title: The importance of genomic copy number changes in the prognosis of glioblastoma multiforme.
abstract: Glial tumors are the most common tumors of the nervous system, affecting individuals at any age. Since understanding of the molecular pathologies underlying human gliomas is still very poor, the treatment and therefore prognosis of this malignancy could not yet be improved. In order to determine whether different glioblastoma-associated genomic aberrations may serve as prognostic markers in combination with histopathological findings, 20 primary glioblastoma multiforme tumors were screened by comparative genomic hybridization, and the results were compared with histopathological and clinical features. All tumors showed genomic copy aberrations detected by comparative genomic hybridization. Regional and numerical increases in chromosome 7 copy number were the most frequently seen abnormality (10/20 tumors), followed by loss of chromosome 10 (8/20). Both of these aberrations were associated with shorter surveillance time. Chromosome 12q amplification was detected in seven tumors. Loss of 17p, 1p, and 19q in combination was seen in three cases. One of them was a giant cell GBM, whereas the remaining two cases were still alive. Combination of chromosome 1p and 19q deletions was also seen in a case with long surveillance. According to the preliminary findings of this study, in addition to the EGFR gene, amplification of other genes on chromosome 7 and the deletion of PTEN gene and other cancer-related genes on chromosome 10 appeared important to the development of glioblastoma multiforme and were associated with poor prognosis, whereas the combination of chromosome 1p and 19q deletions seems to be an informative molecular marker for better prognosis. The clinical features and genetic alterations of primary and secondary glioblastoma multiforme should be compared in large series to clarify the effective prognostic markers; and further molecular analyses focused on chromosomes 7 and 10 will be very helpful for understanding the molecular mechanisms underlying the progression of glioblastoma.
authors.affiliation: Department of Neurosurgery, University of Osmangazi, Eskisehir, Turkey. aali@ogu.edu.tr
authors.forename: Ali
authors.initials: A
authors.lastname: Arslantas
authors.forename: Sevilhan
authors.initials: S
authors.lastname: Artan
authors.forename: Ulkü
authors.initials: U
authors.lastname: Oner
authors.forename: Hamza
authors.initials: H
authors.lastname: Müslümanoğlu
authors.forename: Ramazan
authors.initials: R
authors.lastname: Durmaz
authors.forename: Erhan
authors.initials: E
authors.lastname: Cosan
authors.forename: Metin Ant
authors.initials: MA
authors.lastname: Atasoy
authors.forename: Nurettin
authors.initials: N
authors.lastname: Başaran
authors.forename: Eşref
authors.initials: E
authors.lastname: Tel
mesh_terms: D000328:Adult; D000368:Aged; D001932:Brain Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D005260:Female; D018628:Gene Dosage; D005819:Genetic Markers / Q000235:genetics; D005909:Glioblastoma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009693:Nucleic Acid Hybridization; D011379:Prognosis
chemical_list: D005819:Genetic Markers