Fig. 1: Transcriptional profiling identifies AML-like T-ALLs that are enriched for immature myeloid and thymic progenitor transcriptional signatures. | Leukemia

Fig. 1: Transcriptional profiling identifies AML-like T-ALLs that are enriched for immature myeloid and thymic progenitor transcriptional signatures.

From: A transcriptomic continuum of differentiation arrest identifies myeloid interface acute leukemias with poor prognosis

Fig. 1

a Unsupervised hierarchical clustering (HC) of the transcriptional profiles of 124 acute leukemias, comprising 48 T-ALLs and 76 AMLs. A subset of T-ALL cases segregates with the AML cluster. b GSEA analysis of pathways significantly enriched in AML-like T-ALLs vs the rest of the T-ALL cohort. The MSigDB C2 collection of genesets was used and only selected genesets with FDR < 0.05 are shown. NES normalized enrichment score. c Enrichment of selected normal hematopoietic progenitor transcriptional signatures derived from the indicated published datasets or our own analysis of thymic subpopulations (gene-sets provided in Supplementary Table S1) in AML-like T-ALLs by GSEA. NES normalized enrichment score, crossed out boxes indicate gene-sets that are not significantly enriched (FDR > 0.05). HSC hematopoietic stem cell, CMP common myeloid progenitor, GMP granulocyte-monocyte progenitor, MEP megakaryocytic-erythroid progenitor, MLP multi-lymphoid progenitor, LMPP lymphoid-primed multipotent progenitor, MDCP monocyte-dendritic cell progenitor, LMDP lymphoid-mono-dendritic progenitor, ELP early lymphoid precursor. d 2D PCA map of umbilical cord blood stem and progenitor populations and T-ALL gene expression patterns [38]; distribution of AML-like T-ALLs (blue squares) is significantly different to that of other T-ALLs (PC1: p = 0.003; PC2: p = 4.1 × 10–5 by two-sided t-test).

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