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Androgen receptor in triple negative breast cancer

K M McNamara1, T Yoda, K Takagi

  • 1Department of Anatomical Pathology, Tohoku University School of Graduate Medicine, Japan. kmcnamara@patholo2.med.tohoku.ac.jp

The Journal of Steroid Biochemistry and Molecular Biology
|September 18, 2012
PubMed

Insights

Triple negative breast cancer (TNBC) management is difficult. Androgen receptor (AR) presence in TNBC cells offers potential therapeutic targets, but its role remains unclear, necessitating further research.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Triple-negative breast cancer (TNBC) presents significant clinical challenges due to its aggressive nature and limited targeted therapies.
  • A subset of TNBC cases expresses the androgen receptor (AR), suggesting potential therapeutic avenues through androgen signaling manipulation or AR-targeted treatments.

Purpose of the Study:

  • To review and summarize existing studies on AR positivity rates in TNBC patients.
  • To consolidate findings on the effects of androgens in TNBC cell lines.
  • To investigate the biological significance of AR in TNBC.

Main Methods:

  • Systematic review of literature assessing AR positivity in TNBC patient cohorts.
  • Analysis of in vitro studies examining androgenic effects on TNBC cell lines.
  • Examination of clinical data and survival analyses related to AR expression in TNBC.

Main Results:

  • Reported rates of AR positivity in TNBC vary widely (0-53%), likely due to methodological differences in AR analysis.
  • Most cell line studies indicate androgens promote TNBC proliferation.
  • Preliminary clinical data suggest AR antagonists may improve outcomes for AR-positive TNBC patients.

Conclusions:

  • Conflicting evidence exists regarding AR's role in TNBC: cell line studies suggest proliferation promotion, while some clinical and transfection studies indicate a benign or favorable prognostic role.
  • Discrepancies between in vitro and clinical findings highlight the need for further translational research into androgen action mechanisms in TNBC.

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