KRAS, Hedgehog, Wnt and the twisted developmental biology of pancreatic ductal adenocarcinoma

John P. Morris; Sam C. Wang; Matthias Hebrok

doi:10.1038/nrc2899

KRAS, Hedgehog, Wnt and the twisted developmental biology of pancreatic ductal adenocarcinoma

John P. Morris
, Sam C. Wang
, Matthias Hebrok

University of California San Francisco

Research output: Contribution to journal › Review article › peer-review

497 Scopus citations

Abstract

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-β-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-2-catenin signalling dictate the specification and oncogenic properties of PDAC.

Original language	English
Pages (from-to)	683-695
Number of pages	13
Journal	Nature Reviews Cancer
Volume	10
Issue number	10
DOIs	https://doi.org/10.1038/nrc2899
State	Published - Oct 2010
Externally published	Yes

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10.1038/nrc2899

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title = "KRAS, Hedgehog, Wnt and the twisted developmental biology of pancreatic ductal adenocarcinoma",

abstract = "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-β-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-2-catenin signalling dictate the specification and oncogenic properties of PDAC.",

author = "Morris, \{John P.\} and Wang, \{Sam C.\} and Matthias Hebrok",

note = "Funding Information: The authors thank R. Vanderlaan and A. Folias for critical reading of the manuscript and stimulating discussions. Work in the M.H. laboratory on pancreatic cancer is supported by grants from the National Institutes of Health (NIH) (CA112537) and American Association for Cancer Research Pancreatic Cancer Network (PanCAN). S.C.W. is supported by the NIH under the Ruth L. Kirschstein National Research Service Award F32 from the National Cancer Institute and the American College of Surgeons Resident Research Scholarship.",

year = "2010",

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doi = "10.1038/nrc2899",

language = "English",

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AU - Wang, Sam C.

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N1 - Funding Information: The authors thank R. Vanderlaan and A. Folias for critical reading of the manuscript and stimulating discussions. Work in the M.H. laboratory on pancreatic cancer is supported by grants from the National Institutes of Health (NIH) (CA112537) and American Association for Cancer Research Pancreatic Cancer Network (PanCAN). S.C.W. is supported by the NIH under the Ruth L. Kirschstein National Research Service Award F32 from the National Cancer Institute and the American College of Surgeons Resident Research Scholarship.

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N2 - 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-β-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-2-catenin signalling dictate the specification and oncogenic properties of PDAC.

AB - 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-β-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-2-catenin signalling dictate the specification and oncogenic properties of PDAC.

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M3 - Review article

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JF - Nature Reviews Cancer

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ER -

KRAS, Hedgehog, Wnt and the twisted developmental biology of pancreatic ductal adenocarcinoma

Abstract

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