (MS), associated BM (AML+MS BM), and AML BM without myeloid sarcoma (AML BM) from bulk RNA-seq data. C. Differential expression analysis comparing myeloid sarcoma (MS) to HD counterpart, AML BM with myeloid sarcoma (AML+MS) and AML BM without myeloid sarcoma (AML) hematopoietic stem and progenitor cells (HSPC) or myeloid cells in the <t>single</t> cell data, or MS to AML or AML+MS in bulk deconvoluted malignant cells. Dotplot summarizes the Hallmark pathway enrichment analysis in up-regulated genes in myeloid sarcoma. Only pathways enriched in at least two comparisons are shown. EMT: epithelial to mesenchymal transition. D. Violin plot showing enrichment of “KRAS activity up” Hallmark pathway in myeloid sarcoma (MS) compared to AML and AML+MS BM. Wilcoxon and Kruskal-Wallis tests were used to evaluate statistical significance. E. Average single-cell data group expression of differentially expressed genes in more than four comparisons from the “allograft rejection” (allo. rej.), “epithelial-mesenchymal transition” (EMT), “interferon alpha response” (IFNα), “interferon gamma response” (IFNγ), “KRAS signaling up” (KRAS) Hallmark pathways. The bottom rows annotate the pathway(s) to which each <t>gene</t> belongs; grey indicates the gene does not belong to the pathway. F. Differentially expressed genes between AML BMs with (AML+MS BM) and without (AML BM) myeloid sarcoma in bulk RNA-seq data. G. Differentially expressed genes comparing deconvoluted myeloid sarcoma and AML BM malignant cells of patients with myeloid sarcoma (AML+MS BM). H. UMAP representation of T cells from AML BM, AML+MS BM and MS. I. Quantification of CD8 + cytotoxic T cells in AML BM, AML+MS BM and myeloid sarcoma (MS). J. Quantification of T Reg in AML BM, AML+MS BM and myeloid sarcoma (MS). K. Effector T cell scores in paired bulk RNA-Seq data of AML+MS BM and MS.
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A ) Uniform manifold approximation and projection (UMAP) representing the healthy donors, malignant cells and microenvironment cells from AML BM,, AML+MS BM and myeloid sarcoma, colored by the <t>cell</t> type. B. Principal component analysis of BayesPrism deconvoluted malignant cell <t>expression</t> profiles of myeloid sarcoma (MS), associated BM (AML+MS BM), and AML BM without myeloid sarcoma (AML BM) from bulk RNA-seq data. C. Differential expression analysis comparing myeloid sarcoma (MS) to HD counterpart, AML BM with myeloid sarcoma (AML+MS) and AML BM without myeloid sarcoma (AML) hematopoietic stem and progenitor cells (HSPC) or myeloid cells in the <t>single</t> cell data, or MS to AML or AML+MS in bulk deconvoluted malignant cells. Dotplot summarizes the Hallmark pathway enrichment analysis in up-regulated genes in myeloid sarcoma. Only pathways enriched in at least two comparisons are shown. EMT: epithelial to mesenchymal transition. D. Violin plot showing enrichment of “KRAS activity up” Hallmark pathway in myeloid sarcoma (MS) compared to AML and AML+MS BM. Wilcoxon and Kruskal-Wallis tests were used to evaluate statistical significance. E. Average single-cell data group expression of differentially expressed genes in more than four comparisons from the “allograft rejection” (allo. rej.), “epithelial-mesenchymal transition” (EMT), “interferon alpha response” (IFNα), “interferon gamma response” (IFNγ), “KRAS signaling up” (KRAS) Hallmark pathways. The bottom rows annotate the pathway(s) to which each <t>gene</t> belongs; grey indicates the gene does not belong to the pathway. F. Differentially expressed genes between AML BMs with (AML+MS BM) and without (AML BM) myeloid sarcoma in bulk RNA-seq data. G. Differentially expressed genes comparing deconvoluted myeloid sarcoma and AML BM malignant cells of patients with myeloid sarcoma (AML+MS BM). H. UMAP representation of T cells from AML BM, AML+MS BM and MS. I. Quantification of CD8 + cytotoxic T cells in AML BM, AML+MS BM and myeloid sarcoma (MS). J. Quantification of T Reg in AML BM, AML+MS BM and myeloid sarcoma (MS). K. Effector T cell scores in paired bulk RNA-Seq data of AML+MS BM and MS.
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A ) Uniform manifold approximation and projection (UMAP) representing the healthy donors, malignant cells and microenvironment cells from AML BM,, AML+MS BM and myeloid sarcoma, colored by the <t>cell</t> type. B. Principal component analysis of BayesPrism deconvoluted malignant cell <t>expression</t> profiles of myeloid sarcoma (MS), associated BM (AML+MS BM), and AML BM without myeloid sarcoma (AML BM) from bulk RNA-seq data. C. Differential expression analysis comparing myeloid sarcoma (MS) to HD counterpart, AML BM with myeloid sarcoma (AML+MS) and AML BM without myeloid sarcoma (AML) hematopoietic stem and progenitor cells (HSPC) or myeloid cells in the <t>single</t> cell data, or MS to AML or AML+MS in bulk deconvoluted malignant cells. Dotplot summarizes the Hallmark pathway enrichment analysis in up-regulated genes in myeloid sarcoma. Only pathways enriched in at least two comparisons are shown. EMT: epithelial to mesenchymal transition. D. Violin plot showing enrichment of “KRAS activity up” Hallmark pathway in myeloid sarcoma (MS) compared to AML and AML+MS BM. Wilcoxon and Kruskal-Wallis tests were used to evaluate statistical significance. E. Average single-cell data group expression of differentially expressed genes in more than four comparisons from the “allograft rejection” (allo. rej.), “epithelial-mesenchymal transition” (EMT), “interferon alpha response” (IFNα), “interferon gamma response” (IFNγ), “KRAS signaling up” (KRAS) Hallmark pathways. The bottom rows annotate the pathway(s) to which each <t>gene</t> belongs; grey indicates the gene does not belong to the pathway. F. Differentially expressed genes between AML BMs with (AML+MS BM) and without (AML BM) myeloid sarcoma in bulk RNA-seq data. G. Differentially expressed genes comparing deconvoluted myeloid sarcoma and AML BM malignant cells of patients with myeloid sarcoma (AML+MS BM). H. UMAP representation of T cells from AML BM, AML+MS BM and MS. I. Quantification of CD8 + cytotoxic T cells in AML BM, AML+MS BM and myeloid sarcoma (MS). J. Quantification of T Reg in AML BM, AML+MS BM and myeloid sarcoma (MS). K. Effector T cell scores in paired bulk RNA-Seq data of AML+MS BM and MS.
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Image Search Results


