Summary

Monoclonal antibodies that target various specific antigens can be used to kill the tumor cells expressing specific antigens, especially in hematologic cancers. Rituximab, one of the commonly used monoclonal antibodies, was suggested to mediate its action mechanism via antibody-dependent cellular cytotoxicity (ADCC),

From: Cancer Drug Discovery and Development: Genomics and Pharmacogenomics in Anticancer Drug Development and Clinical Response Edited by: F. Innocenti, DOI: 10.1007/978-1-60327-088-5.12, © Humana Press, Totowa, NJ

complement-dependent cytotoxicity (CDC), or a direct pro-apoptotic effect. It has been proposed that the inter-individual variation of gene expression is a consequence of single nucleotide polymorphisms (SNPs) and that the response to a monoclonal antibody can be affected by the SNPs in the host genes corresponding to the drug binding to the target cells or the metabolism of the drug.

This chapter reviews the current understanding of the mechanism of action of monoclonal antibodies (especially rituximab), the role of Fcy receptor and Fcy receptor gene polymorphisms, and their impact on treatment outcomes in hematologic malignancies including follicular lymphoma (FL), diffuse large B-cell lymphoma (DLBCL), Waldenstrom's macroglobulinemia (WM), and chronic lymphocytic leukemia (CLL). In addition, we discuss the approaches augmenting its clinical activity, especially focusing on Fcy receptor re-engineered monoclonal antibody

Key Words: Polymorphisms; monoclonal antibody; hematologic malignancies; rituximab

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