Notch1 functions as a tumor suppressor in a model of K-ras-induced pancreatic ductal adenocarcinoma

Linda Hanlon; Jacqueline L Avila; Renée M Demarest; Scott Troutman; Megan Allen; Francesca Ratti; Anil K Rustgi; Ben Z Stanger; Fred Radtke; Volkan Adsay; Fenella Long; Anthony J Capobianco; Joseph L Kissil

doi:10.1158/0008-5472.CAN-09-4645

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Notch1 functions as a tumor suppressor in a model of K-ras-induced pancreatic ductal adenocarcinoma

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Notch1 functions as a tumor suppressor in a model of K-ras-induced pancreatic ductal adenocarcinoma

Linda Hanlon, Jacqueline L Avila, Renée M Demarest, Scott Troutman, Megan Allen, Francesca Ratti, Anil K Rustgi, Ben Z Stanger, Fred Radtke, Volkan Adsay, …

Cancer research (Chicago, Ill.), Vol.70(11), pp.4280-4286

2010-06-01

DOI: https://doi.org/10.1158/0008-5472.CAN-09-4645

PMCID: PMC2880196

PMID: 20484026

Abstract

Notch1

Pancreatic Adenocarcinoma

Ras

tumor suppressor

K-ras is the most commonly mutated oncogene in pancreatic cancer and its activation in murine models is sufficient to recapitulate the spectrum of lesions seen in human pancreatic ductal adenocarcinoma (PDAC). Recent studies suggest that Notch receptor signaling becomes reactivated in a subset of PDACs, leading to the hypothesis that Notch1 functions as an oncogene in this setting. To determine whether Notch1 is required for K-ras-induced tumorigenesis, we employed a mouse model in which an oncogenic allele of K-ras is activated and Notch1 is deleted simultaneously in the pancreas. Unexpectedly, the loss of Notch1 in this model resulted in increased tumor incidence and progression implying that Notch1 can function as a tumor suppressor gene in PDAC.

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Collaboration types: Domestic collaboration; International collaboration
Citation topics: 1 Clinical & Life Sciences; 1.108 Molecular & Cell Biology - Cancer & Development; 1.108.579 Drosophila
Web Of Science research areas: Oncology
ESI research areas: Clinical Medicine

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Title: Notch1 functions as a tumor suppressor in a model of K-ras-induced pancreatic ductal adenocarcinoma
Creators: Linda Hanlon - Molecular and Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Jacqueline L Avila - Molecular and Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Renée M Demarest - Molecular and Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Scott Troutman - Molecular and Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Megan Allen - Molecular and Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Francesca Ratti - Molecular and Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Anil K Rustgi - Division of Gastroenterology, Departments of Medicine and Genetics, Abramson Cancer Center, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Ben Z Stanger - Division of Gastroenterology, Departments of Medicine and Genetics, Abramson Cancer Center, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Fred Radtke - Ecole Polytechnique Fédérale de Lausanne, EPFL SV ISREC, 1015 Lausanne, Switzerland
Volkan Adsay - Pathology & Laboratory Medicine, Emory University School of Medicine, H180-B EUH Atlanta, Georgia. USA
Fenella Long - Faculty of Pathobiology, University of Pennsylvania, School of Veterinary Medicine, Philadelphia, PA 19104-6051, USA
Anthony J Capobianco - Molecular and Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Joseph L Kissil - Molecular and Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Publication Details: Cancer research (Chicago, Ill.), Vol.70(11), pp.4280-4286
Academic Unit: Miller School of Medicine; UMMG Department of Surgery; UMMG Dept of Surgery - Div of Surgical Oncology
Language: English
Resource Type: Journal article
PMID: 20484026
PMCID: PMC2880196
Record Identifier: 991031615305202976