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The clinical course of astrocytoma grade 2 (A2) is highly variable and is not reflected by morphological characteristics. Earlier studies using small series of A2 cases suggest that in situ hybridization (ISH) with chromosome-specific DNA probes allows for frequent detection of aneusomy 1, trisomy 7, and monosomy 10. The role of trisomy 7 in astrocytoma carcinogenesis is disputed, however, because of its presence in non-neoplastic brain tissue, as detected by karyotyping. Our objective was to investigate whether there was a correlation between chromosomal aberrations and survival in a series of 47 cases of A2. All cases were evaluated for numerical aberrations of chromosomes 1, 7, and 10 by ISH. Chromosomal aberrations were detected in 68% of cases of A2. Trisomy/polysomy 7 was seen in 31 cases (66%), 22 of which (47%) had a high percentage of this numerical aberration. Only 11 of these 22 cases also showed aneusomy for 1 or 10. No cells or only a few cells with aberrations were detected in non-neoplastic control samples. Using Kaplan-Meier analysis, trisomy/polysomy 7 correlated significantly with shorter survival. Hence, as determined by ISH, trisomy/polysomy 7 is absent in non-neoplastic brain tissue and is frequently detected in A2, correlating with the malignant progression of the disease.

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The authors examined the use of chromosomal analysis by in situ hybridization to differentiate between nonneoplastic reactive gliosis and astrocytomas in cases in which routine histology was inconclusive. Numerical chromosomal aberrations were found in 80% of low-grade astrocytoma specimens and in none of the reactive gliosis specimens. Aneusomic tumor cells were detected in four of 13 stereotactic samples with an initially inconclusive tissue diagnosis, three of which were later diagnosed as astrocytoma. The in situ hybridization procedure may have additional value in the differential diagnosis of reactive gliosis versus low-grade astrocytoma.