Genes Chromosomes and Cancer · 1996 · 99 citations · 16 references
Life SciencesGeneticsMolecular GeneticsCancer GeneticsCytogeneticsMolecular OncologyChromosomal AbnormalitiesComparative Genomic HybridizationLoss Of HeterozygosityMolecular CytogeneticsNumerical Chromosome AbnormalitiesTurner SyndromeAneuploidy In Pediatric TumorsChromosomal RearrangementsChromosome 17P LossGainTurner Syndrome CytogeneticsTurner Syndrome Genetics
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.
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