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. Author manuscript; available in PMC: 2021 Feb 3.
Published in final edited form as: JCO Precis Oncol. 2021 Jan 12;5:145–152. doi: 10.1200/PO.20.00360

Figure 2.

Figure 2

Summary of whole exome sequencing of samples taken from three different timepoints; diagnosis, prior to BCR-targeted therapy and at the time of relapse. Mutations and copy number changes are indicated within each cell. Grey indicates no mutation/copy number change identified. (B) A simplified schematic showing the critical signaling components of the BCR pathway that converge onto activation of canonical NFKB. Components targeted pharmacologically in this patient are indicated. Created with BioRender.com. (C) Sanger sequencing from samples at the indicated timepoints confirm the acquisition of an A to C mutation in CARD11, which results in the activating, coiled-coil domain K215T mutation. (D) Ibrutinib sensitivity assay in the ABC DLBCL line U2932 transduced with either empty vector or CARD11 WT or K215T. Data show mean and SEM of 5 independent experiments.