KRAS mutations take different trajectories to drive pancreatic transformation.

Abstract excerpt

KRAS mutations are highly prevalent in pancreatic cancer and are critical for epithelial reprogramming during tumor initiation. In this issue of Developmental Cell, Grimont et al.1 demonstrate that the three most common KRAS mutations differentially activate downstream signaling pathways, resulting in distinct capacities to develop pancreatic pre-neoplastic lesions.

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