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Immune checkpoint inhibitors are increasingly being used in the clinic to treat patients with advanced lung cancer. Even when these agents are effective, acquired resistance to immune checkpoint inhibitors can occur and very little is known about the mechanisms of resistance to these agents. Through this grant, we investigated genomic and transcriptional mechanisms of resistance in patient specimens and identified new potential mechanisms affecting antigen presentation, interferon signaling and other pathways that can affect innate immune cells and exclude immune cells from tumors. We also optimized immunocompetent mouse models to study resistance and to validate mechanisms in vivo including loss of b2-microglobulin and the tumor suppressor gene Pten. Finally, we investigated mechanisms to overcome resistance using these models