A specific mutation has been linked with acquired resistance in immunotherapy drugs used to treat non–small lung cancer (NSCLC).
A specific mutation has been linked with acquired resistance in immunotherapy drugs used to treat non—small lung cancer (NSCLC).
Researchers led by cancer biologist Katerina Politi, PhD, associate professor in the Yale Department of Pathology and Medical Oncology, have discovered that a mutation in a viral protein called B2M prevents the immune activation needed for immunotherapy agents to function. The discovery of this new resistance mechanism explains why some patients develop resistance later on in treatment and may also steer the evolution of future NSCLC drug development.1
For patients with NSCLC who are not candidates for other targeted therapies, immunotherapy is considered to be a viable treatment alternative. Immunotherapy drugs that have earned FDA approval to treat NSCLC include breakthrough therapies like nivolumab and pembrolizumab, as well as the most recent agent, atezolizumab.