PMID- 10398423
OWN - NLM
STAT- MEDLINE
DCOM- 19990805
LR  - 20071114
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 25
IP  - 4
DP  - 1999 Aug
TI  - Analysis of ovarian borderline tumors using comparative genomic hybridization and 
      fluorescence in situ hybridization.
PG  - 307-15
AB  - It is unclear whether ovarian borderline tumors (tumors of low malignant 
      potential) are independent entities or whether they are part of a continuum of 
      tumor progression that culminates in ovarian carcinoma. Little is known about 
      genetic abnormalities in borderline tumors because of the difficulty of growing 
      them in culture for chromosome studies, and because the low ratio of tumor to 
      nontumor cells can interfere with molecular genetic examination. To circumvent 
      these problems, we performed comparative genomic hybridization (CGH) on 10 serous 
      borderline tumors from nine patients, using microdissection to enrich the samples 
      for tumor DNA and reduce contamination from stromal and inflammatory cells. CGH 
      analysis revealed that three of the tumors had detectable chromosomal imbalances, 
      whereas seven were in a balanced state. In those tumors with imbalances, the 
      number of abnormalities ranged from 3-6 per tumor. Additional studies by 
      fluorescence in situ hybridization (FISH) on disaggregated nuclei confirmed the 
      imbalances detected by CGH, revealed one tumor to be hypertriploid, and indicated 
      that the remaining tumors were diploid and in a balanced state. All abnormalities 
      observed in the aneuploid cases are consistent with chromosomal aberrations 
      previously reported for ovarian carinomas, providing further evidence that some 
      borderline tumors are part of a continuum of tumor progression. These results 
      also suggest that there may be different mechanisms leading to borderline tumor 
      formation, including one associated with multiple chromosomal imbalances, and 
      others that do not involve imbalances detectable by CGH. Genes Chromosomes Cancer 
      25:307-315, 1999.
CI  - Copyright 1999 Wiley-Liss, Inc.
FAU - Wolf, N G
AU  - Wolf NG
AD  - Department of Genetics and Center for Human Genetics, Case Western Reserve 
      University and University Hospitals of Cleveland, Ohio 44124, USA.
FAU - Abdul-Karim, F W
AU  - Abdul-Karim FW
FAU - Farver, C
AU  - Farver C
FAU - Schrock, E
AU  - Schrock E
FAU - du Manoir, S
AU  - du Manoir S
FAU - Schwartz, S
AU  - Schwartz S
LA  - eng
GR  - CA-67515/CA/NCI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (DNA, Neoplasm)
SB  - IM
MH  - Adult
MH  - Chromosome Aberrations/genetics
MH  - Chromosome Disorders
MH  - DNA, Neoplasm/analysis
MH  - Female
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Middle Aged
MH  - Nucleic Acid Hybridization
MH  - Ovarian Neoplasms/*genetics
MH  - Ploidies
MH  - Precancerous Conditions/*genetics
EDAT- 1999/07/09 00:00
MHDA- 1999/07/09 00:01
CRDT- 1999/07/09 00:00
PHST- 1999/07/09 00:00 [pubmed]
PHST- 1999/07/09 00:01 [medline]
PHST- 1999/07/09 00:00 [entrez]
AID - 10.1002/(SICI)1098-2264(199908)25:4<307::AID-GCC1>3.0.CO;2-1 [pii]
PST - ppublish
SO  - Genes Chromosomes Cancer. 1999 Aug;25(4):307-15.