Journal: Cell Death Discovery
Article Title: Cell cycle regulator MYBL2 is a distinct vulnerability in acute myeloid leukemia
doi: 10.1038/s41420-025-02810-4
Figure Lengend Snippet: A Workflow of potential target selection from the CRISPR-Cas9 24Q2 (Chronos) dataset (DepMap). B Analysis of the DepMap’s public genome-scale CRISPR-Cas9 24Q2 (Chronos) essentiality screen dataset comparing dependency scores of AML cell lines ( n = 26) to cancer cell lines of other entities ( n = 1124). Volcano plot represents the median difference between AML cell lines and non-AML cell lines for each gene ( n = 17,931) and the significance (−log10 p value). In green are the top 200 most significant genes with a median difference below 0. Analysis and t test were performed with R version 4.3.2. C KEGG terms from pathway enrichment analysis using g:Profiler obtained from the top 200 ranked genes. D Overlaps from each step in the analysis are represented in a Venn diagram. E Genes from ( C ) filtered for genes essential in AML (dependency score <−0.5) and non-essential in non-AML (dependency score >−0.5), ranked based on significance. F Violin plot of MYBL2 dependency scores from the DepMap data set. In green are all AML cell lines ( n = 26). In blue are all other included cancer cell lines ( n = 1076). The line shows the median for each, and the quartiles are represented as dotted lines, two-sided t test. G Box plot representing dependency scores across cancer entities. Cancer entities that had a minimum of 15 cell lines within the data set were included and ranked based on the median dependency score. Data from all cell lines can be found in supplementary Table . AML is highlighted in green. H Violin plot of MYBL2 expression from the DepMap Expression_Public_24Q2 data set in AML cell lines ( n = 43) (green) and in non-AML cell lines ( n = 1394) (blue).
Article Snippet: dCas9-KRAB expressing AML cell lines were generated with lentiviral transduction with pLV hUbC-dCas9 KRAB-T2A-GFP (addgene #67620, a gift from Charles Gersbach).
Techniques: Selection, CRISPR, Expressing