A 'Trojan Horse' Assault on Cancer

New technology destroys blood vessels that feed tumors

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TUESDAY, June 11, 2002 (HealthDayNews) -- A new type of technology that uses a "Trojan horse" approach to selectively destroy blood vessels supplying malignant cancer tumors has been developed by Texas researchers.

Researchers at M.D. Anderson Cancer Center in Houston and Southwestern Medical Center at Dallas jointly demonstrated that a new drug formed by linking a vascular endothelial growth factor (VEGF) to a toxin will target and destroy blood vessels that feed a malignant tumor, says a report in today's issue of the Proceedings of the National Academy of Sciences journal.

In effect, the tumor starves after its blood supply is cut off, the researchers say. Blood vessels in healthy tissue are not affected.

VEGF is a substance made by cells that stimulates growth of new blood vessels. Tumors use it to grow the blood vessels that keep them nourished.

For this study, mice were injected with human melanoma and human prostate cancer cells. Some of those mice received VEGF combined with a genetically engineered toxin called gelonin. The combination is called VEGF/rGel, the researchers say.

Tumor growth in the mice that received VEGF/rGel was reduced to 16 percent of that of untreated mice, the study says. Destruction of tumor blood vessels was observed as early as 48 hours after the mice were given VEGF/rGel. There was no visible damage in any healthy organs, including the kidneys, of the treated mice.

These results suggest that VEGF/rGel has potential as an anti-tumor treatment for human cancer patients, the researchers say. A clinical trial to test the technology in humans is expected to begin within a year.

Therapies that attack tumor blood vessels are a focus of current cancer research because these treatments avoid the major problem associated with chemotherapy -- the tumor cells' ability to mutate and develop resistance to chemotherapy drugs, the researchers say.

More information

To learn more about blood vessels and their role in cancer, visit The Angiogenesis Foundation.

SOURCE: University of Texas, news release, June 10, 2002

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