Fig. 3: CALCRL is required for leukemic stem cell maintenance.
From: Adrenomedullin-CALCRL axis controls relapse-initiating drug tolerant acute myeloid leukemia cells
a Barplot shows the percentage of CALCRLpositive cells in (n = 11 primary AML samples) in cells classified as HSC-like, progenitor-like, GMP-like, Promonocyte-like, Monocyte-like, or cDC-like malignant cells (Van Galen et al. 2019)31. b Heatmap shows the percentage of CALCRLpositive cells in each patient individually. c SPRING visualization of single-cell transcriptomes. Points are color-coded by indicated cell-type annotations. d Phenotypic distribution and number of CALCRLpositive cells. e GSEA of stem cell signatures functionally identified by Eppert et al.2 or phenotypically defined by Gentles et al.3 or Ng et al.4 was performed using transcriptomes of cells expressing low (blue) vs high (red) levels of CALCRL gene (TCGA, AML cohort, Enrichment Score based on a Kolmogorov-Smirnov statistic). f Primary AML samples or cells from primary mice were collected and treated ex vivo with siCTR or siCALCRL and transplanted in limiting doses into primary or secondary recipients. Human marking of >0.1% was considered positive for AML engraftment except for AML#31 for which the cut-off was 0.5% because the sample was hCD33− (Poisson statistic). g Engraftment results. Data are mean ± error bars (upper and lower limit, Poisson statistic).
