Fig. 1: Prevalence and clinical impact of recurrent mutations of CTDNEP1 in G3 MBs. | Nature Communications

Fig. 1: Prevalence and clinical impact of recurrent mutations of CTDNEP1 in G3 MBs.

From: Loss of phosphatase CTDNEP1 potentiates aggressive medulloblastoma by triggering MYC amplification and genomic instability

Fig. 1: Prevalence and clinical impact of recurrent mutations of CTDNEP1 in G3 MBs.The alternative text for this image may have been generated using AI.

a Frequency of known and recurrent genetic variants in pediatric G3 MBs. b The significance enrichment plot of somatic recurrent mutated genes in G3-MB compared with other MB subgroups. P values were calculated based on Fisher’s exact test and were then adjusted for multiple testing by Bonferroni correction methods. c Frequency of CTDNEP1 LOF variants in different MB subgroups. d Somatic CTDNEP1 mutation profile in patients with MBs. fs, Frameshift. e Association between somatic CTDNEP1 LOF variants and somatic chromosomal alterations (n = 136 G3-MB). p values were calculated using Bayesian logistic regression analysis, likelihood ratio tests, and adjusted for multiple testing based on 5% false discovery rate (FDR) correction. f Kaplan–Meier analysis of overall survival of patients with WNT, SHH, G3, and G4 MB based on the CTDNEP1 high and low expression across subgroups in publicly available MB cohorts. Log-rank test. g Kaplan-Meier analysis of overall survival of patients with CTDNEP1 (CTD) mutation and no MYC amplification (CTD w/o MYC), MYC amplification and no CTDNEP1 mutation (MYC w/o CTD), CTDNEP1 mutation and MYC amplification (CTD + MYC) and other G3 MB patients (other G3). Log-rank test. n.s., not significant. Source data are provided as a Source Data file.

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