Pancreatic cancer modeling using retrograde viral vector delivery and in vivo CRISPR/Cas9-mediated somatic genome editing

  1. Monte M. Winslow1,7,8,12
  1. 1Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA;
  2. 2Department of Developmental Biology, Stanford University School of Medicine, Stanford, California 94305, USA;
  3. 3Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305, USA;
  4. 4Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey 08903, USA;
  5. 5Department of Surgery, Rutgers Robert Wood Johnson University Medical School, New Brunswick, New Jersey 08903, USA;
  6. 6Department of Pharmacology, Rutgers Robert Wood Johnson University Medical School, New Brunswick, New Jersey 08903, USA;
  7. 7Cancer Biology Program, Stanford University School of Medicine, Stanford, California 94305, USA;
  8. 8Stanford Cancer Institute, Stanford University School of Medicine, Stanford, California 94305, USA;
  9. 9Transgenic, Knockout, and Tumor Model Center, Stanford University School of Medicine, Stanford, California 94305, USA;
  10. 10Department of Comparative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA;
  11. 11Department of Pathology, University of California at San Francisco, San Francisco, California 94143, USA;
  12. 12Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA
  1. Corresponding author: mwinslow{at}stanford.edu
  1. 13 These authors contributed equally to this work.

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a genomically diverse, prevalent, and almost invariably fatal malignancy. Although conventional genetically engineered mouse models of human PDAC have been instrumental in understanding pancreatic cancer development, these models are much too labor-intensive, expensive, and slow to perform the extensive molecular analyses needed to adequately understand this disease. Here we demonstrate that retrograde pancreatic ductal injection of either adenoviral-Cre or lentiviral-Cre vectors allows titratable initiation of pancreatic neoplasias that progress into invasive and metastatic PDAC. To enable in vivo CRISPR/Cas9-mediated gene inactivation in the pancreas, we generated a Cre-regulated Cas9 allele and lentiviral vectors that express Cre and a single-guide RNA. CRISPR-mediated targeting of Lkb1 in combination with oncogenic Kras expression led to selection for inactivating genomic alterations, absence of Lkb1 protein, and rapid tumor growth that phenocopied Cre-mediated genetic deletion of Lkb1. This method will transform our ability to rapidly interrogate gene function during the development of this recalcitrant cancer.

Keywords

Footnotes

  • Received April 29, 2015.
  • Accepted June 19, 2015.

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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