Figure 1.
Identification of human EVI1–dependent AML cell lines. (A) Reanalysis of CRISPR-based loss-of-function screens of 102 hematopoietic cell lines. Each dot represents a distinct screen. Gene effects were normalized to false discovery rate (FDR)–adjusted median effects size of defined core essential and nonessential genes. (B) Reanalysis of RNAi-based loss-of-function screens of 61 hematopoietic cell lines retrieved from the Cancer Dependency Map (depmap.org). Each dot represents a distinct screen. Gene effects are normalized using DEMETER2.29 (C) Competitive proliferation assay in human AML cell lines. Illustrated as color-coded percentage of dsRed–positive cells expressing indicated short hairpin RNAs (shRNAs) over 18 days. The nontargeting shRNA Ren.713 is used as negative control and the MYC-targeting shRNA as positive control. Results are normalized to day 8 after transduction and are shown as the mean of 3 biological replicates. (D) Comparative analysis of 2 CRISPR-based loss-of-function screens in MOLM-13 cells using the data set of this study (Institute of Molecular Pathology [IMP]) and the publicly available Avana data set.26 Gray dots represent all genes. Axis shows enrichment/depletion as log2 fold change (FC). Orange dots represent genes defined as core essential, whereas dark gray dots represent nonessential genes. Dashed lines indicate median log2-fold depletion of core essential genes. (E) Comparative analysis of CRISPR-based loss-of-function screens of HNT-34 vs MOLM-13 cells. Red dots represent genes that selectively impair HNT-34 cells upon knockout (log2 FC in HNT-34 < −2, at least 2 log2 difference compared with MOLM-13 and log2 FC in MOLM-13 > −2.5). Blue dots represent genes that selectively impair MOLM-13 cells upon knockout (log2 FC < −2 in MOLM-13, at least 2 log2 difference compared with HNT-34, and log2 FC in HNT-34 > −2.5). (F) GO term analysis of genes with selective effects within HNT-34 compared with MOLM-13.

Identification of human EVI1–dependent AML cell lines. (A) Reanalysis of CRISPR-based loss-of-function screens of 102 hematopoietic cell lines. Each dot represents a distinct screen. Gene effects were normalized to false discovery rate (FDR)–adjusted median effects size of defined core essential and nonessential genes. (B) Reanalysis of RNAi-based loss-of-function screens of 61 hematopoietic cell lines retrieved from the Cancer Dependency Map (depmap.org). Each dot represents a distinct screen. Gene effects are normalized using DEMETER2.29 (C) Competitive proliferation assay in human AML cell lines. Illustrated as color-coded percentage of dsRed–positive cells expressing indicated short hairpin RNAs (shRNAs) over 18 days. The nontargeting shRNA Ren.713 is used as negative control and the MYC-targeting shRNA as positive control. Results are normalized to day 8 after transduction and are shown as the mean of 3 biological replicates. (D) Comparative analysis of 2 CRISPR-based loss-of-function screens in MOLM-13 cells using the data set of this study (Institute of Molecular Pathology [IMP]) and the publicly available Avana data set.26 Gray dots represent all genes. Axis shows enrichment/depletion as log2 fold change (FC). Orange dots represent genes defined as core essential, whereas dark gray dots represent nonessential genes. Dashed lines indicate median log2-fold depletion of core essential genes. (E) Comparative analysis of CRISPR-based loss-of-function screens of HNT-34 vs MOLM-13 cells. Red dots represent genes that selectively impair HNT-34 cells upon knockout (log2 FC in HNT-34 < −2, at least 2 log2 difference compared with MOLM-13 and log2 FC in MOLM-13 > −2.5). Blue dots represent genes that selectively impair MOLM-13 cells upon knockout (log2 FC < −2 in MOLM-13, at least 2 log2 difference compared with HNT-34, and log2 FC in HNT-34 > −2.5). (F) GO term analysis of genes with selective effects within HNT-34 compared with MOLM-13.

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