A particular class of anti-inflammatory drugs may help cancer patients with aggressive tumors, a new research by the Washington School of Medicine in St Louis reveals.
Researchers found that certain aggressive tumors may benefit from anti-inflammatory drugs used to treat rheumatoid arthritis.
The team explained that some aggressive tumors depend on an antiviral pathway that appears to drive inflammation. The tumors that activate this particular antiviral pathway always have dysfunctional forms of the proteins p53 and ARF. These are encoded by genes known for being highly mutated in various cancers.
The team found that these two genes paid off for each other. When both are mutated, the tumors that form are aggressive than if only one of these genes is working, researchers explained in a press release.
"It's probably inaccurate to say that ARF completely replaces p53, which is a robust tumor suppressor with multiple ways of working," said senior author Jason D. Weber, PhD, associate professor of medicine. "But it appears the cell has set up a sort of backup system with ARF. It's not surprising that these are the two most highly mutated tumor suppressors in cancer. Because they're backing one another up, the most aggressive tumors form when you lose both."
The team examined triple-negative breast cancer because these tumors mostly show mutations in both p53 and ARF.
"It's not the level of activation you would see in a true antiviral response, but it's higher than normal," Weber said. "We are interested in studying whether this antiviral response is creating a local environment of inflammation that supports more aggressive tumors."
"There are JAK inhibitors in use for rheumatoid arthritis and being tested against a number of other conditions. Our data suggest that these anti-inflammatory drugs may be a way to treat some patients missing both p53 and ARF."
The study has been reported in the recent issue of the journal Cell Reports.
