Germline Brca2 heterozygosity promotes Kras(G12D) -driven carcinogenesis in a murine model of familial pancreatic cancer.

@article{Skoulidis2010GermlineBH,
  title={Germline Brca2 heterozygosity promotes Kras(G12D) -driven carcinogenesis in a murine model of familial pancreatic cancer.},
  author={Ferdinandos Skoulidis and Liam D Cassidy and Venkat Pisupati and J{\'o}n Gunnlaugur J{\'o}nasson and Hordur Bjarnason and Jorunn Erla Eyfjord and Florian A. Karreth and Michael Lim and Lorraine M Barber and Susan A Clatworthy and Susan E. Davies and Kenneth P. Olive and David A Tuveson and Ashok R. Venkitaraman},
  journal={Cancer cell},
  year={2010},
  volume={18 5},
  pages={499-509}
}
Inherited heterozygous BRCA2 mutations predispose carriers to tissue-specific cancers, but somatic deletion of the wild-type allele is considered essential for carcinogenesis. We find in a murine model of familial pancreatic cancer that germline heterozygosity for a pathogenic Brca2 truncation suffices to promote pancreatic ductal adenocarcinomas (PDACs) driven by Kras(G12D), irrespective of Trp53 status. Unexpectedly, tumor cells retain a functional Brca2 allele. Correspondingly, three out of… CONTINUE READING
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