Both p16
            <sup>Ink4a</sup>
            and the p19
            <sup>Arf</sup>
            -p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse

Bardeesy, Nabeel; J. Aguirre, Andrew; C. Chu, Gerald; Cheng, Kuang-hung; V. Lopez, Lyle; F. Hezel, Aram; Feng, Bin; Brennan, Cameron; Weissleder, Ralph; Mahmood, Umar; Hanahan, Douglas; S. Redston, Mark; Chin, Lynda; A. DePinho, Ronald

doi:10.1073/pnas.0601273103

Public

Both p16 Ink4a and the p19 Arf -p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse

Shared by NobleBlocks on Apr 11, 2006 • 12:00 AM UTC

Authors:

Nabeel Bardeesy

Andrew J. Aguirre

Gerald C. Chu

Abstract

Activating KRAS mutations and p16 Ink4a inactivation are near universal events in human pancreatic ductal adenocarcinoma (PDAC). In mouse models, Kras G12D initiates formation of premalignant pancreatic ductal lesions, and loss of either Ink4a / Arf ( p16 Ink4a / p19 Arf ) or p53 enables their malig...

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