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Triple-negative breast cancer (TNBC) is an aggressive malignancy marked by high heterogeneity, metastatic potential, and a lack of established targeted therapies. This review explores emerging dual-target strategies that concurrently address key biological mechanisms in TNBC, including DNA damage repair, cell cycle regulation, epigenetic modulation, metabolic reprogramming, and immune microenvironment remodeling. By acting on multiple signaling nodes, these strategies demonstrate enhanced efficacy, an ability to overcome resistance, and a potential to reverse immunosuppression. Although challenges in patient selection, toxicity, and mechanistic understanding remain-with most strategies in preclinical or early clinical development-this approach offers a promising path toward precision medicine and improved outcomes for TNBC patients.
Meng et al. (Tue,) studied this question.