Dopamine prevents tumors from gaining a blood supply, studies suggest
SATURDAY, March 15 (HealthDay News) -- The drug dopamine -- currently used to treat patients with conditions such as Parkinson's disease, pituitary tumors and heart attack -- may also prove effective in cancer patients, a Mayo Clinic study finds.
In laboratory and mouse tests, researchers found dopamine can help prevent the development of new blood vessels, something that would slow the progression of cancer. The findings were published in the online edition of the Journal of Clinical Investigation.
"Researchers can now test this concept in solid tumors where angiogenesis (formation of new blood vessels) plays a critical role in the growth and progression of these cancers," Dr. Sujit Basu, a Mayo Clinic oncologist, said in a prepared statement.
Specifically, Basu and colleagues found that dopamine prevents the transfer of endothelial progenitor cells (which help form new blood vessels) from bone marrow into the circulatory system. The drug does this by binding to a specific receptor on the surface of the progenitor cells. This suppresses the activity of an enzyme (MMP-9) that enables the progenitor cells to move out of bone marrow.
In their experiments, the researchers found that dopamine significantly decreased movement of progenitor cells from bone marrow and decreased MMP-9 expression.
"Sometimes new drugs may not be the answer. We looked instead at a novel use for an established product, and have found very promising results," Basu said.
Natural dopamine is a neurotransmitter in the brain that regulates movement and affects behavior. The drug is a synthetic form of the natural brain chemical.
"This is the first time it has been shown that an important neurotransmitter like dopamine is regulating the mobilization of these progenitor cells from the bone marrow. This is very important, and represents why these findings are so unique," Basu said.
The U.S. National Cancer Institute has more about angiogenesis.
-- Robert Preidt
SOURCE: Mayo Clinic, news release, March 13, 2008
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