| Literature DB >> 8703845 |
E Schröck1, C Blume, M C Meffert, S du Manoir, W Bersch, M Kiessling, T Lozanowa, G Thiel, R Witkowski, T Ried, T Cremer.
Abstract
Consistent tumor-specific chromosomal aberrations have not been described in low-grade astrocytic tumors. The most frequent genetic alterations are mutations of the TP53 tumor suppressor gene and/or loss of heterozygosity (LOH) on 17p that occur in about 30% of the cases in adult patients but that are uncommon in childhood tumors. We used comparative genomic hybridization (CGH) to map DNA copy number alterations in 18 primary low-grade astrocytic tumors (ten adult patients and eight children). A gain of chromosome arm 7q was the most frequent event detected in five of ten astrocytomas (50%) from adult patients, followed by DNA amplification on chromosome arm 8q and gain on 12p (two cases). Loss of chromosomal regions on 1p, 4q, and the X chromosome was observed in two of ten cases [including one patient afflicted with Turner syndrome (45,X)]. In contrast, no consistent changes were observed in low-grade astrocytomas in children. A loss of the X chromosome was the sole aberration detected in two of eight cases using DNA extracted from the normal brain tissue. The findings suggest that a gain of 7q is an early event in the initiation of astrocytomas in adult patients. The discrepant findings in low-grade astrocytic tumors in adults compared to tumors in children support the the hypothesis that there might be different mechanisms responsible for tumor development.Entities:
Mesh:
Year: 1996 PMID: 8703845 DOI: 10.1002/(SICI)1098-2264(199604)15:4<199::AID-GCC1>3.0.CO;2-X
Source DB: PubMed Journal: Genes Chromosomes Cancer ISSN: 1045-2257 Impact factor: 5.006