Each therapy alone had limited or no benefit on the tumor, because tumors are skilled at circumventing individual therapies and finding new ways to grow. But together, the two therapies more potently inhibited a tumor's ability to sustain and nourish itself by growing new blood vessels around the tumor.
Most importantly, the scientists clarified how this master switch, Hypoxia Inducible Factor or HIF-1, promotes a cancer cell's ability to grow, nourish, energize and develop blood vessels that support its growth.
The answers they yielded are complex, yet promising, for the future treatment of cancer patients, said Mark Dewhirst, Ph.D., DVM, professor of radiation oncology at Duke.
Results of the research, led by Dewhirst and conducted by M.D./Ph.D. candidate Ben Moeller, will be published in the August 15, 2005, issue of Cancer Cell.
"We've shown that blocking HIF-1 at the wrong time therapeutically in a cancer cell yields no benefit and can actually impede other cancer treatments," said Dewhirst. "But when we block HIF-1 at the appropriate time, it substantially increases a tumor's response to radiation therapy."
Specifically, they found that blocking HIF-1 immediately after radiation prevented new blood vessels from developing and nourishing cancer cells that survived radiation. Two days after tumors were irradiated, there was almost no detectable vasculature ?blood vessels feeding the tumor.
"We've employed a treatment strategy where we accomplish two hits ?killing the cancer cells with radiation and then blocking their blood vessel survival a