Abstract
Tumor reactive monoclonal antibodies (mAb) have been developed and tested as anti-tumor therapy. Some mAb have shown efficacy and are now approved as clinical cancer therapy. The mechanism of action for the antitumor effect includes tumor cell destruction by effector cells with Fc receptors such as natural killer (NK) cells and macrophages. These cells recognize the mAb binding to the tumor cells and mediate antibody-dependent cellular cytotoxicity (ADCC). Enhanced ADCC is mediated by effector cells that have been activated by exposure to the cytokine IL-2 (1). Thus, in murine models, enhanced tumor destruction is produced when tumor bearing animals are treated with a combination of antitumor mAb and IL-2 (2). Clinical testing of mAb and IL-2 is underway.
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References
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Hank, J.A., Surfus, J.E., Gan, J., Ostendorf, A., Gillies, S.D., Sondel, P.M. (2003). Determination of Peak Serum Levels and Immune Response to the Humanized Anti-Ganglioside Antibody-Interleukin-2 Immunocytokine. In: Buolamwini, J.K., Adjei, A.A. (eds) Novel Anticancer Drug Protocols. Methods in Molecular Medicine, vol 85. Humana Press. https://doi.org/10.1385/1-59259-380-1:123
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DOI: https://doi.org/10.1385/1-59259-380-1:123
Publisher Name: Humana Press
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