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PANCREATIC CANCER

Unlocking PDAC initiation with AP-1

Nature Cancer volume 2, pages 14–15 (2021)Cite this article

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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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Authors and Affiliations

  1. David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA

    Lindsay M. LaFave

  2. Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA

    Lindsay M. LaFave

  3. Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA

    Lindsay M. LaFave & Jason D. Buenrostro

  4. Broad Institute of MIT and Harvard, Cambridge, MA, USA

    Jason D. Buenrostro

Authors
  1. Lindsay M. LaFave
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  2. Jason D. Buenrostro
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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). https://doi.org/10.1038/s43018-020-00158-5

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