Notch1 functions as a tumor suppressor in a model of K-ras-induced pancreatic ductal adenocarcinoma.
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ABSTRACT:
SUBMITTER: Hanlon L
PROVIDER: S-EPMC2880196 | biostudies-literature | 2010 Jun
REPOSITORIES: biostudies-literature
Publications
Notch1 functions as a tumor suppressor in a model of K-ras-induced pancreatic ductal adenocarcinoma.
Hanlon Linda L Avila Jacqueline L JL Demarest Renée M RM Troutman Scott S Allen Megan M Ratti Francesca F Rustgi Anil K AK Stanger Ben Z BZ Radtke Fred F Adsay Volkan V Long Fenella F Capobianco Anthony J AJ Kissil Joseph L JL
Cancer research 20100518 11
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 used a mouse model in which an oncogeni ...[more]
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2014-01-24 | E-GEOD-54328 | biostudies-arrayexpress
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