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Targeting the androgen receptor in triple-negative breast cancer: current perspectives
Alain Mina1, Rachel Yoder2, Priyanka Sharma1
1Division of Medical Oncology, Department of Internal Medicine, University of Kansas Medical Center, Westwood.
Abstract:
Triple-negative breast cancer (TNBC) is an aggressive subtype associated with frequent recurrence and metastasis. Unlike hormone receptor-positive subtypes, treatment of TNBC is currently limited by the lack of clinically available targeted therapies. Androgen signaling is necessary for normal breast development, and its dysregulation has been implicated in breast tumorigenesis. In recent years, gene expression studies have identified a subset of TNBC that is enriched for androgen receptor (AR) signaling. Interference with androgen signaling in TNBC is promising, and AR-inhibiting drugs have shown antitumorigenic activity in preclinical and proof of concept clinical studies. Recent advances in our understanding of androgenic signaling in TNBC, along with the identification of interacting pathways, are allowing development of the next generation of clinical trials with AR inhibitors. As novel AR-targeting agents are developed and evaluated in clinical trials, it is equally important to establish a robust set of biomarkers for identification of TNBC tumors that are most likely to respond to AR inhibition.
Insights
Triple-negative breast cancer (TNBC) treatment is limited, but targeting androgen receptor (AR) signaling shows promise. Identifying responsive tumors with biomarkers is key for new AR-inhibiting therapies.
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- Triple-negative breast cancer (TNBC) is aggressive with limited targeted therapy options.
- Androgen receptor (AR) signaling is implicated in breast cancer development and progression.
- A subset of TNBC exhibits enrichment for AR signaling.
Purpose of the Study:
- To explore the therapeutic potential of targeting androgen signaling in TNBC.
- To review recent advances in understanding AR signaling in TNBC.
- To highlight the need for biomarkers to guide AR inhibitor therapy.
Main Methods:
- Review of gene expression studies identifying AR-enriched TNBC.
- Analysis of preclinical and early clinical data on AR inhibitors in TNBC.
- Examination of emerging understanding of AR signaling pathways and interactions.
Main Results:
- AR signaling interference demonstrates antitumorigenic activity in TNBC models.
- Novel AR-targeting agents are advancing to next-generation clinical trials.
- Biomarker identification is crucial for patient selection in AR inhibitor trials.
Conclusions:
- Targeting AR signaling represents a promising therapeutic strategy for a subset of TNBC.
- Further research into AR pathways and biomarkers will refine treatment approaches.
- Development of AR inhibitors and companion diagnostics is advancing TNBC treatment.