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Unlocking PDAC initiation with AP-1

Chronic pancreatitis is a risk factor for pancreatic cancer; however, the mechanisms underlying cellular susceptibility to oncogenic transformation are complex. A recent study reports a damage-associated progenitor cell state, controlled by the transcription factors KLF5 and members of the AP-1 family, that initiates tumorigenesis in mouse models of pancreatic cancer in which the proto-oncogene KRAS is altered.

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Fig. 1: PLDPs serve as a cell of origin in KrasG12D-mutant pancreatic adenocarcinomas.


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Correspondence to Lindsay M. LaFave or Jason D. Buenrostro.

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LaFave, L.M., Buenrostro, J.D. Unlocking PDAC initiation with AP-1. Nat Cancer 2, 14–15 (2021).

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