p53 expression, DNA content and cell proliferation in primary and synchronous metastatic lesions from ovarian surface epithelial-stromal tumours

Eur J Cancer. 1996 Jul;32A(8):1388-93. doi: 10.1016/0959-8049(96)00101-3.

Abstract

The aim of this study was to investigate biological heterogeneity between primary and metastatic ovarian cancer lesions from individual patients as a means of elucidating steps in clinical progression. Cancer tissue from 61 untreated patients with ovarian surface epithelial-stromal tumours was examined. p53 expression detected immunocytochemically by the PAb1801 antibody, DNA content evaluated by flow cytometry, and cell proliferation evaluated as the [3H]thymidine labelling index were investigated in primary tumours and corresponding synchronous metastases. The frequency of p53 positivity was similar in primary (62%) and metastatic (66%) sites, with an agreement between the two lesions from the same patient in 97% of the cases. Similarly, aneuploidy frequency (80%) and DNA indices were superimposable in primary and metastatic lesions from the same patient, with a 94% agreement. The frequency of aneuploidy was higher in p53-positive than in p53-negative lesions. An overall poor agreement (rs = 0.44) was observed for proliferative activity of primary and metastatic lesions, due to a heterogeneous profile in omental with respect to primary tumours, which was mainly evident in p53-positive cancers. Conversely, cell proliferation of peritoneal, abdominal and pelvic lesions was qualitatively similar to that of the primary tumour in 88% of patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Division
  • DNA, Neoplasm / analysis*
  • Female
  • Humans
  • Mitotic Index
  • Neoplasm Proteins / metabolism*
  • Ovarian Neoplasms / genetics*
  • Ovarian Neoplasms / pathology
  • Ploidies
  • Sex Cord-Gonadal Stromal Tumors / genetics*
  • Sex Cord-Gonadal Stromal Tumors / pathology
  • Sex Cord-Gonadal Stromal Tumors / secondary
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • DNA, Neoplasm
  • Neoplasm Proteins
  • Tumor Suppressor Protein p53