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Androgenic pathway in triple negative invasive ductal tumors: its correlation with tumor cell proliferation

Keely M McNamara1, Tomomi Yoda, Yasuhiro Miki

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

Cancer Science
|February 5, 2013
PubMed

Insights

Androgen receptor (AR) and synthesizing enzymes in triple negative breast cancer (TNBC) may indicate a better prognosis. Their presence correlates with lower cell proliferation, suggesting a potential therapeutic target for TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Triple negative breast cancer (TNBC) lacks targeted therapies, leading to aggressive clinical courses.
  • Androgen receptor (AR) expression is common in TNBC, but its role in disease progression is debated.
  • Androgen synthesis pathways may influence TNBC behavior.

Purpose of the Study:

  • To investigate the expression of AR and androgen synthesizing enzymes (5αR1, 17βHSD5) in TNBC.
  • To correlate AR and enzyme status with clinicopathological features and patient survival.
  • To elucidate the role of androgen signaling in TNBC progression.

Main Methods:

  • Immunohistochemical analysis of AR, 5αR1, and 17βHSD5 in 203 TNBC patient samples.
  • Correlation of protein expression with clinicopathological data (age, stage, tumor size, metastasis, Ki-67).
  • Survival analysis using Kaplan-Meier and Cox proportional hazards models.

Main Results:

  • AR+/enzyme+ TNBC cases showed a significantly lower Ki-67 labeling index.
  • AR and enzyme status correlated positively with tumor diameter, lymph node invasion, and metastasis.
  • Lower Ki-67 was significantly associated with AR and 5αR1 expression.
  • Ki-67 and tumor stage were independent predictors of survival; AR/5αR1 negativity suggested a worse outcome.

Conclusions:

  • Androgen synthesizing pathways and AR expression in TNBC may suppress cell proliferation.
  • The presence of AR and androgen synthesis enzymes could be associated with a better clinical outcome in TNBC.
  • Targeting androgen signaling pathways represents a potential therapeutic strategy for TNBC.

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