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Study raises safety concerns about experimental cancer approach
Date:1/25/2011

system in the experimental mice. Endothelial cells line blood vessels, allowing them to expand and contract as blood is pumped through the body. For reasons the researchers don't yet understand, endothelial cells in the liver were most affected. Ninety percent of the proliferating liver endothelial cells in the experimental mice had lost the Notch1 signal.

Notch plays many roles in the body, depending on the cellular context. In some instances, Notch can spur tumor growth and in others suppress it. The researchers suspect that loss of the Notch1 signal in the experimental mice releases the brakes on endothelial cell division, allowing the cells to proliferate uncontrollably, particularly in the liver.

Anti-notch compounds now in preclinical and clinical trials include gamma secretase inhibitors, originally developed to treat Alzheimer's disease. These drugs block an enzyme all Notch receptors rely on. Other drugs in the pipeline are called DLL4 antibodies, which also disrupt Notch signaling and blood vessel formation. Anti-Notch1 antibodies are also being developed.

Kopan, however, says he is not optimistic about the prospects for any of them.

"The therapeutic window for any kind of anti-Notch1 therapy that's the dosage of a drug that is both safe and effective is extremely small, perhaps even nonexistent, for these compounds in their current form," he says. "We need to do additional research to try to find out how we can open that window."


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Contact: Caroline Arbanas
arbanasc@wustl.edu
314-286-0109
Washington University School of Medicine
Source:Eurekalert  

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