Isolated nuclei prepared from fresh-frozen tissue specimens were used to investigate structural aberrations of chromosome 17 in 18 malignant gliomas (7 anaplastic astrocytomas, 11 glioblastomas). Nuclear DNA was hybridized with four DNA probes specific for centromeric (D17ZI), telomeric (Tel 17p, Tel 17q) and 17p 13.1 sequences (p53) of chromosome 17, using fluorescence in situ hybridization (FISH). The rates of nuclei with one signal (OS) for Tel 17p and p53 were significantly higher than those for D17ZI and Tel 17q. This indicated that the majority of chromosome 17 aberrations was a deletion of the short arm including the p53 gene. When compared with the histological grading, the rates of OS for Tel 17p and p53 in anaplastic astrocytomas were higher than those of glioblastomas, suggesting that the deletion may be associated with the early events in tumorigenesis and that some glioblastomas without chromosome 17 aberrations may be independent from tumour progression via low-grade gliomas.