Brentuximab-vedotin induces apoptosis in neoplastic MCs. (A) HMC-1 cells, MCPV-1.1 cells, MCPV-1.4 cells, and C2 cells were incubated in control medium or in medium containing brentuximab-vedotin (2.5-10 µg/mL) at 37°C for 96 hours. Cells were then stained for Annexin V and PI (left panel) or active caspase-3 (right panel) by flow cytometry. Apoptosis was evaluated in CD30⁺ MCPV-1.1 cells (black bars), CD30⁺ C2 cells (light gray bars), CD30^+/− HMC-1.1 cells (gray bars), CD30⁻ HMC-1.2 cells (open bars), and CD30⁻ MCPV-1.4 cells (dark gray bars). Results are expressed as percentage of positive cells and represent the mean ± SD from 3 independent experiments. *P < .05. (B) Primary BM cells obtained from 3 patients with CD30⁺ SM (ASM, n = 2; MCL, n = 1) and 3 patients with CD30⁻ SM (ISM-AHNMD, n = 2; MCL, n = 1) were incubated in control medium or brentuximab-vedotin (2.5-10 µg/mL) at 37°C for 96 hours. (Left panel) Cells were stained with a mAb against CD117 for MC detection, and for Annexin V. (Right panel) Cells were stained with a mAb against CD117 and a mAb against active caspase-3. Apoptosis was analyzed in CD30⁺ MCs (black bars) and in CD30⁻ MCs (gray bars). Results are expressed as percentage of DAPI⁺/KIT⁺ cells (left panel) or as the percentage of KIT⁺ cells (right panel) and represent the mean ± SD from 3 independent experiments in each group of patients. *P < .05 compared with control.