Pan-cancer analysis of whole genomes identifies driver rearrangements promoted by LINE-1 retrotransposition View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2020-02-05

AUTHORS

Bernardo Rodriguez-Martin, Eva G. Alvarez, Adrian Baez-Ortega, Jorge Zamora, Fran Supek, Jonas Demeulemeester, Martin Santamarina, Young Seok Ju, Javier Temes, Daniel Garcia-Souto, Harald Detering, Yilong Li, Jorge Rodriguez-Castro, Ana Dueso-Barroso, Alicia L. Bruzos, Stefan C. Dentro, Miguel G. Blanco, Gianmarco Contino, Daniel Ardeljan, Marta Tojo, Nicola D. Roberts, Sonia Zumalave, Paul A. W. Edwards, Joachim Weischenfeldt, Montserrat Puiggròs, Zechen Chong, Ken Chen, Eunjung Alice Lee, Jeremiah A. Wala, Keiran Raine, Adam Butler, Sebastian M. Waszak, Fabio C. P. Navarro, Steven E. Schumacher, Jean Monlong, Francesco Maura, Niccolo Bolli, Guillaume Bourque, Mark Gerstein, Peter J. Park, David C. Wedge, Rameen Beroukhim, David Torrents, Jan O. Korbel, Inigo Martincorena, Rebecca C. Fitzgerald, Peter Van Loo, Haig H. Kazazian, Kathleen H. Burns, Peter J. Campbell, Jose M. C. Tubio

ABSTRACT

About half of all cancers have somatic integrations of retrotransposons. Here, to characterize their role in oncogenesis, we analyzed the patterns and mechanisms of somatic retrotransposition in 2,954 cancer genomes from 38 histological cancer subtypes within the framework of the Pan-Cancer Analysis of Whole Genomes (PCAWG) project. We identified 19,166 somatically acquired retrotransposition events, which affected 35% of samples and spanned a range of event types. Long interspersed nuclear element (LINE-1; L1 hereafter) insertions emerged as the first most frequent type of somatic structural variation in esophageal adenocarcinoma, and the second most frequent in head-and-neck and colorectal cancers. Aberrant L1 integrations can delete megabase-scale regions of a chromosome, which sometimes leads to the removal of tumor-suppressor genes, and can induce complex translocations and large-scale duplications. Somatic retrotranspositions can also initiate breakage–fusion–bridge cycles, leading to high-level amplification of oncogenes. These observations illuminate a relevant role of L1 retrotransposition in remodeling the cancer genome, with potential implications for the development of human tumors. More... »

PAGES

306-319

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  • Journal

    TITLE

    Nature Genetics

    ISSUE

    3

    VOLUME

    52

    Author Affiliations

  • Biomedical Research Centre (CINBIO), University of Vigo, Vigo, Spain
  • Transmissible Cancer Group, Department of Veterinary Medicine, University of Cambridge, Cambridge, UK
  • Department of Zoology, Genetics and Physical Anthropology, Universidade de Santiago de Compostela, Santiago de Compostela, Spain
  • Institucio Catalana de Recerca i Estudis Avançats (ICREA), Barcelona, Spain
  • Department of Human Genetics, University of Leuven, Leuven, Belgium
  • Cancer Ageing and Somatic Mutation Programme, Wellcome Sanger Institute, Cambridge, UK
  • Genomes and Disease, Centre for Research in Molecular Medicine and Chronic Diseases (CIMUS), Universidade de Santiago de Compostela, Santiago de Compostela, Spain
  • Galicia Sur Health Research Institute, Vigo, Spain
  • Faculty of Science and Technology, University of Vic—Central University of Catalonia (UVic-UCC), Vic, Spain
  • Oxford Big Data Institute, University of Oxford, Oxford, UK
  • Department of Biochemistry and Molecular Biology, Universidade de Santiago de Compostela, Santiago de Compostela, Spain
  • Medical Research Council (MRC) Cancer Unit, University of Cambridge, Cambridge, UK
  • Department of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Baltimore, MD, USA
  • Department of Biochemistry, Genetics and Immunology, University of Vigo, Vigo, Spain
  • Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK
  • European Molecular Biology Laboratory (EMBL), Genome Biology Unit, Heidelberg, Germany
  • Barcelona Supercomputing Center (BSC-CNS), Barcelona, Spain
  • Department of Genetics and Informatics Institute, University of Alabama at Birmingham (UAB) School of Medicine, Birmingham, AL, USA
  • Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
  • The Broad Institute of Harvard and MIT, Cambridge, MA, USA
  • Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA
  • Department of Computer Science, Yale University, New Haven, CT, USA
  • Department of Human Genetics, McGill University, Montreal, Québec, Canada
  • Department of Medical Oncology and Hematology, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy
  • Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA
  • Department of Biomedical Informatics, Harvard Medical School, Boston, MA, USA
  • Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Baltimore, MD, USA
  • Department of Haematology, University of Cambridge, Cambridge, UK
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41588-019-0562-0

    DOI

    http://dx.doi.org/10.1038/s41588-019-0562-0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1124596160

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/32024998


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