Researchers at UCSF Cancer Center are recruiting patients with advanced lung cancer for a clinical trial of a novel drug they hope will inhibit the growth of blood vessels that nourish tumor cells.
The drug, developed by Genentech, Inc., is a protein known as an antibody that represses a growth factor called VEGF, or vascular endothelial cell growth factor. This therapy has been shown to inhibit the growth of cancer cells in animal laboratory studies.
The antibody to VEGF, called rhuMAb VEGF, belongs to a class of drugs known as anti-angiogenesis therapies that are intended to block the growth of blood vessels in and around tumor cells, thereby starving the tumor by cutting off its supply of nutrients and oxygen.
Many cells produce VEGF to help stimulate the growth and migration of blood vessels that supply nutrients to cells in a beneficial way, for example, during wound healing. But many types of human cancer cells also produce VEGF, and they produce higher than normal levels.
During the clinical trial of the anti-VEGF antibody, UCSF cancer specialists will determine whether or not the therapy will impede the growth of solid tumors and possibly lead to the shrinkage of tumors, especially when administered in combination with standard chemotherapy.
"We are excited about finally bringing new approaches like anti-angiogenesis therapies that make sense intellectually from the laboratory to the clinic," says David Jablons, MD, UCSF assistant professor of surgery and principal investigator of the study. "In this approach, rather than targeting the malfunctioning genome of cancer cells, we are targeting normal cells with stable genomes around the tumor that respond better than cancer cells to growth signals like the anti-VEGF therapy."
Despite the modest improvements of patients with non-small cell lung cancer
(NSCLC), which accounts for approximately 70 percent of all lung cancers, the
overall mortality rate for lung cancer patients is un
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Contact: Abby Sinnott
sinnott@itsa.ucsf.edu
(415) 885-7277
University of California - San Francisco
30-Jul-1998