Activated Kras and Ink4a/Arf Deficiency cooperate to produce Metastatic Pancreatic Ductal Adenocarcinoma

We assessed the cooperative interactions of two signature mutations in mice engineered to sustain pancreas-specific Pre-mediated activation of a mutant Kras allele and deletion of a conditional Ink4a/Arf tumor suppressor allele. Our findings in the mouse provided experimental support for the widely accepted model of human pancreatic adenocarcinoma in which activated KRAS initiates PanIN lesions, and the INK4A/ARF tumor suppressors function to constrain the malignant conversion of these PanIN lesions into lethal ductal adenocarcinoma.

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