Researchers at the Keck School of Medicine of USC have identified a biological feedback loop that helps explain why certain colorectal cancers—known as microsatellite instability (MSI) and deficient DNA mismatch repair (dMMR) tumors—respond better to immunotherapy. Using mouse models and patient tumor data, the team found that two genes, DR5 and Lig3, drive a cycle of tumor cell death and immune activation by promoting the release of extrachromosomal circular DNA, which amplifies the immune response. Tumors with higher DR5 and Lig3 activity were more likely to respond to immune checkpoint inhibitors, suggesting a potential pathway to improve treatment and better predict which patients will benefit from immunotherapy.

A major national cooperative group clinical trial led by Mayo Clinic researchers found that continuing maintenance therapy with lenalidomide beyond two years after initial treatment for standard-risk multiple myeloma did not improve overall survival compared with stopping treatment after two years.