Timing Is Everything: Brca2 and p53 Mutations in Pancreatic Cancer Jennifer P. Morton, Colin W. Steele, Owen J. Sansom  Gastroenterology  Volume 140, Issue 4, Pages 1143-1146 (April 2011) DOI: 10.1053/j.gastro.2011.02.026 Copyright © 2011 AGA Institute Terms and Conditions

Figure 1 A mouse model for pancreatic cancer initiation in BRCA2 kindreds. In this model, 1 copy of Brca2 is inactivated from birth. LOH before the acquisition of further mutations is not sufficient to drive tumorigenesis, instead promoting chromosomal instability. Intriguingly, even in the presence of Kras activation, LOH at Brca2 inhibits tumor formation as long as wild-type p53 remains. When p53 is mutated, however, loss of the second copy of Brca2 accelerates pancreatic tumorigenesis in a Kras-independent manner. Gastroenterology 2011 140, 1143-1146DOI: (10.1053/j.gastro.2011.02.026) Copyright © 2011 AGA Institute Terms and Conditions