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• W1969201526 abstract "Initiation of pancreatic ductal adenocarcinoma (PDA) is definitively linked to activating mutations in the KRAS oncogene. However, PDA mouse models show that mutant Kras expression early in development gives rise to a normal pancreas, with tumors forming only after a long latency or pancreatitis induction. Here, we show that oncogenic KRAS upregulates endogenous EGFR expression and activation, the latter being dependent on the EGFR ligand sheddase, ADAM17. Genetic ablation or pharmacological inhibition of EGFR or ADAM17 effectively eliminates KRAS-driven tumorigenesis in vivo. Without EGFR activity, active RAS levels are not sufficient to induce robust MEK/ERK activity, a requirement for epithelial transformation." @default.
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• W1969201526 date "2012-09-01" @default.
• W1969201526 modified "2023-10-18" @default.
• W1969201526 title "EGF Receptor Is Required for KRAS-Induced Pancreatic Tumorigenesis" @default.
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• W1969201526 doi "https://doi.org/10.1016/j.ccr.2012.07.024" @default.
• W1969201526 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3443395" @default.
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