Abstract
Mismatch-repair deficiency (dMMR) is a hallmark of Lynch syndrome-associated cancers, often resulting from inactivating mutations in MLH1 or MSH2. These tumors have a high likelihood of responding to immune checkpoint inhibitors (ICI). Still, intrinsic or acquired resistance mechanisms impair patients’ outcomes. Here, we compared the therapeutic potential of an anti-PD-L1 inhibitor with the CDK4/6 inhibitor abemaciclib in two preclinical mouse models of dMMR-driven carcinogenesis.
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