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This article is part of the supplement: Abstracts of the 16th International Charles Heidelberger Symposium on Cancer Research

Open Access Poster presentation

Identification of copy number variations of chromosomes 7, 9 and 10 in human glioblastomas by SNP-arrays

Inês Crespo12*, Maria D Tabernero345, Ana B Nieto4, Olinda Rebelo6, Hermínio Tão7, Fernando Gomes7, Catarina R Oliveira18, Maria C Lopes12 and Alberto Orfao4

Author Affiliations

1 Centre for Neurosciences and Cell Biology, University of Coimbra, Coimbra, Portugal

2 Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal

3 Instituto de Estudios de Ciencias de la Salud de Castilla y León, Soria, Spain

4 Centre for Cancer Research (CIC IBMCC-CSIC/USAL), Salamanca, Spain

5 Research Unit of the University Hospital of Salamanca, Salamanca, Spain

6 Neuropathology Laboratory, Neurology Service, University Hospital of Coimbra, Coimbra, Portugal

7 Neurosurgery Service, University Hospital of Coimbra, Coimbra, Portugal

8 Faculty of Medicine, University of Coimbra, Coimbra, Portugal

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BMC Proceedings 2010, 4(Suppl 2):P53  doi:10.1186/1753-6561-4-S2-P53

The electronic version of this article is the complete one and can be found online at:

Published:24 September 2010

© 2010 Crespo et al; licensee BioMed Central Ltd.

Poster presentation

Glioblastomas (GBM) are the most frequent and malignant tumors of the central nervous system. Despite advances in treatment modalities, their prognosis remains dismal and a better knowledge at the molecular and genomic level is still required.

We have previously reported the cytogenetic heterogeneity of gliomas [1]. The aim of the present study was to identify genetically distinct subgroups of GBM, according to similar copy number (CN) profiles for chromosome 7, 9 and 10, and to establish the prognostic value of the different subsets. We also correlated those genetic subgroups with the clinical and biological features of the tumors.

Single-nucleotide polymorphism (SNP)-arrays (Affymetrix 500K) were performed in a group of 35 GBM, to screen for gains, losses, loss of heterozygosity (LOH) and CN neutral LOH (cnLOH).

We identified gains of chromosome 7 (97%) and deletions of chromosome 9 (60%) and chromosome 10 (83%), as the most frequent events in GBM. According to the CN variation observed in these chromosomes four subgroups were disclosed, revealing strong association with patients’ overall survival. GBM with EGFR amplification showed longer survival times when compared to those with no amplification (p = 0.006), or to the other subgroups (p =0.0006).

In conclusion, our results support the concept that the characterization of genomic changes underlying GBM development, along with the recognition of genetic subsets within these tumors, may be useful to predict prognosis behaviour and to better stratify patients.


  1. Vital AL, Tabernero MD, Crespo I, Rebelo O, Tão H, Gomes F, Lopes MC, Orfao A: Intratumoral patterns of clonal evolution in gliomas.

    Neurogenetics 2010, 11:227-39. PubMed Abstract | Publisher Full Text OpenURL