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The heterogeneity of triple-negative breast cancer (TNBC) has spurred the exploration of precision therapies based on molecular subtypes, with the androgen receptor (AR)-positive subtype emerging as a potential therapeutic target. The treatment of AR-positive TNBC relies primarily on androgen receptor antagonists, such as enobosarm, bicalutamide, and enzalutamide. To enhance efficacy, researchers are investigating combination therapies that integrate anti-androgen agents with chemotherapy, immunotherapy, or PARP inhibitors. Additionally, studies have revealed that the AR signaling pathway regulates the tumor microenvironment, and AR inhibition may potentiate the efficacy of immune checkpoint inhibitors. However, anti-AR therapies face significant limitations and challenges due to multifaceted factors, necessitating further resolution. With continued advancements, AR-targeted therapy holds promise as a critical component of personalized treatment strategies for TNBC.
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http://dx.doi.org/10.1007/s11596-025-00094-4 | DOI Listing |
Breast Cancer Res Treat
September 2025
Department of Pharmacy, Duke University Hospital, Durham, NC, USA.
Purpose: Limited data is available assessing sequencing of antibody drug conjugates (ADCs) in patients with hormone receptor-positive (HR +), human epidermal growth factor 2 (HER2)-negative, HER2-low, and triple-negative metastatic breast cancer (MBC), including patients with brain metastases (BrM) or leptomeningeal disease (LMD). This study assesses the efficacy and safety of sequential sacituzumab govitecan (SG) and trastuzumab deruxtecan (T-DXd) in MBC and impact on chemotherapy (CTX).
Methods: This is a single-center, retrospective, cohort study in adult patients with HR + , HER2-negative, or low MBC who received T-DXd and/or SG.
Oncogene
September 2025
Department of Breast Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Cholesterol biosynthesis is more activated in triple negative breast cancer (TNBC) than in other subtype breast cancer and plays essential role in facilitating TNBC. However, the regulatory network and how cholesterol biosynthesis contribute to TNBC development and progression are not well elucidated. Here, we found that reticulum membrane protein complex 2 (EMC2) is highly expressed in TNBC and predicts short survival of patients.
View Article and Find Full Text PDFMethods Cell Biol
September 2025
LR18ES03 Laboratory of Neurophysiology, Cellular Physiopathology and Valorisation of Biomolecules, Faculty of Science of Tunis, University Tunis El Manar, Tunis, Tunisia. Electronic address:
Breast cancer (BC) represents a major socio-economic challenge worldwide due to its high morbidity and mortality rates. Despite various therapeutic strategies, the heterogeneity of breast cancer and the resistance of tumour cells often lead to treatment failure. Consequently, the use of animal models of BC is crucial for understanding the cellular and molecular mechanisms involved in the different stages of carcinogenesis and for screening new drugs to assess their efficacy, potential safety and side effects.
View Article and Find Full Text PDFCell Signal
September 2025
School of Forensic Medicine, Xinxiang Medical University, Xinxiang, Henan 453003, People's Republic of China.
Triple-negative breast cancer (TNBC) presents a formidable therapeutic challenge due to its aggressive behavior, molecular heterogeneity, and lack of actionable targets. This study identifies activation-induced cytidine deaminase (AID) as a pivotal epigenetic driver reprogramming the tumor microenvironment (TME) via non-canonical regulation of NOTCH signaling. Mechanistically, AID recruits histone acetyltransferase 1 (HAT1) to form a chromatin-remodeling complex that binds the JAG1 promoter region (-1.
View Article and Find Full Text PDFBiochim Biophys Acta Mol Cell Res
September 2025
Institute of Cellular and Organismic Biology, Academia Sinica, Taiwan. Electronic address:
Paclitaxel resistance is a major obstacle to achieving long-term remission in patients with triple-negative breast cancer (TNBC), and effective strategies to overcome drug resistance would have significant clinical impact. In this study, we established a paclitaxel-resistant cell clone, T50R, from the human TNBC cell line MDA-MD-231. Intriguingly, these drug-resistant T50R cells required paclitaxel for proliferation.
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