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Letters to the Editor
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Figure 3. Daratumumab depletes multiple myeloma cells in patient samples
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as depicted by (A) counts of CD38 CD138 , (B) percent depletions of
CD138+CD38+, and (C) percent depletion of CD27dimCD138+ multiple myelo- ma cells.a Peripheral blood mononuclear cells or bone marrow mononuclear cells from multiple myeloma (MM) patients were obtained from MM patients according to the guidelines of the Ethics Committee of the Discovery Life Sciences (Huntsville, AL, USA) and in compliance with Declaration of Helsinki protocols. Cells were thawed and measured for viability/density, and 200,000 live cells were seeded to assay plates. MM patient cells were treated with daratumumab, isatuximab (ISA) analog, or TAK-079 analog at specified con- centrations in the presence of 10% human complement. After 3 days, MM cell numbers were measured using Precision Count BeadsTM (BioLegend) and by gating on live CD19-CD20–CD138+CD38+ (HuMab; does not compete with tested CD38 monoclonal antibodies). The percent cytotoxicity was deter- mined relative to the corresponding IgG1 control. Complement was present in each experiment. Data are shown as representative experiment at 10 mg/mL treatment. aPeripheral blood mononuclear cells or bone marrow–derived macrophages from MM patients (n=5 donors).
remains to be determined in clinical trials if these in vitro differences lead to differences in clinical benefit.
Michelle Kinder,1 Nizar J. Bahlis,2 Fabio Malavasi,3 Bart de Goeij,4 Alexander Babich,1 Jocelyn Sendecki,1 Joshua Rusbuldt,1 Kevin Bellew,1 Colleen Kane1
and Niels W.C.J. van de Donk5
1Janssen Research & Development, LLC, Spring House, PA, USA; 2University of Calgary, Arnie Charbonneau Cancer Institute, Calgary, Canada; 3Department of Medical Science, University of Turin and Fondazione Ricerca Molinette, Turin, Italy; 4Genmab B.V., Utrecht, the Netherlands and 5Department of Hematology, Amsterdam University Medical Center, Vrije Universiteit Amsterdam, Cancer Center Amsterdam, Amsterdam, the Netherlands
Correspondence: NIELS W.C.J. VAN DE DONK n.vandedonk@amsterdamumc.nl
doi:10.3324/haematol.2020.268656 Received: August 4, 2020.
Accepted: December 21, 2020. Pre-published: January 14, 2021.
Disclosures: MK was an employee of Janssen and owns stock/shares in Johnson & Johnson; NJB received research funding from Celgene, served in a consulting or advisory role for AbbVie, Amgen, Celgene, Janssen, Sanofi, and Takeda, and had travel, accommodations, or other expenses paid or reimbursed by Celgene and Janssen; FM received research support from Janssen, Celgene, Tusk Therapeutics, and Centrose, and served on advisory boards for Centrose, Tusk Therapeutics, Janssen, Takeda, and Sanofi; BdG is an employee of Genmab; JS, JR, and CK are employees of Janssen and own stock/shares in Johnson & Johnson; AB and KB are employees of Janssen; NWCJvdD received research funding from Amgen, Bristol Myers Squibb, Celgene, Janssen, and Novartis, and
served in a consulting or advisory role for Amgen, Bayer, Bristol Myers Squibb, Celgene, Janssen, Novartis, Servier, and Takeda.
Contributions: all authors developed the manuscript, provided final submission approval, and confirmed that the data were accu- rate and complete.
Acknowledgmemts: the authors would like to thank Amy Wong, Amy Axel, and Mi Ta of Oncology at Janssen Research & Development, LLC, for providing additional experimental support.
Funding: the analysis was funded by Janssen Global Services, LLC; editorial and medical writing support were provided by Tara Abraham, PhD, and Grace Wang, PharmD, of MedErgy, and were funded by Janssen Global Services, LLC.
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