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Chromosomally unstable mouse tumours have genomic alterations similar to diverse human cancers. 2007
Richard S Maser, and
Bhudipa Choudhury, and
Peter J Campbell, and
Bin Feng, and
Kwok-Kin Wong, and
Alexei Protopopov, and
Jennifer O'Neil, and
Alejandro Gutierrez, and
Elena Ivanova, and
Ilana Perna, and
Eric Lin, and
Vidya Mani, and
Shan Jiang, and
Kate McNamara, and
Sara Zaghlul, and
Sarah Edkins, and
Claire Stevens, and
Cameron Brennan, and
Eric S Martin, and
Ruprecht Wiedemeyer, and
Omar Kabbarah, and
Cristina Nogueira, and
Gavin Histen, and
Jon Aster, and
Marc Mansour, and
Veronique Duke, and
Letizia Foroni, and
Adele K Fielding, and
Anthony H Goldstone, and
Jacob M Rowe, and
Yaoqi A Wang, and
A Thomas Look, and
Michael R Stratton, and
Lynda Chin, and
P Andrew Futreal, and
Ronald A DePinho
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA.
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.
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