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Gain of 1q and loss of 22 are the most common changes detected by comparative genomic hybridisation in paediatric ependymoma

Authors

  • Samantha Ward,

    1. University Department of Neurosurgery, Institute of Neurology, University College London, National Hospital for Neurology and Neurosurgery, London, United Kingdom
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  • Brian Harding,

    1. Department of Neuropathology, Great Ormond Street Hospital for Children NHS Trust, London, United Kingdom
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  • Peter Wilkins,

    1. Department of Neuropathology, Atkinson Morley's Hospital, London, United Kingdom
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  • William Harkness,

    1. Department of Neurosurgery, Great Ormond Street Hospital for Children NHS Trust, London, United Kingdom
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  • Richard Hayward,

    1. Department of Neurosurgery, Great Ormond Street Hospital for Children NHS Trust, London, United Kingdom
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  • John L. Darling,

    1. University Department of Neurosurgery, Institute of Neurology, University College London, National Hospital for Neurology and Neurosurgery, London, United Kingdom
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  • David G.T. Thomas,

    1. University Department of Neurosurgery, Institute of Neurology, University College London, National Hospital for Neurology and Neurosurgery, London, United Kingdom
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  • Tracy Warr

    Corresponding author
    1. University Department of Neurosurgery, Institute of Neurology, University College London, National Hospital for Neurology and Neurosurgery, London, United Kingdom
    • University Department of Neurosurgery, Institute of Neurology, University College London, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG
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Abstract

Ependymomas are the third most common brain tumour in the paediatric population. Although cytogenetic and molecular analyses have pinpointed deletions of chromosomes 6q, 17, and 22 in a subset of tumours, definitive patterns of genetic aberrations have not been determined. In the present study, we analysed 40 ependymomas from paediatric patients for genomic loss or gain using comparative genomic hybridisation (CGH). Eighteen of the tumours (45%) had no detectable regions of imbalance. In the remaining cases, the most common copy number aberrations were loss of 22 (25% of tumours) and gain of 1q (20%). Three regions of high copy number amplification were noted at 1q24-31 (three cases), 8q21-23 (two cases), and 9p (one case). Although there was no association with the loss or gain of any chromosome arm or with benign versus anaplastic histologic characteristics, the incidence of gain of 7q and 9p and loss of 17 and 22 was significantly higher in recurrent versus primary tumours. This study has identified a number of chromosomal regions that may contain candidate genes involved in the development of different subgroups of ependymoma. © 2001 Wiley-Liss, Inc.

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