A ) Uniform manifold approximation and projection (UMAP) representing the healthy donors, malignant cells and microenvironment cells from AML BM,, AML+MS BM and myeloid sarcoma, colored by the cell type. B. Principal component analysis of BayesPrism deconvoluted malignant cell expression profiles of myeloid sarcoma (MS), associated BM (AML+MS BM), and AML BM without myeloid sarcoma (AML BM) from bulk RNA-seq data. C. Differential expression analysis comparing myeloid sarcoma (MS) to HD counterpart, AML BM with myeloid sarcoma (AML+MS) and AML BM without myeloid sarcoma (AML) hematopoietic stem and progenitor cells (HSPC) or myeloid cells in the single cell data, or MS to AML or AML+MS in bulk deconvoluted malignant cells. Dotplot summarizes the Hallmark pathway enrichment analysis in up-regulated genes in myeloid sarcoma. Only pathways enriched in at least two comparisons are shown. EMT: epithelial to mesenchymal transition. D. Violin plot showing enrichment of “KRAS activity up” Hallmark pathway in myeloid sarcoma (MS) compared to AML and AML+MS BM. Wilcoxon and Kruskal-Wallis tests were used to evaluate statistical significance. E. Average single-cell data group expression of differentially expressed genes in more than four comparisons from the “allograft rejection” (allo. rej.), “epithelial-mesenchymal transition” (EMT), “interferon alpha response” (IFNα), “interferon gamma response” (IFNγ), “KRAS signaling up” (KRAS) Hallmark pathways. The bottom rows annotate the pathway(s) to which each gene belongs; grey indicates the gene does not belong to the pathway. F. Differentially expressed genes between AML BMs with (AML+MS BM) and without (AML BM) myeloid sarcoma in bulk RNA-seq data. G. Differentially expressed genes comparing deconvoluted myeloid sarcoma and AML BM malignant cells of patients with myeloid sarcoma (AML+MS BM). H. UMAP representation of T cells from AML BM, AML+MS BM and MS. I. Quantification of CD8 + cytotoxic T cells in AML BM, AML+MS BM and myeloid sarcoma (MS). J. Quantification of T Reg in AML BM, AML+MS BM and myeloid sarcoma (MS). K. Effector T cell scores in paired bulk RNA-Seq data of AML+MS BM and MS.

