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British Journal of Cancer (2006) 94, 1217–1220. doi:10.1038/sj.bjc.6603025 www.bjcancer.com
Published online 28 February 2006

The place of VEGF inhibition in the current management of renal cell carcinoma

P Nathan1, D Chao2, C Brock3, P Savage3, M Harries4, M Gore5 and T Eisen5 for the London Biological and Targeted Therapy Group

  1. 1Mount Vernon Cancer Centre, Rickmansworth Road, Northwood, Middlesex, HA6 2RN, UK
  2. 2Royal Free Hospital, Pond Street, London, NW3 2QG, UK
  3. 3Charing Cross Hospital, Fulham Palace Road, London, W6 8RF, UK
  4. 4Guy's and St. Thomas' Hospital, St. Thomas Street, London, SE1 9RT, UK
  5. 5Royal Marsden Hospital, Fulham Road, London, SW3 6JJ, UK

Correspondence: Dr P Nathan, E-mail: p.nathan@nhs.net

Received 30 November 2005; Revised 31 January 2006; Accepted 1 February 2006; Published online 28 February 2006.

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Abstract

Vascular endothelial growth factor (VEGF) is overexpressed in around 80% of patients with clear cell carcinoma of the kidney owing to the inactivation of von Hippel Lindau gene activity. VEGF stimulates angiogenesis and acts as an autocrine growth factor. A number of different agents are now available which target VEGF and its signalling pathways. A significant body of evidence has accumulated demonstrating that antagonism of VEGF and its downstream pathways is clinically useful in a significant proportion of patients with metastatic clear cell carcinoma of the kidney. Enough data is now available to recommend that patients with metastatic clear cell carcinoma of the kidney should at some point during the course of their disease be offered entry into a clinical trial enabling exposure to a targeted inhibitor of VEGF or its signalling pathways. Assuming early clinical trial data is substantiated by ongoing registration studies, efforts should be made to minimise the time taken between licensing and general availability of these active agents.

Keywords:

renal cell carcinoma, VEGF, vascular endothelial growth factor, sorafenib, sunitinib

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