Kankermedicijnen die tumoren doen groeien*
Uit verschillende studies blijkt dat agioneseremmers zoals Avastin de groei van kankercellen en uitzaaiingen kunnen bevorderen. Avastin is een antilichaamtherapie en is specifiek gericht tegen de groeifactor VEGF. Door aan VEGF te binden is de tumor niet meer in staat nieuwe bloedvaten aan te maken en blijft de tumor verstoken van voeding en zuurstof. Het was al langer duidelijk dat Avastin niet het veelbelovende medicijn tegen kanker is ondanks de grote promotiecampagnes. Uit een studie blijk dat agioneseremmers afhankelijk van de hoeveelheid tumorgroei doen stoppen of versnellen. Uit andere studies blijkt ook nog eens dat angiogenese remmers waaronder dus Avastin de agressiviteit van de kankercel stimuleert en ook uitzaaiingen stimuleert. Waarschijnlijk aldus de onderzoekers in hun verklaring, omdat de kankercellen zich teweer stellen tegen de zuurstof- en voedingsblokkering van de bloedvaten om de tumorcel heen en als het ware vluchten naar ander weefsel, zelfs andere organen op afstand.
Cancer drugs 'speed tumour growth'
A cancer treatment that starves tumours of blood can sometimes make the disease worse, research has shown.
Drugs called angiogenesis inhibitors prevent the growth of blood vessels that supply tumours with oxygen and nutrients.
Some of the medicines have already been marketed after proving their effectiveness in clinical trials. Examples include the kidney cancer drug Sutent and Avastin, used to treat bowel, breast and lung cancer.
But new research suggests certain angiogenesis inhibitors may actually promote the growth of tumours.
Scientists made the discovery after studying cilengitide, an experimental angiogenesis inhibitor which has not yet been licensed for patients. The findings appear in the journal Nature Medicine.
Dr Andy Reynolds, from the Breakthrough Breast Cancer Research Centre at the Institute of Cancer Research in London, said: "Our study revealed a previously unknown mechanism through which drugs such as cilengitide behave. It showed that while higher concentrations of cilengitide can block angiogenesis, lower concentrations can actually stimulate the supply of blood to the tumour and can promote its growth.
"These results may explain why initial results from early stage clinical trials have not been as promising as hoped.
"Knowledge of this mechanism will help us develop new ways to make these drugs as effective as possible. In the future, we may be able to combine these inhibitors with other drugs to maximise their effectiveness for patients."
Dr Lesley Walker, director of cancer information at Cancer Research UK, said: "Drugs redirect the body's complex signalling systems. Sometimes very subtle alterations to the way a drug is administered, or subtle changes to a drug's structure, can have a huge impact on its effectiveness.
"This study is important because it may help to explain the mixed results previously seen in patients and turn around disappointing results so people may still benefit from the drug without the potential harm."
Silencing or Fueling Metastasis with VEGF Inhibitors: Antiangiogenesis Revisited
Sonja Loges1, 2, Massimiliano Mazzone1, 2, Philipp Hohensinner1, 2 and Peter Carmeliet1, 2, ,
1Vesalius Research Center, VIB, B-3000 Leuven, Belgium
2Vesalius Research Center, KU Leuven, B-3000 Leuven, Belgium
Clinical practice reveals that therapy with angiogenesis inhibitors often does not prolong survival of cancer patients for more than months, because tumors elicit evasive resistance. In this issue of Cancer Cell, two papers report that VEGF inhibitors reduce primary tumor growth but promote tumor invasiveness and metastasis. These perplexing findings help to explain resistance to these drugs but raise pertinent questions of how to best treat cancer patients with antiangiogenic medicine in the future. We discuss here how VEGF inhibitors can induce such divergent effects on primary tumor growth and metastasis.
Refers to: Accelerated Metastasis after Short-Term Treatment with a Potent Inhibitor of Tumor AngiogenesisCancer Cell, Volume 15, Issue 3, 3 March 2009, Pages 232-239, John M.L. Ebos, Christina R. Lee, William Cruz-Munoz, Georg A. Bjarnason, James G. Christensen, Robert S. Kerbel PDF (1036 K) | Supplementary Content
Refers to: Antiangiogenic Therapy Elicits Malignant Progression of Tumors to Increased Local Invasion and Distant MetastasisCancer Cell, Volume 15, Issue 3, 3 March 2009, Pages 220-231, Marta Pāez-Ribes, Elizabeth Allen, James Hudock, Takaaki Takeda, Hiroaki Okuyama, Francesc Viņals, Masahiro Inoue, Gabriele Bergers, Douglas Hanahan, Oriol Casanovas PDF (2341 K) | Supplementary Content
(April
2009)
