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| From OncoLog,
June 2004, Vol. 49, No. 6 |
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  Understanding Angiogenesis
The human body has a remarkable ability to repair itself. It has countless mechanisms to fight viruses and bacteria, to recover from infections and fevers, and to heal cuts and punctures, but one mechanism we seldom think about is angiogenesis, or the body’s ability to grow new blood vessels.
All tissues need blood
All of the tissues of the body—including skin, cartilage, and bone—must have a constant supply of blood, which provides oxygen and nutrients essential to survival. Any time, from conception until death, that blood vessels are damaged, special proteins and molecules called growth factors go to work at the site of the damage to promote the development of new blood vessels.
Ironically, angiogenesis, which is essential to life itself, has become a primary target in the fight against cancer. Tumors also need a reliable blood supply to survive, and the same angiogenic factors that help maintain vital tissues also help maintain cancerous tissues.
Understanding the process
Scientists have been working for years to understand the mechanisms that control angiogenesis. They have discovered that both healthy tissues and tumors naturally produce proteins and molecules that either promote or inhibit angiogenesis. Experiments on mice have been performed to determine whether angiogenesis is triggered by the tumor itself or by the surrounding host tissue. The findings proved that tumors initiate angiogenesis by releasing growth factors into the surrounding tissue, in a sense ordering the tissue to start making blood vessels. For a tumor to grow, it must release more angiogenesis-promoting factors than inhibiting factors into the surrounding tissue.
The fact that tumors also produce angiogenesis inhibitors happens to be very important in explaining metastasis, which is the spread of cancer to other parts of the body and the main reason for cancer-related deaths. Frequently, tiny, microscopic metastases in areas of the body far away from the primary tumor will remain inactive for years and begin to grow only after the primary tumor is removed. This happens because the primary tumor has been releasing angiogenesis inhibitors into the bloodstream, and when these inhibitors are gone, the microscopic tumors begin to grow. Cancer researchers hope that by preventing angiogenesis, they can prevent these microscopic metastases from growing. Furthermore, if a tumor has not metastasized, or spread to other areas, and has been effectively treated with antiangiogenesis agents, metastasis is much less likely to occur because fewer blood vessels are available to spread cancer cells from the tumor.
Fighting angiogenesis
The almost two dozen angiogenesis inhibitors currently being tested work in many different ways. Some block the growth of vascular endothelial cells, which are the primary cells in blood vessels. Another category of angiogenesis inhibitors indirectly attacks endothelial cell growth. Others are designed to interfere with the signaling that takes place between tumor cells and cells in the surrounding tissue, preventing a tumor’s order to produce blood vessels from ever reaching the host tissue. Yet another category includes angiogenesis inhibitors with different mechanisms of action that are not completely understood.
Looking to the future
The science of stopping tumor angiogenesis is relatively new, and there are many unanswered questions. What are the short-term and long-term side effects of antiangiogenesis therapies? Will cancer cells adapt to render antiangiogenesis drugs ineffective? How long will these treatments last? These questions and others are now being addressed in clinical trials, which you can read about on the National Cancer Institute Web site.
For
more information on this topic or for questions about M. D. Anderson’s treatments,
programs, or services, call askMDAnderson at (877) MDA-6789.
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OncoLog, June 2004 issue:
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