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    Spectrum of copy number changes in low grade paediatric brain tumours detected by comparative genomic hybdidisation

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    Authors
    Warr, Tracy
    Ward, Samantha
    Idowu, Michael O.
    Gregory, S.
    Darling, John L.
    Thomas, David G.
    Issue Date
    2001
    
    Metadata
    Show full item record
    Other Titles
    In: Abstracts from the 14th International Conference on Brain Tumor Research and Therapy. Asheville, North Carolina, USA. May 27-30, 2001. No.180
    Abstract
    Several different types of low-grade brain tumours arise predominantly in the paediatric population, including astrocytoma, craniopharygioma and choroid plexus papilloma (CPP). As yet, the genetic events that contribute to their development have not been well defined. We have used comparative genomic hybridisation (CGH) to identify regions of genetic loss and gain in a series of 30 low grade tumours comprising 7 pilocytic astrocytoma (WHO grade I), 12 grade II astrocytoma, 5 craniopharyngioma (WHO grade I) and 6 CPP (WHO grade I). In the group of astrocytoma, there were no detectable regions of genomic imbalance in all 7 grade I tumours and in 9 of 12 grade II tumours. The copy number changes in the remaining 3 cases of grade II astrocytoma were gain of 7p and 12p; loss of 1p, 12q and 22; gain of 2q, 3, 8q and 18q, respectively. Similarly, 4 of 5 craniopharyngioma appeared to have normal CGH profiles, although multiple changes including gain of 4, 6q, 8q and 18q and loss of 17, 20q and 22 were observed in the sixth case. In contrast, copy number aberrations were detected in 3 of 6 CPP. In one tumour, gain of 7 was the sole change, whereas gain of 3q and 6q and loss of 9q and 21 were detected in a second case. However, in the remaining CPP all chromosomes except X and Y were involved in copy number changes with gain of 1, 7, 9, 12, 15, 16, 18, 20 and 22 and loss of the remaining autosomes. Overall, genomic imbalance was detected in only 7 of these low grade tumours and it was not possible to identify consistent regions of loss and gain. Considerably larger numbers of each tumour type need to be analysed in order to elucidate the genetic pathways involved in tumourigenesis.
    Citation
    Neuro-oncology, 3(Suppl 1): 310
    Publisher
    Society for Neuro-Oncology and Duke University Press
    Journal
    Neuro-oncology
    URI
    http://hdl.handle.net/2436/30199
    DOI
    10.1093/neuonc/3.Supplement_1.S1
    Additional Links
    http://hdl.handle.net/2436/30199
    Type
    Conference contribution
    Language
    en
    Description
    Abstracts from Neuro-Oncology are provided here courtesy of Society for Neuro-Oncology and Duke University Press.
    ISSN
    1522-8517
    ae974a485f413a2113503eed53cd6c53
    10.1093/neuonc/3.Supplement_1.S1
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    Research Institute in Healthcare Science

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