A team of Stanford researchers has developed a protein therapy that disrupts the process that causes cancer cells to break away from original tumor sites, travel through the bloodstream and start aggressive new growths elsewhere in the body.
This process, known as metastasis, can cause cancer to spread with deadly effect. "The majority of patients who succumb to cancer fall prey to metastatic forms of the disease," said Jennifer Cochran, an associate professor of bioengineering who describes a new therapeutic approach in Nature Chemical Biology.
Today doctors try to slow or stop metastasis with chemotherapy, but these treatments are unfortunately not very effective and have severe side effects. The Stanford team seeks to stop metastasis, without side effects, by preventing two proteins, Axl and Gas6, from interacting to initiate the spread of cancer. An engineered Axl ‘decoy receptor’ effectively silences the Gas6-Axl signaling axis
Axl proteins stand like bristles on the surface of cancer cells, poised to receive biochemical signals from Gas6 proteins. When two Gas6 proteins link with two Axls, the signals that are generated enable cancer cells to leave the original tumor site, migrate to other parts of the body and form new cancer nodules.
To stop this process Cochran used protein engineering to create a harmless version of Axl that acts like a decoy. This decoy Axl latches on to Gas6 proteins in the bloodstream and prevents them from linking with and activating the Axls present on cancer cells.