Breast cancer mortality is driven predominantly by metastasis, which affects 20–30% of patients with early-stage disease despite guideline-directed therapies. Because conventional imaging modalities currently lack sensitivity to identify residual disease, molecular-level monitoring must be developed. Circulating tumor DNA (ctDNA) profiling currently enables transformative minimal residual disease (MRD) detection and can quantify tumor burden at low variant allele frequencies. This review provides a comprehensive overview of MRD in breast cancer, including its definition, detection technologies, positivity thresholds, pathophysiology, clinical applications in adjuvant and neoadjuvant settings, ongoing clinical trials, challenges, and future directions. ctDNA-defined MRD has potential as a precision tool for adaptive therapy, and might facilitate post-adjuvant interception, whereby targeted therapies are administered to eradicate micro-metastases before radiographic recurrence. Persistent challenges include MRD assay standardization, subtype-specific MRD thresholds, tumor heterogeneity, and positioning MRD as a potentially valuable tool for precision management in breast cancer.

Pancreatic cancer (PC) is a highly aggressive cancer characterized by a unique tumor microenvironment (TME) that confers resistance to traditional therapies. As the dominant stromal cells in the TME, cancer-associated fibroblasts (CAFs) promote PC progression by modulating the extracellular matrix and interacting with surrounding cells. Numerous PC treatment strategies targeting CAFs have been explored in the past decade. However, targeting different subtypes of CAFs leads to varying therapeutic outcomes, highlighting the intricate and multifaceted nature of CAFs. The heterogeneity and dynamism of CAFs increase the complexity and challenges associated with tumor therapeutics. Currently, combination therapies incorporating CAF-targeted approaches in PC treatment have shown encouraging outcomes in select clinical trials. A comprehensive understanding of CAFs is essential for developing individualized therapeutic approaches. This review outlines the current knowledge of CAF heterogeneity, crosstalk with surrounding cells, and strategies for targeting CAFs in PC, aiming to keep researchers and clinicians up-to-date with the latest information on CAFs in PC.

Tumor cells undergo metabolic reprogramming to adapt to rapid proliferation and harsh microenvironments, as evidenced by aerobic glycolysis. Mitochondria serve as key coordinators of this process. Under internal and environmental stress in tumors, mitochondria reprogram metabolism by balancing energy dynamics, redirecting metabolic routes, communicating via metabolites, and preserving the quality of mitochondria, thus supporting tumor cell survival. Traditional Chinese medicine (TCM) has a key role in modulating mitochondrial reprogramming in tumor cells, possibly disrupting metabolic pathways that are necessary for survival and proliferation. However, the underlying molecular signaling and cellular biological mechanisms need to be elucidated. In this review, we focused on the Key functions of mitochondria in adapting to tumor metabolic reprogramming are the focus of this review and recent advances in and regulatory mechanisms of TCM and nano-pharmaceutical formulations in maintaining mitochondrial homeostasis are discussed. These insights may help understand the role of mitochondria in the pathogenesis of metabolic diseases, such as cancer, and identify therapeutic targets.

Immune checkpoint inhibitors have markedly improved outcomes in patients with multiple advanced malignancies. However, their widespread use has markedly increased the incidence of immune-related adverse events (irAEs). irAEs can affect a wide range of organ systems and are characterized by heterogeneous onset, broad toxicity spectra, and complex management requirements, thus ultimately impairing treatment continuation and patient quality of life. This review systematically summarizes the epidemiological features, clinical progression, and current management of irAEs. Existing guidelines largely focus on acute toxicities but have not provided structured strategies for chronic, delayed-onset, or multisystem irAEs. Moreover, clinical practice is hampered by incomplete multidisciplinary collaboration, insufficient training of oncologists, and fragmented treatment pathways, all of which limit the efficacy of irAE management. We propose incorporating irAE management into core oncology training and call for the establishment of comprehensive interdisciplinary frameworks to ensure the standardized long-term use of immunotherapy.