Recurrent gain of chromosome arm 7q in low-grade astrocytic tumors studied by comparative genomic hybridization

✍ Scribed by Evelin Schröck; Collin Blume; Marie-Christine Meffert; Stanislas du Manoir; Wolf Bersch; Marika Kiessling; Tanka Lozanowa; Gundula Thiel; Regine Witkowski; Thomas Ried; Thomas Cremer

• Book ID: 102655747
• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 526 KB
• Volume: 15
• Category: Article
• ISSN: 1045-2257
• DOI: 10.1002/(sici)1098-2264(199604)15:4<199::aid-gcc1>3.0.co;2-x

✦ Synopsis

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 I7p 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 m s t 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 Ip, 4q, and the X chromosome was observed in two of ten cases each [including one patient afflicted with Turner syndrome (45,X)l. 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 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 hypothesis that there might be different mechanisms responsible for tumor development. Genes Chromosom Cancer 15:199-205 (1996).