Hormones and hormone antagonists: mechanisms of action in carcinogenesis of endometrial and breast cancer

Horm Metab Res. 2001 Aug;33(8):451-7. doi: 10.1055/s-2001-16936.

Abstract

Proliferation of breast and endometrial cells is under the control of ovarian steroid hormones (SHs) such as oestrogen and progesterone. They mediate diverse physiological functions via interaction with nuclear-localised steroid hormone receptors (HRs). The SH receptor complex modifies the expression of SH-regulated genes by binding to conserved binding sites in their promoter region or through cross-talk with other transcription factors. In non-malignant tissues, HRs are in balance with other factors regulating proliferation, differentiation and apoptosis. While dysfunction of the regulatory mechanisms is a part of malignant transformation, functional SH receptors can promote growth of SH-responsive tumours. Therefore, anti-hormones that block the interaction of steroid hormones with the SH receptor are useful tools for the treatment of SH-responsive carcinomas. However, a portion of ER-positive breast cancers and most endometrial cancers do not respond to anti-oestrogens and continued treatment results in hormone resistance, mostly without loss of the ER. This review focuses on the mechanisms of action of hormones and anti-hormones in breast and endometrial carcinomas.

Publication types

  • Review

MeSH terms

  • Animals
  • Binding Sites / physiology
  • Breast Neoplasms / drug therapy
  • Breast Neoplasms / metabolism*
  • Disease Progression
  • Endometrial Neoplasms / drug therapy
  • Endometrial Neoplasms / metabolism*
  • Estrogen Receptor Modulators / metabolism*
  • Estrogen Receptor Modulators / therapeutic use
  • Estrogens / metabolism*
  • Female
  • Gene Expression / physiology
  • Hormone Antagonists / metabolism
  • Hormones / metabolism
  • Humans
  • Receptor Cross-Talk / physiology
  • Receptors, Estrogen / metabolism*
  • Receptors, Steroid / metabolism
  • Steroids / metabolism
  • Transcription Factors / metabolism

Substances

  • Estrogen Receptor Modulators
  • Estrogens
  • Hormone Antagonists
  • Hormones
  • Receptors, Estrogen
  • Receptors, Steroid
  • Steroids
  • Transcription Factors