Fig. 1: Patients with AML displaying a low PRMT2 expression show a higher inflammatory signature.
From: Protein arginine methyltransferase 2 controls inflammatory signaling in acute myeloid leukemia
a PRMT2 gene expression within the Leucegene cohort (non-APL AML, n = 371) at diagnosis with the PRMT2low patients in red (n = 37) and PRMT2high patients in blue (n = 37). b Kaplan-Meier survival curves of the patients depending on their PRMT2 expression: above or below the median of expression of the cohort. c Mutation profile of the PRMT2low (n = 10) and PRMT2high (n = 10) patients for a subset of frequently mutated genes in AML. Blue: mutated gene; gray: non mutated gene. d The bar graph shows the most significantly overrepresented hallmarks after a gene set enrichment analysis (GSEA) of PRMT2low compared to PRMT2high patients with normalized enrichment scores on the right. All gene sets are FDR < 25% and p < 0.01. e GSEA plot for the “TNFA signaling via NFKB” hallmark with FDR and nominal p value indicated. f Heatmap representing the top 20 enriched genes of the “TNFA signaling via NFKB” hallmark. NF-κB-related genes appear in bold.
