Chromosomally unstable mouse tumours have genomic alterations similar to diverse human cancers

Richard S. Maser, Bhudipa Choudhury, Peter J. Campbell, Bin Feng, Kwok-Kin Wong, Alexei Protopopov, Jennifer O’Neil, Alejandro Gutierrez, Elena Ivanova, Ilana Perna, Eric Lin, Vidya Mani, Shan Jiang, Kate McNamara, Sara Zaghlul, Sarah Edkins, Claire Stevens, Cameron Brennan, Eric S. Martin, Ruprecht Wiedemeyer, Omar Kabbarah, Cristina Nogueira, Gavin Histen, Jon Aster, Marc Mansour, Veronique Duke, Letizia Foroni, Adele K. Fielding, Anthony H. Goldstone, Jacob M. Rowe, Yaoqi A. Wang, A. Thomas Look, Michael R. Stratton, Lynda Chin, P. Andrew Futreal and Ronald A. DePinho ()
Additional contact information
Richard S. Maser: Department of Medical Oncology,
Bhudipa Choudhury: Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK
Peter J. Campbell: Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK
Bin Feng: Center for Applied Cancer Science of the Belfer Institute for Innovative Cancer Science,
Kwok-Kin Wong: Department of Medical Oncology,
Alexei Protopopov: Center for Applied Cancer Science of the Belfer Institute for Innovative Cancer Science,
Jennifer O’Neil: Boston, Massachusetts 02115, USA
Alejandro Gutierrez: Boston, Massachusetts 02115, USA
Elena Ivanova: Center for Applied Cancer Science of the Belfer Institute for Innovative Cancer Science,
Ilana Perna: Center for Applied Cancer Science of the Belfer Institute for Innovative Cancer Science,
Eric Lin: Agilent Technologies, Palo Alto, California 94304, USA
Vidya Mani: Department of Medical Oncology,
Shan Jiang: Department of Medical Oncology,
Kate McNamara: Department of Medical Oncology,
Sara Zaghlul: Department of Medical Oncology,
Sarah Edkins: Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK
Claire Stevens: Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK
Cameron Brennan: Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
Eric S. Martin: Department of Medical Oncology,
Ruprecht Wiedemeyer: Department of Medical Oncology,
Omar Kabbarah: Department of Medical Oncology,
Cristina Nogueira: Department of Medical Oncology,
Gavin Histen: Department of Pathology,
Jon Aster: Department of Pathology,
Marc Mansour: Royal Free and University College Medical School, London NW3 2PF, UK
Veronique Duke: Royal Free and University College Medical School, London NW3 2PF, UK
Letizia Foroni: Royal Free and University College Medical School, London NW3 2PF, UK
Adele K. Fielding: Royal Free and University College Medical School, London NW3 2PF, UK
Anthony H. Goldstone: University College London Hospitals, London NW1 2BU, UK
Jacob M. Rowe: Rambam Medical Center and Technion, Haifa 31096, Israel
Yaoqi A. Wang: Department of Medical Oncology,
A. Thomas Look: Boston, Massachusetts 02115, USA
Michael R. Stratton: Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK
Lynda Chin: Department of Medical Oncology,
P. Andrew Futreal: Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK
Ronald A. DePinho: Department of Medical Oncology,

Nature, 2007, vol. 447, issue 7147, 966-971

Abstract: Abstract Highly rearranged and mutated cancer genomes present major challenges in the identification of pathogenetic events driving the neoplastic transformation process. Here we engineered lymphoma-prone mice with chromosomal instability to assess the usefulness of mouse models in cancer gene discovery and the extent of cross-species overlap in cancer-associated copy number aberrations. Along with targeted re-sequencing, our comparative oncogenomic studies identified FBXW7 and PTEN to be commonly deleted both in murine lymphomas and in human T-cell acute lymphoblastic leukaemia/lymphoma (T-ALL). The murine cancers acquire widespread recurrent amplifications and deletions targeting loci syntenic to those not only in human T-ALL but also in diverse human haematopoietic, mesenchymal and epithelial tumours. These results indicate that murine and human tumours experience common biological processes driven by orthologous genetic events in their malignant evolution. The highly concordant nature of genomic events encourages the use of genomically unstable murine cancer models in the discovery of biological driver events in the human oncogenome.

Date: 2007
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DOI: 10.1038/nature05886

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