Steroid Hormone Receptor Signaling in Cancer

  • Shinta Cheng
  • Steven P. Balk
Part of the Cancer Treatment and Research book series (CTAR, volume 115)

Summary and Conclusions

SHRs function as hormone activated, sequence specific DNA binding transcription factors that recruit multiple coactivator and other proteins to specific genes and generally stimulate transcription of these genes. SHR may have further genomic actions, that do not involve direct DNA binding, through protein-protein interactions with other sequence specific transcription factors, although these may still involve weak binding to nonconsensus steroid responsive elements in vivo. SHRs also appear to have nongenomic effects mediated through interactions with cytoplasmic signaling proteins. The major functions of SHRs in normal adult tissues appear to involve stimulation of differentiation, rather than proliferation. In contrast, the ERα and AR directly stimulate the growth of breast and prostate cancers, respectively, indicating a critical change in their functions. The ERα and AR appear to undergo further adaptation in tumor cells in response to hormonal therapies, that render these therapies ineffective. Understanding the molecular basis for these changes in SHR function during cancer development and progression may provide new targets for the generation of drugs to prevent and treat steroid stimulated cancers.


Prostate Cancer Estrogen Receptor Androgen Receptor Androgen Deprivation Therapy Estrogen Receptor Alpha 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© Kluwer Academic Publishers 2004

Authors and Affiliations

  • Shinta Cheng
    • 1
  • Steven P. Balk
    • 1
  1. 1.Cancer Biology Program Hematology-Oncology Division Beth Israel Deaconess Medical CenterHarvard Medical SchoolBoston

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