Fig. 3: Mutational signature of EBV+ DLBCL (NOS). | Blood Cancer Journal

Fig. 3: Mutational signature of EBV+ DLBCL (NOS).

From: Genomic insights into the pathogenesis of Epstein–Barr virus-associated diffuse large B-cell lymphoma by whole-genome and targeted amplicon sequencing

Fig. 3

Panel (A) depicts an oncoplot of all genes harboring mutations in at least two samples of our discovery WGS cohort. Panel (B) illustrates the mutational landscape in our discovery and extension cohort of EBV + DLBCL (NOS) by tNGS. Mutations in ANKRD11 were identified as indicators of superior relapse-free but not overall survival (C). Moreover, distinct molecular subtypes exhibiting combined alterations of ARID1A and DAPK1 are shown to exhibit inferior overall survival (D). The corresponding endpoint analysis for (C) and (D) (overall survival for ANKRD11 mutation status and progression-free survival for our combined mutation set of ARID1A and DAPK1) is provided in Supplementary Fig. 7. For information on outcome according to these two mutational markers in the subset of R-CHOP treated patients, please see Supplementary Fig. 8. Further, we found mutations in both KMT2D as well as NOTCH2 to be significantly enriched in 6q wild-type patients (E). Lollipop plots illustrating the localized distribution of mutational patterns affecting ARID1A, KMT2A, ANKRD11, and NOTCH2 in our combined cohorts; green dots refer to missense mutations; gray to truncating mutations (F–I).

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