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- W4361242583 abstract "<div>Abstract<p><i>K-ras</i> 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 oncogenic allele of <i>K-ras</i> is activated and <i>Notch1</i> is deleted simultaneously in the pancreas. Unexpectedly, the loss of <i>Notch1</i> in this model resulted in increased tumor incidence and progression, implying that <i>Notch1</i> can function as a tumor suppressor gene in PDAC. Cancer Res; 70(11); 4280–6. ©2010 AACR.</p></div>" @default.
- W4361242583 created "2023-03-31" @default.
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- W4361242583 date "2023-03-30" @default.
- W4361242583 modified "2023-10-01" @default.
- W4361242583 title "Data from Notch1 Functions as a Tumor Suppressor in a Model of K-ras–Induced Pancreatic Ductal Adenocarcinoma" @default.
- W4361242583 doi "https://doi.org/10.1158/0008-5472.c.6501183" @default.
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