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Abstract
Monoclonal antibodies targeting key receptors that inhibit T cell function such as CTLA-4 and PD-1 have demonstrated the potency of checkpoint blockade, highlighted by long-term complete responses for metastatic cancers once thought incurable. However, only a subset of patients will respond to checkpoint blockade due to a multitude of factors including an immunosuppressive tumor microenvironment and the mutational burden of the cancer.