title: Numerical chromosomal aberrations in borderline, benign, and malignant epithelial tumors of the ovary: correlation with p53 protein overexpression and Ki-67.
abstract: OBJECTIVE
  Ovarian tumors of low malignant potential (borderline tumors) have a 5-year survival rate of 69-98%, illustrating that while the prognosis is better than in the typical epithelial carcinoma, a significant number of women still succumb to this disease. The aim of our study was to elucidate the role of numerical chromosomal aberrations in borderline tumors of the ovary in comparison with benign and malignant epithelial tumors in an effort to develop parameters to differentiate prospectively borderline lesions from benign and invasive tumors.
  
  
  METHODS
  Cytologic imprints of surgical specimens of 46 ovarian tumors of low-malignant potential, 17 invasive epithelial carcinomas of the ovary, and 18 benign epithelial tumors of the ovary were examined for numerical chromosomal aberrations (trisomy 7, trisomy 12, and trisomy 17) by fluorescence in situ hybridization (FISH).
  
  
  RESULTS
  In benign tumors no evidence of trisomy 7 and 17 was present. Trisomy 12 was detected in six cases (33.3%). We did not find p53 protein overexpression in any case. Ki-67 stained positive in three cases (16.7%). In borderline tumors trisomy 12 was detected in 33 patients (71.7%). Numerical aberrations of chromosome 17 were absent in all cases. Fourteen patients (30.4%) showed trisomy 7. No immunohistochemical staining reaction for p53 protein was found. Staining of the proliferation marker Ki-67 was observed in two cases (4.3%). In malignant epithelial tumors of the ovary, trisomy 7, trisomy 12, and trisomy 17 were detected in 14 (82.3%), 11 (64.7%), and 5 (29.4%) cases, respectively. Four tumors (23.5%) showed immunohistochemically detected p53 protein overexpression. Thirteen tumors (76.5%) stained for Ki-67.
  
  
  CONCLUSIONS
  Our results indicate that trisomy 7 argues against benign disease. Trisomy 17 was specific for invasive disease, while trisomy 12 is common in borderline tumors of the ovary.
authors.affiliation: Department of Gynecology and Obstetrics, University of Vienna, Medical School, Austria.
authors.forename: P D
authors.initials: PD
authors.lastname: Kohlberger
authors.forename: D G
authors.initials: DG
authors.lastname: Kieback
authors.forename: C
authors.initials: C
authors.lastname: Mian
authors.forename: H
authors.initials: H
authors.lastname: Wiener
authors.forename: C
authors.initials: C
authors.lastname: Kainz
authors.forename: G
authors.initials: G
authors.lastname: Gitsch
authors.forename: G
authors.initials: G
authors.lastname: Breitenecker
mesh_terms: D000328:Adult; D000368:Aged; D002869:Chromosome Aberrations / Q000235:genetics*; D002881:Chromosomes, Human, Pair 12; D002886:Chromosomes, Human, Pair 17; D002897:Chromosomes, Human, Pair 7; D005260:Female; D016158:Genes, p53 / Q000235:genetics*; D006801:Humans; D007150:Immunohistochemistry; D017404:In Situ Hybridization, Fluorescence; D019394:Ki-67 Antigen / Q000235:genetics*; D008875:Middle Aged; D010051:Ovarian Neoplasms / Q000235:genetics / Q000473:pathology*; D014314:Trisomy / Q000235:genetics*; D015854:Up-Regulation
chemical_list: D019394:Ki-67 Antigen