A protein that triggers the growth of blood vessels appears to play a key role in the development of Kaposi's sarcoma. The discovery, published in the tomorrow of the Proceedings of the National Academy of Sciences, may lead to better treatments for the disfiguring and potentially fatal cancer that strikes nearly a third of AIDS patients.
pathologist Parkash Gill and his colleagues at the University of Southern California School of Medicine had suspected that vascular endothelial growth factor (VEGF), a protein that regulates the permeability of blood vessels and stimulate growth, could be involved in Kaposi's sarcoma, because tumors - that appear as purple spots on the skin - twisted masses of disorganized blood vessels and capillaries that leak. The team found that the Kaposi sarcoma cells indeed produce scads of VEGF. They also noted that tumor cells with elevated levels of two receptor proteins that bind to VEGF, whereas the skin cells from the adjacent unaffected areas had no receptors.
Gill group next tried to block VEGF with the hope of preventing tumor growth. They injected with antisense DNA - a mirror image so of the DNA segment in the gene encoding the VEGF protein - into mice with tumors. The antisense DNA can bind to the cell an RNA template for the protein, thus strangling its production. The treatment seems to work :. Tumors in mice that received the antisense DNA has not increased as rapidly as those mice that received random DNA fragments
"If it holds up that VEGF is an very central player "in Kaposi sarcoma, said Harvard University cell biologist Judah Folkman, it may open multiple avenues of treatment. Although the initial antisense DNA tests were promising, Gill said compounds that block VEGF receptors can also be a weapon against cancer, which can kill patients when tumors invade the lungs or other organs.
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