Journal
NATURE REVIEWS CANCER
Volume 10, Issue 10, Pages 683-695Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrc2899
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Funding
- National Institutes of Health (NIH) [CA112537]
- American Association for Cancer Research Pancreatic Cancer Network
- NIH, National Cancer Institute
- American College of Surgeons
- NATIONAL CANCER INSTITUTE [R01CA112537] Funding Source: NIH RePORTER
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Pancreatic ductal adenocarcinoma (PDAC) is characterized by near-universal mutations in KRAS and frequent deregulation of crucial embryonic signalling pathways, including the Hedgehog (Hh) and Wnt-beta-catenin cascades. The creation of mouse models that closely resemble the human disease has provided a platform to better understand when and in which cell types these pathways are misregulated during PDAC development. Here we examine the central part that KRAS plays in the biology of PDAC, and how the timing and location of Hh and Wnt-beta-catenin signalling dictate the specification and oncogenic properties of PDAC.
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