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Glioblastomas with oligodendroglial component – common origin of the different histological parts and genetic subclassification

Article type: Research Article

Authors: Klink, Barbara; | Schlingelhof, Ben | Klink, Martin; | Stout-Weider, Karen; | Patt, Stephan | Schrock, Evelin

Affiliations: Institut für Klinische Genetik, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany | Institut für Pathologie, Medizinische Fakultät, Friedrich-Schiller Universität Jena, Jena, Germany

Note: [] Corresponding author: Barbara Klink, Institute of Clinical Genetics, University of Technology, Dresden, Fetscherstr. 74, D-01307 Dresden, Germany. Tel.: +49 351 458 2894; Fax: +49 351 458 6337; E-mail: [email protected].

Note: [] Current address: Deutscher Wetterdienst, 14473 Potsdam, Germany.

Note: [] Current address: Charité-Universitätsmedizin Berlin, Institut für Medizinische Genetik, Augustenburger Platz 1, 13353 Berlin, Germany.

Keywords: Glioblastoma, oligodendroglial component, GBMO, genetics, CGH, Interphase-FISH, genetic subclassification

DOI: 10.3233/ACP-CLO-2010-0530

Journal: Analytical Cellular Pathology, vol. 33, no. 1, pp. 37-54, 2010

Published: 2010
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Abstract

Background: Glioblastomas are the most common and most malignant brain tumors in adults. A small subgroup of glioblastomas contains areas with histological features of oligodendroglial differentiation (GBMO). Our objective was to genetically characterize the oligodendroglial and the astrocytic parts of GBMOs and correlate morphologic and genetic features with clinical data.

Methods: The oligodendroglial and the “classic” glioblastoma parts of 13 GBMO were analyzed separately by interphase fluorescence in situ hybridization (FISH) on paraffin sections using a custom probe set (regions 1p, 1q, 7q, 10q, 17p, 19q, cen18, 21q) and by comparative genomic hybridization (CGH) of microdissected paraffin embedded tumor tissue.

Results: We identified four distinct genetic subtypes in 13 GBMOs: an “astrocytic” subtype (9/13) characterized by +7/−10; an “oligodendroglial” subtype with −1p/−19q (1/13); an “intermediate” subtype showing +7/−1p (1/13), and an “other” subtype having none of the former aberrations typical for gliomas (2/13). The different histological tumor parts of GBMO revealed common genetic changes in all tumors and showed additional aberrations specific for each part.

Conclusion: Our findings demonstrate the monoclonal origin of GBMO followed by the development of the astrocytic and oligodendroglial components. The diagnostic determination of the genetic signatures may allow for a better prognostication of the patients.

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