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Blood, 15 July 2006, Vol. 108, No. 2, pp. 705-710.
Prepublished online as a Blood First Edition Paper on March 21, 2006; DOI 10.1182/blood-2005-11-4607.
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NEOPLASIA
Effective therapy for a murine model of human anaplastic large-cell lymphoma with the anti-CD30 monoclonal antibody, HeFi-1, does not require activating Fc receptors
Meili Zhang,
Zhengsheng Yao,
Zhuo Zhang,
Kayhan Garmestani,
Carolyn K. Goldman,
Jeffrey V. Ravetch,
John Janik,
Martin W. Brechbiel, and
Thomas A. Waldmann
From the Metabolism Branch, Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD; and the Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, NY.
CD30 is a member of the tumor necrosis factor receptor family. Overexpression of CD30 on some neoplasms versus its limited expression on normal tissues makes this receptor a promising target for antibody-based therapy. Anaplastic large-cell lymphoma (ALCL) represents a heterogeneous group of aggressive non-Hodgkin lymphomas characterized by the strong expression of CD30. We investigated the therapeutic efficacy of HeFi-1, a mouse IgG1 monoclonal antibody, which recognizes the ligand-binding site on CD30, and humanized anti-Tac antibody (daclizumab), which recognizes CD25, in a murine model of human ALCL. The ALCL model was established by intravenous injection of karpas299 cells into nonobese diabetic/severe combined immuno-deficient (SCID/NOD) wild-type or SCID/NOD Fc receptor common  chain–deficient (FcR–/–) mice. HeFi-1, given at a dose of 100 µg weekly for 4 weeks, significantly prolonged survival of the ALCL-bearing SCID/NOD wild-type and SCID/NOD FcR–/– mice (P < .01) as compared with the control groups. In vitro studies showed that HeFi-1 inhibited the proliferation of karpas299 cells, whereas daclizumab did not inhibit cell proliferation. We demonstrated that the expression of FcR on polymorphonuclear leukocytes and monocytes was not required for HeFi-1–mediated tumor growth inhibition in vivo, although it was required for daclizumab.
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