PMID- 9360232
OWN - NLM
STAT- MEDLINE
DCOM- 19980205
LR  - 20061115
IS  - 1071-5576 (Print)
IS  - 1071-5576 (Linking)
VI  - 4
IP  - 5
DP  - 1997 Sep-Oct
TI  - Numerical chromosomal aberrations in borderline, benign, and malignant epithelial 
      tumors of the ovary: correlation with p53 protein overexpression and Ki-67.
PG  - 262-4
AB  - 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. CONCLUSION: 
      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.
FAU - Kohlberger, P D
AU  - Kohlberger PD
AD  - Department of Gynecology and Obstetrics, University of Vienna, Medical School, 
      Austria.
FAU - Kieback, D G
AU  - Kieback DG
FAU - Mian, C
AU  - Mian C
FAU - Wiener, H
AU  - Wiener H
FAU - Kainz, C
AU  - Kainz C
FAU - Gitsch, G
AU  - Gitsch G
FAU - Breitenecker, G
AU  - Breitenecker G
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Soc Gynecol Investig
JT  - Journal of the Society for Gynecologic Investigation
JID - 9433806
RN  - 0 (Ki-67 Antigen)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Chromosome Aberrations/*genetics
MH  - *Chromosomes, Human, Pair 12
MH  - *Chromosomes, Human, Pair 17
MH  - *Chromosomes, Human, Pair 7
MH  - Female
MH  - Genes, p53/*genetics
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Hybridization, Fluorescence
MH  - Ki-67 Antigen/*genetics
MH  - Middle Aged
MH  - Ovarian Neoplasms/genetics/*pathology
MH  - Trisomy/*genetics
MH  - Up-Regulation
EDAT- 1997/11/14 00:00
MHDA- 1997/11/14 00:01
CRDT- 1997/11/14 00:00
PHST- 1997/11/14 00:00 [pubmed]
PHST- 1997/11/14 00:01 [medline]
PHST- 1997/11/14 00:00 [entrez]
AID - S1071-5576(97)00061-0 [pii]
PST - ppublish
SO  - J Soc Gynecol Investig. 1997 Sep-Oct;4(5):262-4.