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 Blood, 1 April 2008, Vol. 111, No. 7, pp. 3403-3406.
Prepublished online as a Blood First Edition Paper on January 23, 2008; DOI 10.1182/blood-2007-11-125526.

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Submitted November 27, 2007
Accepted January 15, 2008

CD32B is highly expressed on clonal plasma cells from patients with systemic light-chain amyloidosis and provides a target for monoclonal antibody-based therapy

Ping Zhou, Raymond L Comenzo*, Adam B Olshen, Ezio Bonvini, Scott Koenig, Peter G Maslak, Martin Fleisher, James Hoffman, Suresh Jhanwar, James W. Young, Stephen D Nimer, and Adam M Boruchov

Department of Medicine, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY, United States
Division of Hematologic Oncology, Memorial Sloan-Kettering Cancer Center, New York, NY, United States
Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY, United States
MacroGenics Inc., Rockville, MD, United States
Department of Clinical Laboratories, Memorial Sloan-Kettering Cancer Center, New York, NY, United States

* Corresponding author; email: comenzor{at}mskcc.org.

Despite advances in therapy, many patients with systemic light-chain amyloidosis (AL) die less than 3 years from diagnosis. The humanized 2B6 monoclonal antibody (MoAb) is specific for the low-affinity IgG Fc-receptor CD32B and effective in a human CD32B+ B-cell lymphoma murine xenograft model. Because MoAb therapy could improve outcomes in AL, we studied CD32B expression by clonal plasma cells obtained from 48 patients with AL. Transcript profiling showed that expression of CD32B was significantly higher than expression of all other Fc-receptor family members. RT-PCR using double-enriched CD138+ plasma cells showed uniform expression of the stable cell-surface CD32B1 isoform at diagnosis and relapse, and flow cytometry showed intense CD32B cell-surface staining on 99% of CD138+ plasma cells at diagnosis and relapse. These data provide a rationale for the novel therapeutic targeting of CD32B using the humanized 2B6 MoAb in patients with systemic AL-amyloidosis.


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