© 2000 by Society
© 2000 by the Society forNeuro-Oncology
Comparative genetic patterns of glioblastoma multiforme: Potentialdiagnostic tool for tumor classification
Departments of Pathology (R.N.W., B.K.A.R., H.S.F.,S.H.B.), Surgery (H.S.F., A.H.F.), and Pediatrics (H.S.F.), Duke University, Durham, NC27710
1 Address correspondence and reprint requests to Sandra H. Bigner, DukeUniversity Medical Center, Department of Pathology, PO Box 3712, Durham, NC27710.
| Abstract |
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Cytogenetic and molecular genetic studies of glioblastoma multiforme (GBM)have shown that the most frequent alterations are gains of chromosome 7,losses of 9p loci and chromosome 10, and gene amplification, primarily of theepidermal growth factor receptor (EGFR) gene. Although this profileis potentially useful in distinguishing GBM from other tumor types, thetechniques used tend to be labor intensive, and some can detect only gains orlosses of genetic loci. Comparative genomic hybridization (CGH) is a powerfultechnique capable of identifying both gains and losses of DNA sequences. Thepresent study compares the CGH evaluation of 22 GBM with classic cytogenetics,loss of heterozygosity by allelotyping, and gene amplification by Southernblot analysis to determine the reliability of CGH in the geneticcharacterization of GBM. The CGH and karyotypic data were consistent inshowing gain of chromosome 7 accompanied by a loss of chromosome 10 as themost frequent abnormality, followed by a loss of 9p in 17 of 22 GBM cases.Loss of heterozygosity of chromosomes 10 (19/22) and 9p (9/22) loci confirmedthe underrepresentation by CGH. Genomic amplifications were observed by CGH in5 of the 10 cases where gene amplification was detected by Southern blotanalysis. The data show that CGH is equally reliable, compared with the moreestablished genetic methods, for recognizing the prominent genetic alterationsassociated with GBM and support its use as a plausible adjunct to gliomaclassification.
Received March 2, 2000; Accepted April 24, 2000
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