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Molecular dynamics driving phenotypic divergence among KRAS mutants in pancreatic tumorigenesis
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DOI:10.1016/j.devcel.2026.06.016.png)
Abstract
En 中文
• Inflammation induces lineage reversion in pancreatic acinar cells • Enhancer rewiring, initiated by injury, is co-opted by KrasG12D in tumorigenesis • KrasG12V/R are not able to sustain enhancer reprogramming and neoplastic commitment • Deficient KrasG12R EGFR and RAC1 signaling are rescued by enforced AKT activation
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