Role of steroid receptor and coregulator mutations in hormone-dependent cancers

J Clin Invest. 2017 Apr 3;127(4):1126-1135. doi: 10.1172/JCI88885. Epub 2017 Apr 3.

Abstract

Steroid hormones mediate critical lineage-specific developmental and physiologic responses. They function by binding their cognate receptors, which are transcription factors that drive specific gene expression programs. The requirement of most prostate cancers for androgen and most breast cancers for estrogen has led to the development of endocrine therapies that block the action of these hormones in these tumors. While initial endocrine interventions are successful, resistance to therapy often arises. We will review how steroid receptor-dependent genomic signaling is affected by genetic alterations in endocrine therapy resistance. The detailed understanding of these interactions will not only provide improved treatment options to overcome resistance, but, in the future, will also be the basis for implementing precision cancer medicine approaches.

Publication types

  • Review

MeSH terms

  • Androgens / genetics
  • Androgens / metabolism
  • Animals
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / therapy
  • Drug Resistance, Neoplasm / genetics*
  • Estrogens / genetics
  • Estrogens / metabolism
  • Female
  • Humans
  • Male
  • Mutation*
  • Neoplasm Proteins* / genetics
  • Neoplasm Proteins* / metabolism
  • Prostatic Neoplasms*
  • Receptors, Steroid* / genetics
  • Receptors, Steroid* / metabolism
  • Signal Transduction / genetics*

Substances

  • Androgens
  • Estrogens
  • Neoplasm Proteins
  • Receptors, Steroid