Adding an anti-inflammatory drug to anti-PD1 checkpoint inhibitor immunotherapy has shown great promise as a new strategy against advanced lung cancer, based on results from a clinical trial led by investigators at the Abramson Cancer Center at the Perelman School of Medicine.
The results, published in Science, are based the strategy on an accumulating body of evidence for the dual nature of inflammation—it can be beneficial against infectious pathogens and cancers in the short term, but can also lead to a weakened immune system when it becomes chronic. Signs of this chronic inflammatory response, particularly involving a cytokine called interferon, are often seen in patients taking anticancer immunotherapies and are linked to worse outcomes.
“Many oncologists might find it surprising to combine a JAK inhibitor with immunotherapy since the focus has typically been on creating a strong inflammatory response for effective anti-PD1 treatment. However, there’s a growing understanding that chronic inflammation, especially chronic interferon, can be harmful. Our study’s high response rate and the improvements in immune cells suggest that our approach could help control inflammation and interferon levels before they become detrimental,” says co-senior author Andy Minn, professor of radiation oncology and director of the Mark Foundation Center for Immunotherapy, Immune Signaling, and Radiation.
The researchers now plan to follow up with a larger confirmatory clinical trial as well as additional investigations into the role of JAK1 inhibition in patients with disease progression on immunotherapy, an area of great clinical need.
Read more at Penn Medicine News.