Extended Data Fig. 2: Clinical relevance of coexisting IDH2 and SRSF2 mutations in AML.
From: Coordinated alterations in RNA splicing and epigenetic regulation drive leukaemogenesis
a–c, Kaplan–Meier survival analysis of patients with AML from the Manchester/Christie Biobank dataset (a: based on IDH2 and SRSF2 genotype (n = 258); b: based on cytogenetic risk (n = 284)) and the TCGA (c; n = 161; based on IDH1, IDH2 and SRSF2 genotypes (log-rank (Mantel–Cox) test (two-sided)). d, Age at diagnosis of patients from the TCGA, Beat AML, and Manchester/Christie Biobank cohorts combined (the line represents mean, box edges show 25th and 75th percentiles and whiskers represent 2.5th and 97.5th percentiles; samples below 2.5th percentile and above 97.5th percentile are shown as dots; one-way ANOVA with Tukey’s multiple comparison test). e, Distribution of French–American–British (FAB) classification of patients with AML with the indicated genotypes from the TCGA cohort. f–h, Mutations coexisting with IDH2 and SRSF2 double-mutant and SRSF2 single-mutant AML from the TCGA (f), Beat AML (g), and Manchester/Christie Biobank (h) cohorts are shown with FAB classification, cytogenetic risk, prior history of myeloid disorders, and genetic risk stratification based on European LeukaemiaNet (ELN) 2008 and ELN2017 guidelines (the number of patients is indicated; P values on the right represent statistical significance of co-occurrence (red and orange) or mutual exclusivity (blue and light blue) of each gene mutation with SRSF2 (including those in IDH2 and SRSF2 double-mutant AML) or coexisting IDH2 and SRSF2 mutations; Fisher’s exact test (two-sided)). *P < 0.05, **P < 0.01, ***P < 0.001.
