A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns

@article{Notta2016ARM,
  title={A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns},
  author={Faiyaz Notta and Michelle A. Chan-Seng-Yue and Mathieu Lemire and Yilong Li and Gavin W. Wilson and Ashton A. Connor and Robert E Denroche and Sheng-ben Liang and Andrew M. K. Brown and Jaeseung C. Kim and Tao Wang and Jared T. Simpson and Timothy Beck and Ayelet Eppel Borgida and Nicholas B. Buchner and Dianne Chadwick and Sara Hafezi-Bakhtiari and John E Dick and Lawrence Heisler and Michael Anthony Hollingsworth and Emin Ibrahimov and Gun Ho Jang and Jeremy Johns and Lars G. T. Jorgensen and C. Law and Olga Ludkovski and Ilinca Mihaela Lungu and Karen Ng and Danielle Pasternack and G. M. van Petersen and Liran I. Shlush and Lee Timms and Ming-Sound Tsao and Julie M. Wilson and Christina K. Yung and George Zogopoulos and John M. S. Bartlett and Ludmil B. Alexandrov and Francisco X Real and Sean P. Cleary and Michael H. A. Roehrl and John D. McPherson and Lincoln D. Stein and Thomas J. Hudson and Peter J. Campbell and Steven Gallinger},
  journal={Nature},
  year={2016},
  volume={538},
  pages={378-382}
}
Pancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory… CONTINUE READING

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