Fig. 6

KMT2C truncations enhance MYC target gene expression and correlate with reduced DFS for PCa patients. a HALLMARK gene sets enriched in patients with KMT2C truncation mutations versus wild type forms of KMT2C. Gene sets enriched at an FDR < 0.05 are depicted. Dotted lines: adj. P value = -log10(0.05). b fGSEA plots of KMT2C truncated versus KMT2C wild type (wt) prostate cancer patient samples showing an enrichment for MYC target genes (HALLMARK_MYC_TARGETS_V1, HALLMARK_MYC_TARGETS_V2). c-d MYC (c) and CDKN2A (d) mRNA expression levels in prostate cancer patients with wild type (n = 461) or truncated (n = 15) forms of KMT2C. Data are shown as box and whiskers (min to max) plots, and P values were determined by a Mann–Whitney test for non-normal distribution (c) or a two-tailed unpaired Student’s t-test (d). e fGSEA plots of KMT2C truncated versus KMT2C wild type (wt) prostate cancer patient samples showing an enrichment of transcriptional signatures upregulated during G1/S phase transition (REACTOME_G1_S_TRANSITION, FISCHER_G1_S_CELL_CYCLE). f Disease free survival for prostate cancer patients dependent of the KMT2C mutational status. Frameshift and nonsense mutations were grouped as truncation mutations (wild type KMT2C: n = 724; truncated KMT2C: n = 11). Samples with alterations that were not classified as truncation mutations were excluded from the analysis. Data were retrieved from the ICGC Data Portal and analysed by a log-rank (Mantel-Cox) test. (a-e) Data were derived from the TCGA-PRAD dataset