Review Series 10.1172/JCI88885

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

Anna C. Groner1,2,3 and Myles Brown1,2

1Department of Medical Oncology and

2Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA.

3Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland.

Address correspondence to: Myles Brown, 450 Brookline Ave., Dana 730, Boston, Massachusetts 02215, USA. Phone: 617.632.3948; E-mail: Myles_Brown@dfci.harvard.edu.

Find articles by Groner, A. in: JCI | PubMed | Google Scholar

1Department of Medical Oncology and

2Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA.

3Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland.

Address correspondence to: Myles Brown, 450 Brookline Ave., Dana 730, Boston, Massachusetts 02215, USA. Phone: 617.632.3948; E-mail: Myles_Brown@dfci.harvard.edu.

Find articles by Brown, M. in: JCI | PubMed | Google Scholar

First published April 3, 2017 - More info

Published in Volume 127, Issue 4 (April 3, 2017)
J Clin Invest. 2017;127(4):1126–1135. doi:10.1172/JCI88885.
Copyright © 2017, American Society for Clinical Investigation

Published April 3, 2017

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.

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