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New blood vessels are generally beneficial to our bodies. They help our wounds heal, and they help our babies develop.
But new blood vessels can also help turn a small, harmless group of cancerous cells into a malignant tumor. Experiments have shown that if you block blood vessel formation, specifically by inhibiting a protein called VEGF, you can block the growth of tumors. But VEGF is only one of the proteins involved in forming new blood vessels.
Now a team of Carolina researchers at the Lineberger Comprehensive Cancer Center has identified 55 more proteins involved in blood vessel formation in breast cancer tumors. They hope that further research will help identify which, if any, of these proteins could become targets for new cancer drugs.
The team, led by Nancy Klauber-DeMore, associate professor of surgery, examined vascular cells from both cancerous and normal breast tissues. When researchers looked at the genetic activity in these tissues, they found 55 genes that created either proteins or RNA at much higher rates than did the genes in the normal cells.
Then the team found that seven of those genes encode proteins that either sit on the surface of the vascular cell or get secreted from it, making them relatively easy targets for drug development.
Next, Klauber-DeMore and the Lineberger team will attempt to figure out which, if any, of these proteins actually trigger blood vessel formation. This work, which is now being conducted through Carolina’s University Cancer Research Fund, can then help in the development of new drugs to block blood vessel formation in tumors. (The University Cancer Research Fund, approved by the North Carolina General Assembly last year, will provide $50 million a year toward the prevention, diagnosis and treatment of cancer.)
A report of the study appeared in the American Journal of Pathology. Funding for the study came from the National Cancer Institute, the Department of Defense, the American Society of Surgical Oncology, the Breast Cancer Research Foundation and the Sidney Kimmel Foundation.
Provided by Research and Economic Development
Editor: Neil Caudle
Writer: Jason Smith