Inflammation-induced NFATc1-STAT3 transcription complex promotes pancreatic cancer initiation by KrasG12D.

@article{Baumgart2014InflammationinducedNT,
  title={Inflammation-induced NFATc1-STAT3 transcription complex promotes pancreatic cancer initiation by KrasG12D.},
  author={Sandra Baumgart and Na Chen and Jens T. Siveke and A. Koenig and Jin-San Zhang and Shiv K. Singh and Elmar Wolf and Marek Bartkuhn and Irene Esposito and Elisabeth Hessmann and Johanna Reinecke and Julius Nikorowitsch and Marius Brunner and Garima R. Singh and Martin E Fernandez-Zapico and Thomas T Smyrk and William R. Bamlet and Martin Eilers and Albrecht Neesse and Thomas Matthias Gress and Daniel D Billadeau and David A Tuveson and Raul A Urrutia and Volker Ellenrieder},
  journal={Cancer discovery},
  year={2014},
  volume={4 6},
  pages={
          688-701
        }
}
UNLABELLED Cancer-associated inflammation is a molecular key feature in pancreatic ductal adenocarcinoma. Oncogenic KRAS in conjunction with persistent inflammation is known to accelerate carcinogenesis, although the underlying mechanisms remain poorly understood. Here, we outline a novel pathway whereby the transcription factors NFATc1 and STAT3 cooperate in pancreatic epithelial cells to promote Kras(G12D)-driven carcinogenesis. NFATc1 activation is induced by inflammation and itself… CONTINUE READING
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