HCK transcription is driven by mutated MYD88. (A) HCK transcript levels in MYD88-mutated WM (BCWM.1 and MWCL-1) and ABC DLBCL (TMD-8, HBL-1, OCI-Ly3, and SU-DHL2) cells, and MYD88 WT (OCI-Ly7 and OCI-Ly19 GCB DLBCL, Ramos Burkitt, MM1.S, and RPMI-8226 myeloma) cells by qRT-PCR. (B) HCK transcription using TaqMan Gene Expression Assay in primary LPCs (CD19⁺) from MYD88 L265P expressing WM patients, and HD-derived nonmemory (CD19⁺CD27⁻) and memory (CD19⁺CD27⁺) B cells. P < .01 for comparison of WM LPC vs either HD non-memory or memory B-cells. The number of healthy donors that were evaluated for nonmemory (open circles) and memory (open triangles) B cells, as well as the number of WM patients that were evaluated for LPC (open diamonds) are shown. (C) Fold change in HCK transcription following lentiviral transduction with vector control, Flag-tagged MYD88 L265P or MYD88 WT protein in cell lines expressing mutated or WT MYD88. At the bottom of (C), total Flag-tagged MYD88 L265P or WT protein levels are shown for all transduced cell lines to demonstrate relative translation efficiency for MYD88 L265P and WT vectors, as well as GAPDH protein levels as protein loading controls.