Background: Colorectal cancers in Lynch syndrome (LS) carriers, characterized by microsatellite instability (MSI) and pronounced immune infiltration, can develop via three pathways: progression from mismatch repair-proficient (MMRp) or MMR-deficient (MMRd) adenomas and MMRd crypt foci. We recently reported changes in the immune environment in normal mucosa and carcinomas from LS carriers. Here, we analyzed the LS adenoma immune phenotype and its relation to clinicopathological features with particular focus on its dependence on MMRd/MSI. …
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