Chromosome abnormalities in human epithelial ovarian malignancies

Gynecol Oncol. 1990 Sep;38(3):473-7. doi: 10.1016/0090-8258(90)90094-2.

Abstract

Karyotypic analysis of tumor specimens from 29 patients with untreated epithelial ovarian carcinoma was performed at the University of Kentucky Medical Center. Twenty-three of the twenty-nine tumors had adequate cells for analysis. Seventeen of these tumors exhibited chromosome abnormalities. Chromosome alterations were complex, with an average of seven different abnormal chromosomal patterns per tumor (range 2-14). Chromosomes 1 and 11 were the most commonly involved, being abnormal in 89 and 83% of tumors, respectively. Chromosomes 3 and 7 were also frequently abnormal. In contrast to invasive tumors, alterations in chromosomes 1 and 11 were not seen in the two tumors of borderline malignant potential. Evidence for DNA amplification of IGF2, Ha-ras-1, and c-ets was not observed. Amplification of the c-erbB-2 oncogene was present in two tumors. These findings indicate that multiple karyotypic abnormalities occur in untreated epithelial ovarian malignancies, with chromosomes 1 and 11 being the most frequently abnormal. These data also suggest that alterations of these chromosomes may be associated with the biologically aggressive behavior of frankly invasive ovarian tumors.

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Blotting, Southern
  • Chromosome Aberrations*
  • Chromosomes, Human, Pair 1
  • Chromosomes, Human, Pair 11
  • Chromosomes, Human, Pair 3
  • Chromosomes, Human, Pair 7
  • ErbB Receptors
  • Female
  • Genes, ras / genetics
  • Humans
  • Insulin-Like Growth Factor II / genetics
  • Karyotyping
  • Middle Aged
  • Multigene Family
  • Ovarian Neoplasms / genetics*
  • Protein-Tyrosine Kinases / genetics
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins c-ets
  • Transcription Factors*

Substances

  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-ets
  • Transcription Factors
  • Insulin-Like Growth Factor II
  • ErbB Receptors
  • Protein-Tyrosine Kinases