Experimental cancer drug shows promise

By WES ALLISON

© St. Petersburg Times, published September 28, 2000

TAMPA -- Scientists have known for years they could kill a cancerous tumor by cutting off its blood supply. The tough question has always been how best to do it.

Now researchers at the Moffitt Cancer Center in Tampa and Yale University report they have developed a drug that stops the growth of human tumors in mice by suppressing the formation of new blood vessels, essentially depriving the tumor of nourishment.

If it works as well in people as it has in mice, the finding could lead to an important new class of drugs to fight solid tumors throughout the body -- from the brain to the lungs to breasts to the pancreas, researchers say.

The findings are published in the October issue of Nature Biotechnology, a sister publication of the British journal Nature.

"We're hoping, and there's no way of knowing until you try it," said Dr. Said Sebti, co-author of the study and director of drug discovery at the Moffitt Cancer Center at the University of South Florida.

"If it does, it would really be big because . . . this is designed to attack a very critical character of the tumor."

The news was welcomed by other leading cancer researchers, although tests in people are at least a year and a half away. Just one in 20 drugs at this stage of development makes it to clinical trials, but Sebti said he thinks this one may have a good chance.

The formation of new blood vessels is called angiogenesis, and many researchers believe that preventing the growth of new vessels -- called anti-angiogenesis -- offers the best hope for beating many common cancers.

Research hospitals and drug companies across the United States have been scrambling to find the best way to do that since Harvard surgeon Dr. Judah Folkman first used it to kill tumors in mice four years ago.

Several anti-angiogenesis drugs are being tested in humans, but Sebti and his partner at Yale, chemist Andrew Hamilton, have taken a different path. Other researchers on Wednesday said that is helpful because it expands the knowledge of how angiogenesis works and may provide another important weapon.

"Based on past history of anti-cancer drugs, you often want to have more than just one," said Dr. Christopher C. Widnell, scientific program director at the American Cancer Center in Atlanta, which funded Folkman's early work on anti-angiogenesis.

"And you want them working by different mechanisms, because that greatly enhances your chance of therapeutic" success.

One of the chemicals vital to building blood vessels in tumors is called platelet derived growth factor, or PDGF. The PDGF works by binding to the surface of existing blood vessel cells, much like Velcro, and encouraging those cells to replicate.

According to the Nature Biotechnology article, this new drug disrupts the interaction of PDGF with blood vessel cells by binding directly to the PDGF. Because the PDGF is tied up by the drug, it cannot bind to the blood vessel cells.

If vessels can't form, the tumor can't grow. And if the tumor can't grow, it will die. Moffitt researchers have tested it in tumors of the brain, lung and pancreas in mice, and believe it should also work with virtually any solid tumor, including those of the breast, ovaries and colon, Sebti said.

The new drug is called GFB-111, short for growth factor binder.

The next step for researchers at Moffitt and Yale is determining whether their GFB-111 is safe to test in humans. It hasn't seemed to hurt the mice, but humans are much more complicated, since the body is more adept at flushing drugs from the body before they have a chance to work.

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