Abstract
Tumor antigen (TA)-specific monoclonal antibodies (mAb) block oncogenic signaling and can also induce Fc gamma receptor (FcγR)-mediated cytotoxicity. A growing body of experimental and clinical evidence suggests that mAb-induced anti-tumor immunity may play a role in the differential clinical responses that have been described in patients treated with rituximab, trastuzumab, and cetuximab. Indeed, preclinical data has suggested that cellular immunity, mediated by natural killer (NK) or T cells may contribute to cetuximab's clinical activity.
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