P1.08-03 Hyper-Interferon Sensitive Influenza Virus Induces Immune Activation and Overcomes Resistance to Anti-PD-1 in Murine NSCLC

Despite recent advances in immunotherapy, many patients with non-small cell lung cancer (NSCLC) fail to respond to immune checkpoint inhibitors (ICI) or acquire resistance after an initial response. Exclusion of T cells from the tumor or the presence of a dysfunctional T cell compartment within the tumor microenvironment (TME) constitute two central hallmarks of resistance to ICI in patients with NSCLC. Seminal studies have identified that loss of LKB1 in KRAS-mutant NSCLC drives resistance to ICI, possibly through the suppression of STING which results in dysregulation of the interferon (IFN) signaling.