Search Here

Some cancer patients with aggressive tumors may benefit from a class of anti-inflammatory drugs used to treat rheumatoid arthritis, a new study has suggested. 

The study found that some aggressive tumors rely on an antiviral pathway that appears to drive inflammation. The tumors that activate this particular antiviral pathways always have dysfunctional forms of the proteins p53 and ARF. These are encoded by the genes known for being highly mutated in various cancers. 

Researchers discovered that these two genes compensated for each other. When both are mutated, the tumors that form are more aggressive than if only one of these genes is lost. 

"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, in the press release. "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."

Researchers studied triple-negative breast cancer as these tumors often 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 added in the press release. "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.