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Both p16(Ink4a) and the p19(Arf)-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse
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 maligna...
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| Hoofdauteurs: | , , , , , , , , , , , , , |
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| Formaat: | Artigo |
| Taal: | Inglês |
| Gepubliceerd in: |
National Academy of Sciences
2006
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| Onderwerpen: | |
| Online toegang: | https://ncbi.nlm.nih.gov/pmc/articles/PMC1458678/ https://ncbi.nlm.nih.gov/pubmed/16585505 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.0601273103 |
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