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Tumour angiogenesis is reduced in the Tc1 mouse model of Down’s syndrome

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  • Louise E. Reynolds

    (Adhesion and Angiogenesis Laboratory, Barts Institute of Cancer, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK)

  • Alan R. Watson

    (Adhesion and Angiogenesis Laboratory, Barts Institute of Cancer, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK)

  • Marianne Baker

    (Adhesion and Angiogenesis Laboratory, Barts Institute of Cancer, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK)

  • Tania A. Jones

    (Neuroscience Centre, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Institute of Cell and Molecular Sciences, 4 Newark Street, London E1 2AD, UK)

  • Gabriela D’Amico

    (Adhesion and Angiogenesis Laboratory, Barts Institute of Cancer, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK)

  • Stephen D. Robinson

    (Adhesion and Angiogenesis Laboratory, Barts Institute of Cancer, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK)

  • Carine Joffre

    (Centre for Tumour Biology, Institute of Cancer, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK)

  • Sarah Garrido-Urbani

    (Centre Medical Universitaire, University of Geneva Medical School (CMU), rue Michel Servet 1, CH-1211 Geneva, Switzerland)

  • Juan Carlos Rodriguez-Manzaneque

    (GENYO, Avenida Del Conocimiento, s/n Armilla 18100, Granada, Spain)

  • Estefanía Martino-Echarri

    (GENYO, Avenida Del Conocimiento, s/n Armilla 18100, Granada, Spain)

  • Michel Aurrand-Lions

    (INSERM, 27, Boulevard Lei Roure, 13009 Marseille, France)

  • Denise Sheer

    (Neuroscience Centre, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Institute of Cell and Molecular Sciences, 4 Newark Street, London E1 2AD, UK)

  • Franca Dagna-Bricarelli

    (Human Genetics Institute, Galliere Hospital, Via Volta 10, 16128 Genoa, Italy)

  • Dean Nizetic

    (Paediatrics Centre, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Institute of Cell and Molecular Sciences, 4 Newark Street, London E1 2AD, UK)

  • Christopher J. McCabe

    (School of Clinical and Experimental Medicine, University of Birmingham)

  • Andrew S. Turnell

    (School of Cancer Sciences, University of Birmingham)

  • Stephanie Kermorgant

    (Centre for Tumour Biology, Institute of Cancer, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK)

  • Beat A. Imhof

    (Centre Medical Universitaire, University of Geneva Medical School (CMU), rue Michel Servet 1, CH-1211 Geneva, Switzerland)

  • Ralf Adams

    (Max Planck Institute for Molecular Biomedicine, Röntgenstrasse 20, D-48149 Münster, Germany)

  • Elizabeth M. C. Fisher

    (UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK)

  • Victor L. J. Tybulewicz

    (MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK)

  • Ian R. Hart

    (Centre for Tumour Biology, Institute of Cancer, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK)

  • Kairbaan M. Hodivala-Dilke

    (Adhesion and Angiogenesis Laboratory, Barts Institute of Cancer, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK)

Abstract

The Down's cancer link Down's syndrome is caused by the presence of an extra copy of chromosome 21 (a state known as trisomy), and it is known that the growth of certain tumours is reduced in this genetic disorder. A study of a mouse model of Down's syndrome points to an antitumour mechanism, the inhibition of tumour angiogenesis by the overexpression of four genes, two putative anti-angiogenic genes (ADAMTS1 and ERG) and two novel endothelial cell-specific genes not previously linked with angiogenesis (JAM-B and PTTG1IP).

Suggested Citation

  • Louise E. Reynolds & Alan R. Watson & Marianne Baker & Tania A. Jones & Gabriela D’Amico & Stephen D. Robinson & Carine Joffre & Sarah Garrido-Urbani & Juan Carlos Rodriguez-Manzaneque & Estefanía Mar, 2010. "Tumour angiogenesis is reduced in the Tc1 mouse model of Down’s syndrome," Nature, Nature, vol. 465(7299), pages 813-817, June.
    • Handle: RePEc:nat:nature:v:465:y:2010:i:7299:d:10.1038_nature09106
    DOI: 10.1038/nature09106
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