Abstract
Even though treatment of several types of solid tumours has improved in the past few years with the introduction of the monoclonal antibodies against epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF), response rates to these targeted therapies are modest. Pharmacogenetic factors have the potential to select patients with higher chance of response to agents that target these pathways. This review provides an overview over germ-line variations in genes that are potentially involved in the pharmacodynamics of the monoclonal antibodies cetuximab, panitumumab and bevacizumab, and which may underlie variable anti-tumour response.