Growth factor receptors and oncogene expression in prostate cells

Am J Clin Oncol. 1988:11 Suppl 2:S1-7. doi: 10.1097/00000421-198801102-00002.

Abstract

Specimens of benign prostatic hypertrophy (BPH) and prostate carcinoma and prostate cells in culture were assessed for their capacity to bind androgens, radioiodinated EGF, and IGF-I, and to express certain cellular protooncogenes. Prostate cell lines contained receptors for both EGF and IGF-I. Similarly, clinical samples of human diseased prostate contained receptors for both of these factors. Prostate carcinoma contained higher concentrations of EGF receptors based on DNA than did BPH, although it is accepted that BPH may not be the appropriate comparison for carcinoma. Increased EGF receptors were associated circumstantially with a decline in androgen receptors with deteriorating differentiation status and with an increase in expression of c-myc. Androgen receptor concentration correlated with increased expression of c-fos. Deteriorating differentiation status was associated with the appearance or increase in secondary sites with lower affinity for IGF-I. Whereas c-myc expression was increased in all grades of carcinoma compared to BPH, expression of c-H-ras accompanied loss of differentiation. Although those alterations are hindered by tissue heterogeneity and correlations are essentially circumstantial, they may provide clues to the progression of prostate cancer that can be validated in prostate cell lines with similar growth response capabilities.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Line
  • ErbB Receptors / analysis*
  • Humans
  • Male
  • Neoplasms, Hormone-Dependent / analysis
  • Neoplasms, Hormone-Dependent / genetics
  • Oncogenes*
  • Phenotype
  • Prostate / analysis
  • Prostate / cytology*
  • Prostatic Hyperplasia / genetics
  • Prostatic Hyperplasia / metabolism*
  • Prostatic Hyperplasia / pathology
  • Prostatic Neoplasms / analysis*
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / pathology

Substances

  • ErbB Receptors