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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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CLINICAL TRIALS AND OBSERVATIONS

Brief Report

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 Zhou1, Raymond L. Comenzo2,3, Adam B. Olshen4, Ezio Bonvini5, Scott Koenig5, Peter G. Maslak2,3, Martin Fleisher3, James Hoffman2, Suresh Jhanwar1,3, James W. Young2, Stephen D. Nimer1,3, and Adam M. Boruchov2

1 Sloan-Kettering Institute; 2 Division of Hematologic Oncology, Department of Medicine; 3 Department of Clinical Laboratories; 4 Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center (MSKCC), New York, NY; and 5 MacroGenics, Rockville, MD

Despite advances in therapy, many patients with systemic light-chain amyloidosis (AL) die within 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. Reverse-transcriptase polymerase chain reaction (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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