Advances in Immunotherapy for DNA Mismatch Repair-Deficient Colon and Rectal Cancers

Approximately 10% to 15% of colorectal cancers (CRCs) exhibit deficient mismatch repair (dMMR), resulting in microsatellite instability–high.1 The prevalence of dMMR declines with advancing stage and is substantially lower in metastatic disease. These hypermutated tumors generate abundant neoantigens that elicit a robust intratumoral immune response.2 Immune checkpoint inhibitors (ICIs), including anti–PD-1 antibodies, restore antitumor immunity by blocking inhibitory PD-1 signaling on activated T cells.