DNA copy number alterations mark disease progression in paediatric chronic myeloid leukaemia

Authors

  • Naomi E. van der Sligte,

    1. Division of Paediatric Oncology/Haematology, Department of Paediatrics, Beatrix Children's Hospital, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands
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    • These authors contributed equally.
  • Manuela Krumbholz,

    1. Department of Paediatrics, University Hospital Erlangen, Erlangen, Germany
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    • These authors contributed equally.
  • Agata Pastorczak,

    1. Laboratory of Paediatric Oncology, Radboud University Medical centre, Nijmegen, The Netherlands
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    • These authors contributed equally.
  • Blanca Scheijen,

    1. Laboratory of Paediatric Oncology, Radboud University Medical centre, Nijmegen, The Netherlands
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  • Josephine T. Tauer,

    1. Department of Paediatrics, University Hospital “Carl Gustav Carus”, Dresden, Germany
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  • Christina Nowasz,

    1. Department of Paediatrics, University Hospital “Carl Gustav Carus”, Dresden, Germany
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  • Edwin Sonneveld,

    1. Dutch Childhood Oncology Group, The Hague, The Netherlands
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  • Geertruida H. de Bock,

    1. Department of Epidemiology, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands
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  • Tiny G. J. Meeuwsen-de Boer,

    1. Division of Paediatric Oncology/Haematology, Department of Paediatrics, Beatrix Children's Hospital, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands
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  • Simon van Reijmersdal,

    1. Department of Human Genetics, Radboud University Medical Centre, Nijmegen, The Netherlands
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  • Roland P. Kuiper,

    1. Department of Human Genetics, Radboud University Medical Centre, Nijmegen, The Netherlands
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  • Jutta Bradtke,

    1. Oncogenetic laboratory, Institute of Pathology, University Hospital Giessen and Marburg, Giessen and Marburg, Germany
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  • Markus Metzler,

    1. Department of Paediatrics, University Hospital Erlangen, Erlangen, Germany
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    • Contributed equally as senior authors.
  • Meinolf Suttorp,

    1. Department of Paediatrics, University Hospital “Carl Gustav Carus”, Dresden, Germany
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    • Contributed equally as senior authors.
  • Evelina S. J. M. de Bont,

    Corresponding author
    1. Division of Paediatric Oncology/Haematology, Department of Paediatrics, Beatrix Children's Hospital, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands
    • Correspondence: Evelina S. J. M. de Bont MD, PhD, Division of Paediatric Oncology/Haematology, Department of Paediatrics, Beatrix Children's Hospital, University Medical Centre Groningen, University of Groningen, PO Box 30.001, Groningen 9700 RB, The Netherlands. E-mail: e.s.j.m.de.bont@umcg.nl

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    • Contributed equally as senior authors.
  • Frank N. van Leeuwen

    1. Laboratory of Paediatric Oncology, Radboud University Medical centre, Nijmegen, The Netherlands
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    • Contributed equally as senior authors.

Errata

This article is corrected by:

  1. Errata: Erratum Volume 167, Issue 4, 584, Article first published online: 27 October 2014

Summary

Early recognition of children with chronic phase chronic myeloid leukaemia (CML-CP) at risk for developing a lymphoid blast crisis (LyBC) is desirable, because therapy options in CML-LyBC are limited. We used Multiplex Ligation-dependent Probe Amplification to determine whether B-cell lymphoid leukaemia-specific copy number alterations (CNAs) (e.g. IKZF1, PAX5, CDKN2A deletions) could be detected in CML-CP and may be used to predict disease progression to LyBC. CNAs were detected in all patients with CML-LyBC, but in none of the 77 patients with CML-CP. Based on this study we conclude that CNAs remain a hallmark of disease progression.

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