| Literature DB >> 28883003 |
Ronan Ulvé1,2,3, Mélanie Rault1,3, Mathieu Bahin1,3, Laetitia Lagoutte1,3, Jérôme Abadie4, Clotilde De Brito1,3, Jean-Michel Coindre5, Nadine Botherel1,3, Audrey Rousseau6, Valentin Wucher1,3, Edouard Cadieu1,3, Catherine Thieblemont7, Christophe Hitte1,3, Laurence Cornevin8, Florian Cabillic8, Laura Bachelot1,3, David Gilot1,3, Benoit Hennuy9, Thierry Guillaudeux3,10, Arnaud Le Goff2,3, Thomas Derrien1,3, Benoît Hédan11,3, Catherine André11,3.
Abstract
Canine cancers represent a tremendous natural resource due to their incidence and striking similarities to human cancers, sharing similar clinical and pathologic features as well as oncogenic events, including identical somatic mutations. Considering the importance of gene fusions as driver alterations, we explored their relevance in canine cancers. We focused on three distinct human-comparable canine cancers representing different tissues and embryonic origins. Through RNA-Seq, we discovered similar gene fusions as those found in their human counterparts: IGK-CCND3 in B-cell lymphoma, MPB-BRAF in glioma, and COL3A1-PDGFB in dermatofibrosarcoma protuberans-like. We showed not only similar partner genes but also identical breakpoints leading to oncogene overexpression. This study demonstrates similar gene fusion partners and mechanisms in human-dog corresponding tumors and allows for selection of targeted therapies in preclinical and clinical trials with pet dogs prior to human trials, within the framework of personalized medicine. Cancer Res; 77(21); 5721-7. ©2017 AACR. ©2017 American Association for Cancer Research.Entities:
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Year: 2017 PMID： 28883003 DOI： 10.1158/0008-5472.CAN-16-2691
Source DB: PubMed Journal: Cancer Res ISSN： 0008-5472 Impact factor: 12.701