Recently, the field of oncology has witnessed the introduction of several
effective chemotherapeutic agents. Still, not all cancers respond to the use of
conventional chemotherapy and thus combination therapy is an emerging weapon in the
battle against cancer. There is emerging evidence in support of the use of Monoclonal
antibodies (MoAbs) in cancer therapy. The mechanisms behind their efficacy are multifaceted;
they can kill tumor cells through antibody-dependent cell-mediated cytotoxicity
(ADCC), complement-dependent cytotoxicity (CDC), and apoptosis as well as target
ligands or growth factor receptors favoring tumor growth. The interaction of the Fc
domains of antibodies with the Fcγ (gamma) receptors is an essential prerequisite for
biological response to antibodies, including ADCC. This interaction is strongly
regulated and is largely dependent upon receptor conformation and number. It is
accepted that germ-line single nucleotide polymorphisms (SNPs) and copy number
variations (CNVs) have the potential to predict the outcome of therapy. The possibility
of predicting patients response to monoclonal antibody therapy is of particular
importance, as response rates are moderate, with the risk of serious side effects all at a
high financial cost. This patent chapter provides an insight into the role of Fcγ receptors
(FcγRs) genetic variation in Monoclonal Antibody-based anti-cancer therapy.
Keywords: ADCC, Alemtuzumab, Bevacizumab, cancer, Cetuximab,
chemotherapeutic agents, copy number variations, drug responses, drug toxicity,
engineered antibodies, Fc gamma receptors, genetic polymorphism, monoclonal
antibody-based therapy, Ofatumumab, oncology, personalized medicine,
pharmacogenomics, single nucleotide polymorphism, Rituximab, Trastuzumab.
