Vascular Endothelial Growth Factor and Inhibiting Agents for Cancer Treatment

Vascular endothelial growth factor (VEGF) is a polypeptide manufactured by cells to facilitate angiogenesis (the production of cells to form new blood vessels). The malignant neoplasm (cancer) tumor implications of vascular growth have been of interest to physicians and cancer researchers dating back to the late 1800s, at which time it was first noted that solid tumors were highly vascularized growths that depended on blood for a supply of oxygen and other much needed nutrients. Early, though, unproven theories of the time speculated that if one could inhibit angiogenesis at tumor sites, growth of the mass could be diminished or the tumor could be eliminated altogether. Turn of the twentieth century theories were one thing, but without today's scientific knowledge of the body's biological, cellular, and genetic mechanisms, cancer researchers had little hope of altering them.

In the twenty-first century, scientists know a great deal about VEGF behaviors, in large part because of discoveries made possible by the Human Genome Project, which clearly identified the genetic and cellular origins of various types of VEGF. Cancer researchers, today, have moved beyond an understanding of how VEGF behaviors affect solid tumors; scientists are now concentrating on the development and administration of anti-angiogenesis biological agents designed to reduce the mass of solid tumors by cutting off their blood supply.

Cancer researchers now know that there are a variety of cellular and biological pathways that allow cancer cells to effect increased vascular growth, and each of these routes offer scientists an opportunity to intervene and inhibit these processes. It should be noted that VEGF studies are most commonly associated with breast, colorectal, and lung cancer, and new anti-angiogenesis drug therapies, to date, have concentrated on solid tumors in these patients. One of the first anti-angiogenesis drugs to win FDA approval is Bevacizumab (Avastin), a monoclonal antibody, which is a synthetic analogue that mimics a specific immune system protein. Avastin attaches itself to VEGF molecules and prevents the protein from binding with receptor cells that would inevitably trigger vascular growth at tumor sites.

Working from the other end of the equation, cancer researchers have developed the drugs Sunitinib (Sutent) and Sorafenib (Nexavar), both of which bind directly to VEGF receptor cells, thus interrupting angiogenesis. Additionally, some cancer studies have shown that existing chemotherapeutic agents, when given in very low doses on a continual (IV drip) basis, can also inhibit angiogenesis, though, researchers are still not sure why this is the case.

Problems With VEGF Research

While some scientists believe VEGF inhibition offers some promise in the battle against cancer, other researchers aren't so sure. A recent University of California at San Diego (UCSD) study seems to indicate that VEGF inhibition can actually increase tumor size. In an animal study involving mice, scientists found that VEGF inhibiting agents reduced the production of vascular structures, though, those blood vessels that did grow were far better organized and actually increased blood flow to tumors that increased in size.

UCSD scientists still believe VEGF inhibitors have some value, and they suggest that further studies should include the administration of drugs such as Avastin in combination with other chemotherapies. Perhaps the right combination of novel drug therapies will produce the tumor reduction results that are hoped for.

Sources for information on this page: Scientific American, American Cancer Society

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