The aim of this investigation was to explore the relationships between pS3 mutation, DNA aneuploidy, 17p deletions, and clinical stage in ovarian cancer. Nuclear suspensions were obtained by tissue disaggregation, stained with propidium iodide, and analysed on a Coulter EPICS Elite flow cytometer. DNA cell cycle analysis was performed using Multicycle software (Phoenix Flow Systems). DNA extracted from paraffin-embedded archival carcinomashon-tumour tissue was used as template for PCR amplification of the microsatellite dinucleotide repeat polymorphism D17SS13, a locus telomeric to pS3 on 17~13.1. Allele loss at D17SS13 was detected in 64.5 per cent of carcinomas (20 of 31 informative cases). DNA aneuploidy was detected in 20 of 54 (37 per cent) carcinomas. Eight of ten cases previously shown to harbour pS3 mutations showed aneuploid DNA content. Although ten other DNA aneuploid cases had shown no p53 mutations, the results show a statistically significant association between pS3 mutation and DNA aneuploidy (P<O.Ol). Furthermore, the mean DNA index of the DNA aneuploid cases was significantly higher in pS3 mutant cases compared with those showing no pS3 mutation (P=0.02). There was also a significant association between p53 mutations and stage, between ploidy and stage, and between allelic deletions at D17SS13 or p53 and stage, but not between these allelic deletions and ploidy. p53 mutations appear to be associated with DNA aneuploidy in ovarian cancer independently of 17p deletions. pS3 mutations, DNA aneuploidy, and 17p deletions are associated with late stage.