The short arm isochromosome of chromosome 12 and trisomy 12 are well-established chromosomal alterations in human ovarian germ cell tumors. However, numerical aberrations of chromosome 12 in epithelial ovarian tumors (EOTs) are highly controversial; both trisomy 12 and monosomy 12 have been observed. We performed chromosomal in situ hybridization in paraffin-embedded and formalin-fixed tissue sections of 31 EOTs. Twenty-five EOTs could be evaluated statistically (2 mucinous, 11 serous, 5 endometrioid, 3 borderline, and 4 other epithelial-type tumors) to examine the copy number of chromosome 12 and 15. The frequency distribution of hybridization signals with alpha-satellite centromeric DNA probes for chromosome 15 revealed disomy in all cases. However, we found the loss of chromosome 12 in 16 of 25 tumor samples. No correlation was found between the presence of monosomy 12 and the clinical stage of the tumors. Frequent loss of chromosome 12 may indicate that this chromosome is involved in the tumorigenesis of EOTs. Further studies are needed to clarify whether loss of chromosome 12 is an early or late event in ovarian carcinogenesis.