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

Faiyaz Notta,Michelle Chan-Seng-Yue,Mathieu Lemire,Yilong Li,Gavin Wilson,Ashton A. Connor,Robert E. Denroche,Sheng-Ben Liang,Andrew M.K. Brown,J. Kim,Tao Wang,Jared T. Simpson,Timothy Beck,Ayelet Borgida,Nicholas Buchner,Dianne Chadwick,Sara Hafezi-Bakhtiari,John E. Dick,Lawrence E. Heisler,Michael A. Hollingsworth,Emin Ibrahimov,Gun Ho Jang,Jeremy Johns,Lars G.T. Jorgensen,Calvin Law,Olga Ludkovski,Ilinca Lungu,Karen Ng,Danielle Pasternack,Gloria M. Petersen,Liran I. Shlush,Lee Timms,Ming Sound Tsao,Julie M. Wilson,Christina K. Yung,George Zogopoulos,John M. S. Bartlett,Ludmil B. Alexandrov,Francisco X. Real,Sean P. Cleary,Michael H.A. Roehrl,John Douglas Mcpherson,Lincoln Stein,Thomas J. Hudson,Peter J. Campbell,Steven Gallinger

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

2016

Pancreatic cancer is not caused by a specific series of genetic alterations that occur sequentially but by one, or few, catastrophic events that result in simultaneous oncogenic genetic rearrangements, giving rise to highly aggressive tumours.

Keywords:

Mutagenesis
Chromothripsis
Carcinoma in situ
Pancreatic cancer
Neoplasm Invasiveness
Mitosis
Genetics
Carcinogenesis
Mutation
Biology
gene rearrangement
KRAS
CDKN2A
Bioinformatics
Cancer

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