Journal: bioRxiv

Article Title: Multiomic characterization, early detection, and therapeutic targeting of myeloid sarcoma

doi: 10.64898/2025.12.04.689069

Figure Lengend Snippet: A ) Uniform manifold approximation and projection (UMAP) representing the healthy donors, malignant cells and microenvironment cells from AML BM,, AML+MS BM and myeloid sarcoma, colored by the cell type. B. Principal component analysis of BayesPrism deconvoluted malignant cell expression profiles of myeloid sarcoma (MS), associated BM (AML+MS BM), and AML BM without myeloid sarcoma (AML BM) from bulk RNA-seq data. C. Differential expression analysis comparing myeloid sarcoma (MS) to HD counterpart, AML BM with myeloid sarcoma (AML+MS) and AML BM without myeloid sarcoma (AML) hematopoietic stem and progenitor cells (HSPC) or myeloid cells in the single cell data, or MS to AML or AML+MS in bulk deconvoluted malignant cells. Dotplot summarizes the Hallmark pathway enrichment analysis in up-regulated genes in myeloid sarcoma. Only pathways enriched in at least two comparisons are shown. EMT: epithelial to mesenchymal transition. D. Violin plot showing enrichment of “KRAS activity up” Hallmark pathway in myeloid sarcoma (MS) compared to AML and AML+MS BM. Wilcoxon and Kruskal-Wallis tests were used to evaluate statistical significance. E. Average single-cell data group expression of differentially expressed genes in more than four comparisons from the “allograft rejection” (allo. rej.), “epithelial-mesenchymal transition” (EMT), “interferon alpha response” (IFNα), “interferon gamma response” (IFNγ), “KRAS signaling up” (KRAS) Hallmark pathways. The bottom rows annotate the pathway(s) to which each gene belongs; grey indicates the gene does not belong to the pathway. F. Differentially expressed genes between AML BMs with (AML+MS BM) and without (AML BM) myeloid sarcoma in bulk RNA-seq data. G. Differentially expressed genes comparing deconvoluted myeloid sarcoma and AML BM malignant cells of patients with myeloid sarcoma (AML+MS BM). H. UMAP representation of T cells from AML BM, AML+MS BM and MS. I. Quantification of CD8 + cytotoxic T cells in AML BM, AML+MS BM and myeloid sarcoma (MS). J. Quantification of T Reg in AML BM, AML+MS BM and myeloid sarcoma (MS). K. Effector T cell scores in paired bulk RNA-Seq data of AML+MS BM and MS.

Article Snippet: Subsequently, the Cell Ranger Single Cell Gene Expression Software (version 5.0, 10x Genomics) was employed to demultiplex and align the raw 3’ library reads to GRCh38 (version 2020-A).

Techniques: Expressing, RNA Sequencing, Quantitative Proteomics, Activity Assay