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Abstract Pathogenic variants in the exonuclease (proofreading) domain of DNA polymerase ε (POLE) are frequently detected in colorectal cancers (CRC) with high tumor mutational burden (TMB), yet their functional role in intestinal tumorigenesis remains unknown. Here, we investigated the impact of mutation in POLE on intestinal homeostasis using a conditional mouse model expressing the PoleP286R pathogenic driver in intestinal epithelial cells.
As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
