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Article

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

3 Apr 2006

Abstract excerpt

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 malignant progression. As recent mouse modeling studies have suggested a less prominent role for p16(Ink4a) in constraining...

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PMID: 16585505
DOI: 10.1073/pnas.0601273103

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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