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    Loss of chromosome 1p/19q in oligodendroglial tumors: refinement of chromosomal critical regions and evaluation of internexin immunostaining as a surrogate marker.

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    Authors
    Buckley, Patrick G
    Alcock, Leah
    Heffernan, Josephine
    Woods, Jack
    Brett, Francesca
    Stallings, Raymond L
    Farrell, Michael A
    Affiliation
    The Royal College of Surgeons in Ireland, Cancer Genetics, 2nd Floor York House, York Street, Dublin, Dublin 2, Ireland. pbuckley@rcsi.ie
    Issue Date
    2011-03
    
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    Citation
    Loss of chromosome 1p/19q in oligodendroglial tumors: refinement of chromosomal critical regions and evaluation of internexin immunostaining as a surrogate marker. 2011, 70 (3):177-82 J. Neuropathol. Exp. Neurol.
    Journal
    Journal of neuropathology and experimental neurology
    URI
    http://hdl.handle.net/10147/126071
    DOI
    10.1097/NEN.0b013e31820c765b
    PubMed ID
    21293300
    Abstract
    Loss of chromosome 1p/19q in oligodendrogliomas represents a powerful predictor of good prognosis. Expression of internexin (INA), a neuronal specific intermediate filament protein, has recently been proposed as a surrogate marker for 1p/19q deletion based on the high degree of correlation between both parameters in oligodendrogliomas. The aim of this study was to assess further the diagnostic utility of INA expression in a set of genetically well-characterized oligodendrogliomas. On the basis of a conservative approach for copy number determination, using both comparative genomic hybridization and fluorescent in situ hybridization, INA expression as a surrogate marker for 1p/19q loss had both reduced specificity (80%) and sensitivity (79%) compared with respective values of 86% and 96% reported in the previous report. The histologic interpretation and diagnostic value of INA expression in oligodendrogliomas should therefore be assessed with greater caution when compared with 1p/19q DNA copy number analysis. In addition, DNA copy number aberrations of chromosomes 10, 16, and 17 were detected exclusively in 1p/19q codeleted samples, suggesting that other regions of the genome may contribute to the 1p/19q-deleted tumor phenotype inthese samples.
    Item Type
    Article
    Language
    en
    ISSN
    0022-3069
    ae974a485f413a2113503eed53cd6c53
    10.1097/NEN.0b013e31820c765b
    Scopus Count
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    Beaumont Hospital

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