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Recurrent gain of chromosome arm 7q in low‐grade astrocytic tumors studied by comparative genomic hybridization
Author(s) -
Schröck Evelin,
Blume Collin,
Meffert MarieChristine,
du Manoir Stanislas,
Bersch Wolf,
Kiessling Marika,
Lozanowa Tanka,
Thiel Gundula,
Witkowski Regine,
Ried Thomas,
Cremer Thomas
Publication year - 1996
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199604)15:4<199::aid-gcc1>3.0.co;2-x
Subject(s) - comparative genomic hybridization , loss of heterozygosity , biology , astrocytoma , chromosome , pathology , fluorescence in situ hybridization , chromosome 7 (human) , glioma , genetics , gene , medicine , allele
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 each [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 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). © 1996 Wiley‐Liss, Inc.