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Therapeutic IgG cytotoxicity requires activation FcR

The anti-CD20 antibody, rituximab, approved for the treatment of non-Hodgkins lymphoma, requires activation FcRs to mediate its anti-tumor effect. Mice bearing human B cell lymphomas were successfully able to arrest tumor growth in response to rituximab treatment if they expressed activation FcRs. Deletion of the activation subunit of the FcRs, the g chain, abrogated the therapeutic efficacy of this anti-tumor antibody. Similar results have been observed with the anti-Her2neu antibody Herceptin and a wide variety of anti-tumor antibodies now in clinical development, demonstrating the dominance of FcR mediated cytotoxicity to the mechanism of action of these therapeutics.

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