Breast Cancer: Targets and Therapy

Breast Cancer Under Therapeutic Pressure: Adaptive States, Resistance and Emerging Vulnerabilities

Breast cancer treatment has advanced substantially through endocrine therapy, chemotherapy, radiotherapy, HER2-targeted agents, CDK4/6 inhibitors, immunotherapy, antibody-drug conjugates, and other emerging strategies. Yet treatment is not simply a process of eliminating cancer cells. It also imposes powerful selective and biological pressures on tumors and their surrounding microenvironment. In response, surviving cancer cells may enter adaptive cellular states, alter their metabolic and signaling programs, acquire stem-like or dormant phenotypes, and reshape interactions with immune, stromal, and vascular cells. These changes can contribute to residual disease, therapeutic resistance, recurrence, and metastasis. Increasingly, breast cancer should therefore be viewed as a dynamic biological system that evolves during treatment. Understanding how therapeutic pressure reshapes tumor cells and their microenvironment may reveal not only the mechanisms through which breast cancers survive treatment, but also previously unrecognized vulnerabilities created by the adaptation process itself.

Therapeutic resistance remains a major obstacle to durable breast cancer control, but resistance is increasingly understood as a dynamic process rather than a fixed tumor property. Treatment can select resistant clones while simultaneously inducing reversible cell-state transitions, cellular plasticity, immune remodeling, metabolic adaptation, senescence, dormancy, and changes in the extracellular environment. Modern single-cell, spatial, multi-omics, liquid-biopsy, and functional approaches now make it possible to investigate these processes with unprecedented resolution and to track how tumors evolve before, during, and after treatment. Importantly, adaptation may come at a biological cost: the same changes that enable tumor survival can create new molecular dependencies, immune susceptibilities, or therapeutic windows. Defining these vulnerabilities could help move the field beyond documenting resistance toward anticipating, intercepting, or therapeutically exploiting tumor adaptation. Such knowledge may ultimately support more rational treatment combinations, biomarker-guided patient stratification, and strategies designed to prevent or overcome recurrent and treatment-refractory breast cancer.

This Article Collection welcomes basic, translational, and clinical research examining how breast cancer responds and adapts to therapeutic pressure. Topics may include treatment-induced cellular plasticity and state transitions; clonal evolution and tumor heterogeneity; cancer stemness, dormancy, and residual disease; immune and stromal remodeling; metabolic and epigenetic adaptation; mechanisms of resistance to endocrine therapy, chemotherapy, radiotherapy, targeted therapies, immunotherapy, and antibody-drug conjugates; biomarkers of treatment response and resistance; and therapeutic strategies that exploit adaptation-associated vulnerabilities. Studies using single-cell or spatial profiling, multi-omics, liquid biopsy, patient-derived models, organoids, and other advanced experimental approaches are encouraged when they provide biological or translational insight. We particularly welcome Original Research and Review Articles, as well as relevant expert opinion or commentary addressing emerging concepts. Contributions should move beyond descriptive associations wherever possible and clarify how treatment-induced biological changes influence therapeutic response, resistance, recurrence, or opportunities for intervention.

Qinan Yin, MD, PhD is a biomedical and translational researcher at Henan University of Science and Technology, China. His research focuses on precision medicine, translational oncology, tumor immunology, molecular biomarkers, and treatment-induced changes in the tumor microenvironment. His work integrates molecular and cellular biology, multi-omics and computational approaches, and experimental and clinical research to investigate mechanisms of cancer progression and therapeutic response. He has particular interests in radiotherapy, tumor–immune interactions, and strategies to translate mechanistic discoveries into clinically relevant therapeutic opportunities.

Xuewei Zheng, PhD is a researcher in the Precision Medicine Laboratory at Henan University of Science and Technology, China. His research focuses on breast cancer biology, tumor immunology, cancer metabolism, molecular biomarkers, and multi-omics approaches. His recent work has investigated immune evasion and tumor microenvironment remodeling in breast cancer, including the COX-2/PGE2 pathway, macrophage polarization, tumor organoids, and metabolic reprogramming. He has expertise in molecular and cellular biology, tumor organoid models, proteomics, metabolomics, transcriptomics, single-cell analysis, bioinformatics, and machine learning.

­­All manuscripts submitted to this Article Collection will undergo a full peer-review; the Guest Advisor for this Collection will not be handling the manuscripts (unless they are an Editorial Board member).

Please review the journal scope and author submission instructions prior to submitting a manuscript.

The deadline for submitting manuscripts is 1st July 2027.

Please contact Rebecca Turner at rebecca.turner@tandf.co.uk with any questions or requests for discount codes relating to this Article Collection.

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