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      Anti-CD47 antibody synergizes with rituximab to promote phagocytosis and eradicate non-Hodgkin lymphoma.

      Cell
      Animals, Antibodies, Monoclonal, immunology, therapeutic use, Antibodies, Monoclonal, Murine-Derived, Antigens, CD47, B-Lymphocytes, Cell Line, Tumor, Humans, Lymphoma, Non-Hodgkin, diagnosis, therapy, Mice, Phagocytosis, Receptors, Fc, Xenograft Model Antitumor Assays

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          Abstract

          Monoclonal antibodies are standard therapeutics for several cancers including the anti-CD20 antibody rituximab for B cell non-Hodgkin lymphoma (NHL). Rituximab and other antibodies are not curative and must be combined with cytotoxic chemotherapy for clinical benefit. Here we report the eradication of human NHL solely with a monoclonal antibody therapy combining rituximab with a blocking anti-CD47 antibody. We identified increased expression of CD47 on human NHL cells and determined that higher CD47 expression independently predicted adverse clinical outcomes in multiple NHL subtypes. Blocking anti-CD47 antibodies preferentially enabled phagocytosis of NHL cells and synergized with rituximab. Treatment of human NHL-engrafted mice with anti-CD47 antibody reduced lymphoma burden and improved survival, while combination treatment with rituximab led to elimination of lymphoma and cure. These antibodies synergized through a mechanism combining Fc receptor (FcR)-dependent and FcR-independent stimulation of phagocytosis that might be applicable to many other cancers. Copyright 2010 Elsevier Inc. All rights reserved.

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