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Open Access Highly Accessed Review

A critical review of the role of Fc gamma receptor polymorphisms in the response to monoclonal antibodies in cancer

James D Mellor1238*, Michael P Brown4, Helen R Irving2, John R Zalcberg56 and Alexander Dobrovic367

Author Affiliations

1 Pharmacy Department, Peter MacCallum Cancer Centre, St Andrew’s Place, East Melbourne, Victoria, 3002, Australia

2 Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, 3052, Australia

3 Molecular Pathology Research and Development Laboratory, Peter MacCallum Cancer Centre, St Andrew’s Place, East Melbourne, Victoria, 3002, Australia

4 Cancer Clinical Trials Unit, Royal Adelaide Hospital, North Terrace, Adelaide, South Australia, 5000, Australia

5 Division of Cancer Medicine, Peter MacCallum Cancer Centre, St Andrew’s Place, East Melbourne, Victoria, 3002, Australia

6 Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, Victoria, 3010, Australia

7 Department of Pathology, University of Melbourne, Parkville, Victoria, 3010, Australia

8 Pharmacy Department, Peter MacCallum Cancer Centre, Locked Bag 1, A’Beckett Street, East Melbourne, Victoria, 8006, Australia

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Journal of Hematology & Oncology 2013, 6:1  doi:10.1186/1756-8722-6-1

Published: 4 January 2013

Abstract

Antibody-dependent cellular cytotoxicity (ADCC) is a major mechanism of action of therapeutic monoclonal antibodies (mAbs) such as cetuximab, rituximab and trastuzumab. Fc gamma receptors (FcgR) on human white blood cells are an integral part of the ADCC pathway. Differential response to therapeutic mAbs has been reported to correlate with specific polymorphisms in two of these genes: FCGR2A (H131R) and FCGR3A (V158F). These polymorphisms are associated with differential affinity of the receptors for mAbs. This review critically examines the current evidence for genotyping the corresponding single nucleotide polymorphisms (SNPs) to predict response to mAbs in patients with cancer.

Keywords:
FCGR2A; FCGR3A; trastuzumab; rituximab; cetuximab; ADCC