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| health > cancer > story page |         |
UCLA doctors move forward on testing new cancer drugJune 28, 1999
By Cathy Lu (WebMD) -- At the UCLA Jonsson Cancer Center, one drug is giving doctors and patients alike hope that life and cancer can coexist. A drug called SU5416 is just one compound in a class of drugs known as angiogenesis inhibitors -- drugs that stop the growth of blood vessels to tumors. After completing Phase I testing of SU5416, doctors are ready to administer the drug to more patients. At the helm of the UCLA study is Dr. Lee Rosen, director of the Cancer Therapy Development Program. One of the most powerful observations Rosen has made so far was in a patient with Kaposi's sarcoma, a tumor common in people with AIDS. In this case, the subject was suffering from lesions so full of fluid that one of his legs grew to three times larger than its normal size. When doctors began administering SU5416, they saw some phenomenal results. "A lot of the side effects and terrible manifestations of his tumor just went right away," said Rosen. "All that fluid leakage went away, and the lesions themselves kind of flattened out. . . . It was a pretty remarkable thing." Like this patient, everyone who participated in UCLA's Phase I study was in an advanced stage of cancer. In some patients, tumor growth slowed down and the cancer stabilized -- all without the side effects associated with chemotherapy, like hair loss and nausea. However, there were a number of patients in whom tumor growth could not be contained. Currently it's impossible to pinpoint why the drug worked on some patients and not others. It's plausible that the drug would not work on certain types of cancers, some tumors were too advanced for treatment, or some of the administered doses weren't high enough to be effective. "If you're looking at advanced-disease patients, growth rates are often very advanced," said Rosen. "They're in sort of the end stages of their tumor, so it's a big race. You don't always have six months or a year to just wait and see if the drug's going to work." SU5416 is one of about 20 drugs that are based on this simple theory: Starve the tumor. At the heart of the process is a growth hormone called vascular endothelial growth factor (VEGF), which helps the body develop new blood vessels. On cancer cells VEGF attaches itself to a receptor called FLK-1, where a signal to spawn new blood vessels is transmitted. SU5416 blocks the FLK-1 receptor so that VEGF cannot attach to the cell. In theory, this prevents blood vessels from growing and cuts off the supply of blood and nutrients to the tumor. The next step for UCLA doctors is to test SU5416 on patients en masse, a process that will take years. With Phase I testing completed, doctors have learned that there are no notable side effects, and they have determined the right dosage to administer for optimal results. The key now is to test the drug on different tumors, like lung and colon cancer, and on patients in earlier stages of cancer. Doctors will also compare the effectiveness of SU5416 combined with chemotherapy to the effectiveness of chemotherapy alone. The assumption is that using the drug on its own won't be enough to fight cancer. Are angiogenesis inhibitors the breakthrough that cancer researchers have been waiting for? "I think that this whole idea that cancer cells have a lot of blood vessels around them is a very important breakthrough," said Rosen. Until more testing is done, though, it's important to clarify that this is not a miracle cure. According to Rosen, 10 years ago immunotherapy drugs like Interleukin-2 were regarded as the cure-alls that would harness the power of the immune system to help fight cancer. As with what happened then, the fear is that angiogenesis inhibitors won't turn out to be the panacea that cancer patients are praying for. "People want the drug for their dogs and cats and horses and for their grandma who's on her death bed and can't move," said Rosen, "like there's some magic drug that's going to somehow raise her from the dead. It's just very difficult."
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