Chromosomal abnormalities in human glioblastomas: Gain in chromosome 7p correlating with loss in chromosome 10q

• Published in: Molecular carcinogenesis Vol. 36; no. 1; pp. 6 - 14
• Main Authors: del Mar Inda, María, Fan, Xing, Muñoz, Jorge, Perot, Christine, Fauvet, Didier, Danglot, Giselle, Palacio, Ana, Madero, Pilar, Zazpe, Idoya, Portillo, Eduardo, Tuñón, Teresa, Martínez-Peñuela, José María, Alfaro, Jorge, Eiras, José, Bernheim, Alain, Castresana, Javier S.
• Format: Journal Article
• Language: English
• Published: New York Wiley Subscription Services, Inc., A Wiley Company 01-01-2003
• Subjects: Brain Neoplasms - genetics; Chromosome Aberrations; Chromosomes, Human, Pair 10; Chromosomes, Human, Pair 7; comparative genomic hybridization; cyclin-dependent kinase inhibitor 2A; deleted in malignant brain tumors-1; epidermal growth factor receptor; Glioblastoma - genetics; Humans; Nucleic Acid Hybridization; phosphatase and tensin homologue deleted in chromosome 10; Polymerase Chain Reaction
• ISSN: 0899-1987; 1098-2744
• DOI: 10.1002/mc.10085

Various genomic alterations have been detected in glioblastoma. Chromosome 7p, with the epidermal growth factor receptor locus, together with chromosome 10q, with the phosphatase and tensin homologue deleted in chromosome 10 and deleted in malignant brain tumors‐1 loci, and chromosome 9p, with the cyclin‐dependent kinase inhibitor 2A locus, are among the most frequently damaged chromosomal regions in glioblastoma. In this study, we evaluated the genetic status of 32 glioblastomas by comparative genomic hybridization; the sensitivity of comparative genomic hybridization versus differential polymerase chain reaction to detect deletions at the phosphatase and tensin homologue deleted in chromosome 10, deleted in malignant brain tumors‐1, and cyclin‐dependent kinase inhibitor 2A loci and amplifications at the cyclin‐dependent kinase 4 locus; the frequency of genetic lesions (gain or loss) at 16 different selected loci (including oncogenes, tumor‐suppressor genes, and proliferation markers) mapping on 13 different chromosomes; and the possible existence of a statistical association between any pair of molecular markers studied, to subdivide the glioblastoma entity molecularly. Comparative genomic hybridization showed that the most frequent region of gain was chromosome 7p, whereas the most frequent losses occurred on chromosomes 10q and 13q. The only statistically significant association was found for 7p gain and 10q loss. © 2002 Wiley‐Liss, Inc.