SUNDAY, Sept. 15 (HealthDay News) -- The cancer drug Zaltrap (aflibercept) could help treat diabetes, suggest findings from research using mice.
Scientists say they've identified a molecular pathway (a series of interactions among proteins) involved in the development of diabetes, and also found that the drug can regulate this pathway.
Zaltrap is approved in the United States to treat metastatic (spreading) colorectal cancer and the wet form of the eye disease macular degeneration. The drug inhibits the vascular endothelial growth factor (VEGF) pathway, thereby blocking the growth of blood vessels into tumors and starving them of oxygen.
The researchers, from the Stanford University School of Medicine, identified a series of proteins that link VEGF inhibitors and blood glucose levels.
"We were surprised to find that this drug currently used in patients for cancer treatment had beneficial effects on diabetes in laboratory mice and could, potentially, in humans," Dr. Calvin Kuo, a professor of medicine, said in a university news release.
Scientists caution, however, that research with animals often fails to provide similar results in humans.
"Proteins involved in this pathway could be targeted for the development of new diabetes therapies," Amato Giaccia, a professor of cancer biology and director of radiation oncology, said in the news release.
The findings appeared online Sept. 15 in two articles in the journal Nature Medicine.
The researchers said there have been indications that VEGF inhibitors such as Zaltrap could influence blood glucose levels in people, but no human studies have been conducted.
"Anecdotally, there have been reports that diabetic patients who have been prescribed VEGF inhibitors to treat their cancer are better able to control their diabetes," Kuo said.
Three co-authors of Kuo's study are employees at Regeneron Pharmaceuticals, which makes aflibercept.
The U.S. National Institute of Diabetes and Digestive and Kidney Diseases has more about diabetes.
SOURCE: Stanford University School of Medicine, news release, Sept. 15, 2013
-- Robert Preidt
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