Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Angiogenesis, the formation of new blood vessels from existing vasculature, plays an essential role in tumour growth, invasion and metastasis. Vascular endothelial growth factor (VEGF) is one of the key factors responsible for its regulation. High expression of VEGF has been observed in many cancers, and is associated with worse survival. When antiangiogenic agents are used alone they typically initially cause reduction in blood flow or vascular permeability, in many types of cancer. In some cases tumour regression occurs, mainly in renal cancer. In combination with chemotherapy, progression-free survival is often prolonged, but overall survival is not. Many tumours fail to respond initially - de novo resistance. Others develop resistance over time, with progression after a few months of treatment. The mechanisms of resistance are not well understood. The theoretical benefits of VEGF inhibitors are more likely to be realised by understanding these mechanisms and modifying therapy accordingly. This article reviews current knowledge on resistance mechanisms and the therapeutic implications.

Original publication




Journal article


Eur J Cancer

Publication Date





1323 - 1332


Angiogenesis Inhibitors, Cell Hypoxia, Disease Progression, Disease-Free Survival, Drug Resistance, Neoplasm, Growth Hormone, Humans, Neoplasms, Neovascularization, Pathologic, Placental Hormones, Vascular Endothelial Growth Factor A