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NCI Researchers Discover Genes That Are Turned on at High Levels in,Tumor-associated Blood Vessels of Mice and Humans

BETHESDA, Md., June 11, 2007--A team of researchers at the National Cancer Institute (NCI), part of the National Institutes of Health (NIH), has uncovered a set of genes that are turned on, or expressed, at high levels only in the blood vessels that feed tumors in mice and humans. These genes, and the proteins they encode, are important new potential targets for novel drugs that could selectively cut off a tumor's blood supply without affecting the blood vessels of healthy tissues, overcoming one of the major concerns of current anticancer therapies targeted at blood vessel growth. The findings are published in the June 2007 issue of the journal "Cancer Cell".

"These results offer new insights into what is an important aspect of tumor development," said NCI Director John E. Niederhuber, M.D. "How blood vessels grow, intertwined with normal tissue in a tumor's microenvironment, is not just an area of scientific interest; it's a research field that is continuing to develop potentially potent and specific anticancer agents that cut off the tumor from a vital support system."

The growth of blood vessels, a process known as angiogenesis, is a normal process in the body that is essential for organ growth and repair. In many diseases, including most forms of cancer, this carefully regulated process becomes imbalanced, and normal blood vessel growth is redirected toward supplying nutrients and oxygen to feed diseased tissue, destroy normal tissues, and in the case of cancer, allow tumor cells to escape and travel to distant sites in the body. Researchers have tried to stop disease-related angiogenesis by identifying the molecules that stimulate blood vessel and developing new drugs to block their action. However, blocking angiogenesis requires a delicate balance between tumor and normal cells as most angiogenesis-related molecules are also critical for normal blood vessel growth in the body -- for example
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