The cells churn out an enzyme that bonds with a protein, creating a protective barrier that deflects damage from radiation or chemotherapy and promotes tumor cell survival. But in laboratory experiments, UF scientists were able to block the union, and the malignant cells died. The findings are opening new avenues of research that could lead to improved cancer therapies, the researchers report this week in the journal Cancer Research.
"We have found a gene called focal adhesion kinase which is produced at very high levels in human tumors, and our work has shown this makes the tumors more likely to survive as they spread throughout the body and grow," said William G. Cance, M.D., a researcher at the University of Florida Shands Cancer Center and chairman of the department of surgery at UF's College of Medicine. "It also makes them more resistant to our attempts to kill them. And we're trying to understand exactly why this gene, which is a small enzyme molecule, is very intimately associated with tumor cell survival."
Focal adhesion kinase, or FAK, is commanding increasing attention and has spawned a flurry of research designed to develop new drug therapies, said Cance, who is known internationally for his genetic investigations of tumor survival. These medicines would prevent FAK from linking with the protein known as vascular endothelial growth factor receptor 3, or VEGFR-3. The protein is tied to the growth of channels in the lymph system that serve as cellular superhighways for cancer spread and is found in breast, colon and thyroid tumors.
Cance and colleagues were the first to pull FAK out of human tumors and to show that human cancers make the mol
Contact: Melanie Fridl Ross
University of Florida