p53 mutations cooperate with oncogenic Kras to promote adenocarcinoma from pancreatic ductal cells-Reference-Cited by-同舟云学术

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p53 mutations cooperate with oncogenic Kras to promote adenocarcinoma from pancreatic ductal cells

Published:2015-11-23 Issue:32 Volume:35 Page:4282-4288
ISSN:0950-9232
Container-title:Oncogene
language:en
Short-container-title:Oncogene

Author:

Bailey J M,Hendley A M,Lafaro K J,Pruski M A,Jones N C,Alsina J,Younes M,Maitra A,McAllister F,Iacobuzio-Donahue C A,Leach S D

Publisher

Springer Science and Business Media LLC

Subject

Cancer Research,Genetics,Molecular Biology

Link

http://www.nature.com/articles/onc2015441.pdf

Reference18 articles.

1. Waddell N, Pajic M, Patch AM, Chang DK, Kassahn KS, Bailey P et al. Whole genomes redefine the mutational landscape of pancreatic cancer. Nature 2015; 518: 495–501.

2. Kopp JL, von Figura G, Mayes E, Liu FF, Dubois CL, JPt Morris et al. Identification of Sox9-dependent acinar-to-ductal reprogramming as the principal mechanism for initiation of pancreatic ductal adenocarcinoma. Cancer Cell 2012; 22: 737–750.

3. Habbe N, Shi G, Meguid RA, Fendrich V, Esni F, Chen H et al. Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN) by acinar cell targeting of oncogenic Kras in adult mice. Proc Natl Acad Sci USA 2008; 105: 18913–18918.

4. Ji B, Tsou L, Wang H, Gaiser S, Chang DZ, Daniluk J et al. Ras activity levels control the development of pancreatic diseases. Gastroenterology 2009; 137: 82 e1–82 e6.

5. von Figura G, Fukuda A, Roy N, Liku ME, Morris IvJP, Kim GE et al. The chromatin regulator Brg1 suppresses formation of intraductal papillary mucinous neoplasm and pancreatic ductal adenocarcinoma. Nat Cell Biol 2014; 16: 255–267.

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