Whole-genome landscapes of major melanoma subtypes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-05-03

AUTHORS

Nicholas K. Hayward, James S. Wilmott, Nicola Waddell, Peter A. Johansson, Matthew A. Field, Katia Nones, Ann-Marie Patch, Hojabr Kakavand, Ludmil B. Alexandrov, Hazel Burke, Valerie Jakrot, Stephen Kazakoff, Oliver Holmes, Conrad Leonard, Radhakrishnan Sabarinathan, Loris Mularoni, Scott Wood, Qinying Xu, Nick Waddell, Varsha Tembe, Gulietta M. Pupo, Ricardo De Paoli-Iseppi, Ricardo E. Vilain, Ping Shang, Loretta M. S. Lau, Rebecca A. Dagg, Sarah-Jane Schramm, Antonia Pritchard, Ken Dutton-Regester, Felicity Newell, Anna Fitzgerald, Catherine A. Shang, Sean M. Grimmond, Hilda A. Pickett, Jean Y. Yang, Jonathan R. Stretch, Andreas Behren, Richard F. Kefford, Peter Hersey, Georgina V. Long, Jonathan Cebon, Mark Shackleton, Andrew J. Spillane, Robyn P. M. Saw, Núria López-Bigas, John V. Pearson, John F. Thompson, Richard A. Scolyer, Graham J. Mann

ABSTRACT

Melanoma of the skin is a common cancer only in Europeans, whereas it arises in internal body surfaces (mucosal sites) and on the hands and feet (acral sites) in people throughout the world. Here we report analysis of whole-genome sequences from cutaneous, acral and mucosal subtypes of melanoma. The heavily mutated landscape of coding and non-coding mutations in cutaneous melanoma resolved novel signatures of mutagenesis attributable to ultraviolet radiation. However, acral and mucosal melanomas were dominated by structural changes and mutation signatures of unknown aetiology, not previously identified in melanoma. The number of genes affected by recurrent mutations disrupting non-coding sequences was similar to that affected by recurrent mutations to coding sequences. Significantly mutated genes included BRAF, CDKN2A, NRAS and TP53 in cutaneous melanoma, BRAF, NRAS and NF1 in acral melanoma and SF3B1 in mucosal melanoma. Mutations affecting the TERT promoter were the most frequent of all; however, neither they nor ATRX mutations, which correlate with alternative telomere lengthening, were associated with greater telomere length. Most melanomas had potentially actionable mutations, most in components of the mitogen-activated protein kinase and phosphoinositol kinase pathways. The whole-genome mutation landscape of melanoma reveals diverse carcinogenic processes across its subtypes, some unrelated to sun exposure, and extends potential involvement of the non-coding genome in its pathogenesis. More... »

PAGES

175-180

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  • Journal

    TITLE

    Nature

    ISSUE

    7653

    VOLUME

    545

    Author Affiliations

  • QIMR Berghofer Medical Research Institute, 4006, Brisbane, Queensland, Australia
  • Discipline of Pathology, Sydney Medical School, The University of Sydney, 2006, Sydney, New South Wales, Australia
  • Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, University of Queensland, 4072, Brisbane, Queensland, Australia
  • Australian Institute of Tropical Health and Medicine, James Cook University, 4878, Cairns, Queensland, Australia
  • Los Alamos National Laboratory, 87545, Los Alamos, New Mexico, USA
  • Melanoma Institute Australia, The University of Sydney, 2065, North SydneySydney, New South Wales, Australia
  • Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain
  • Centre for Cancer Research, Westmead Institute for Medical Research, The University of Sydney, 2145, WestmeadSydney, New South Wales, Australia
  • Children’s Medical Research Institute, The University of Sydney, 2145, WestmeadSydney, New South Wales, Australia
  • Children’s Hospital at Westmead, The University of Sydney, 2145, WestmeadSydney, New South Wales, Australia
  • Bioplatforms Australia, 2109, North RydeSydney, New South Wales, Australia
  • University of Melbourne Centre for Cancer Research, University of Melbourne, 3052, ParkvilleMelbourne, Victoria, Australia
  • School of Mathematics and Statistics, The University of Sydney, 2006, SydneyNew South Wales, Australia
  • Olivia Newton-John Cancer Research Institute, La Trobe University, Austin Health, 3084, HeidelbergMelbourne, Victoria, Australia
  • Macquarie University, 2109, North RydeSydney, New South Wales, Australia
  • Centenary Institute, The University of Sydney, 2006, SydneyNew South Wales, Australia
  • Department of Medical Oncology, Royal North Shore Hospital, St Leonards, 2065, SydneyNew South Wales, Australia
  • Peter MacCallum Cancer Centre and University of Melbourne, 3000, Melbourne, Victoria, Australia
  • Institució Catalana de Recerca i Estudis Avançats (ICREA), 08010, Barcelona, Spain
  • Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Camperdown, 2050, SydneyNew South Wales, Australia
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature22071

    DOI

    http://dx.doi.org/10.1038/nature22071

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1085123990

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28467829


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