Fourteen human adenocarcinoma specimens were analyzed for somatic abnormalities affecting genes of the ras family. No amplification of the 3 ras genes was detected. Allelic deletion of the Ha-rasl gene (11p15.5) was found to be a very common abnormality in human ovarian adenocarcinomas (4 out of 7 informative cases). However, in these neoplasm deletion of a presumed normal Ha-rasl allele is not a contributory factor in strengthening the tumorigenic effect of a mutated allele. More probably, Ha-rasl allelic losses are markers of larger chromosomal deletions. Analyses at gamma globin loci (11p15.5) and int-2 locus (11q13) provided evidence that the deletions may extend from Ha-rasl locus towards the centromere but never involve loss of the entire chromosome 11. These findings may suggest that a putative tumor suppressor gene closely linked to Ha-rasl in 11p15.5 is involved in ovarian cancerogenesis.