Melanoma can find a safe haven from the BRAF inhibitors designed to stop the cancer. And a group of scientists at the Frick Institute say they have some ideas on shutting that haven down.
These investigators note that BRAF inhibitors have played a big role in improving survival stats for a large swath of cancer patients identified with a common gene mutation. Using funds from Cancer Research UK, they've also highlighted animal and cell research that shows how those same drugs have an unusual side effect, prompting healthy cells to come to the rescue of the cancer cells by creating a "safe haven" by triggering cell signals that allow them to linger. And that seriously raises the risk of a recurrence.
But there may be a way to prevent the haven from forming in the first place.
The key may be targeting FAK proteins, an approach that's also been studied in leukemia. There are experimental drugs in the clinic that may fit that role. But the scientists also note that it will likely take years before a FAK drug can be tested in combination with BRAF inhibitors.
"Skin cancers caused by a faulty BRAF gene typically out-maneuver the targeted drugs used to treat them after a few months," says study author Erik Sahai. "Clearly understanding this process is an important first step in improving treatment. We've now mapped how melanoma cells exploit their neighboring cells to survive in the presence of targeted drugs. It's clear that the 'safe haven' offered by the surrounding cells is triggered as a response to the same drugs that target this class of melanoma. Knowing more about this relationship means we can start to improve treatment."
The research was published on April 13 in Cancer Cell.
- here's the release
- read the research article