Precision medicine, which relies on genomic, multi-omic, phenotypic, and environmental data, has the potential to transform healthcare from population-focused heuristics to individualized prevention, diagnosis, and treatment. Moreover, recent advances in sequencing, molecular profiles, wearable sensors, and machine learning have created opportunities for rapid translational innovation: rapid genomic diagnosis in neonatal and paediatric rare diseases, targeted oncology, pharmacogenomic-based prescribing strategies, and individual sport performance. Nevertheless, the vast majority of innovations remain in centers of specialism or pilot programs, rather than routinely or equitably integrated into clinical or athletic practice. This narrative review synthesizes translational evidence across the life course—in pregnancy, paediatrics, adult medicine, geriatrics, and sportomics—to find reproducible clinical and performance examples which enable precision-based alternative approaches to management, outcome, or preparation; and to reshape those examples into pragmatic, scalable priorities which minimize inequity, and maximize benefit. We undertook a structured narrative synthesis of peer-reviewed literature, trials, clinician translation programs, implementation studies, and sportomics reports, prioritizing examples that demonstrate utility, reproducibility, and impact. Important findings suggest that multi-omics and rapid sequencing improve diagnostic yield and time to diagnosis. Molecular profiling and circulating tumor DNA help realize adaptive treatment selection. Integrated genomics, metabolomics, wearable physiology, and AI analytics facilitate individualized training, injury-risk stratification, and recovery optimization. But systematic value is limited by insufficient representative validation, dataset bias, poor interoperability, regulatory uncertainty, workforce preparedness, and inequities of access. Converting a promise into population- and performance-level value requires coordinated action across four fronts: representative validation; interoperable, privacy-preserving infrastructures; clinician- and coach-centered implementation; and templates for scalable, cost-sensitive deployment.

Polymers are fundamental components of modern pharmaceutical manufacturing, serving critical roles as excipients, binders, coatings, and matrices for controlled drug delivery systems. However, the conventional production of pharmaceutical polymers relies heavily on petrochemical feedstocks, energy-intensive processes, and hazardous solvents, leading to significant environmental and economic burdens. In recent years, increasing regulatory pressure, environmental awareness, and sustainability goals have driven the pharmaceutical industry toward greener manufacturing strategies. This review critically examines sustainable green polymer production for pharmaceutical applications, with a focus on both environmental and economic impacts. The review discusses the role of polymers in pharmaceutical manufacturing, outlines the limitations of conventional polymer synthesis, and highlights the relevance of green chemistry principles in addressing these challenges. Key green polymer synthesis techniques, including biopolymer production, enzymatic polymerization, microwave-assisted synthesis, supercritical CO₂ processing, and the use of ionic liquids and deep eutectic solvents, are systematically evaluated. Additionally, life-cycle assessment (LCA) approaches are explored to assess the environmental performance of green polymer processes in comparison with traditional methods. Beyond environmental sustainability, this review emphasizes the importance of pharmacoeconomic evaluation in determining the feasibility of adopting green polymers at an industrial scale. Cost–benefit analyses, manufacturing cost comparisons, long-term economic advantages, and health–economic outcomes are discussed in the context of pharmaceutical supply chains. Regulatory perspectives, industrial implementation challenges, and future directions are also addressed. Overall, this review highlights sustainable polymer innovation as a critical pathway toward environmentally responsible, economically viable, and future-ready pharmaceutical manufacturing.

HER2-low breast cancer, also known as IHC 1+ or IHC 2+ without ERBB2 amplification, is a new concept in the biology of breast cancer that has removed the binary classification of HER2-positive or HER2-negative breast cancer. The recent introduction of antibody-drug conjugates (ADCs), such as trastuzumab deruxtecan (T-DXd), has improved therapeutic outcomes for HER2-low breast cancer by demonstrating high efficacy in HER2-low tumors through efficient payload delivery. However, differences in ADC efficacy exist among HER2-low breast cancer patients, with tumor cells showing resistance to ADCs. Recent research indicates that the tumor microenvironment (TME) plays a critical role in determining the efficacy of ADCs against tumor cells. TME creates a barrier to the delivery of ADCs to tumor cells that show resistance to ADCs. This review article aims to highlight the current understanding of the biology of HER2-low breast cancer and its response to ADCs with reference to the tumor microenvironment.

Brain tumors, particularly glioblastoma, remain among the most lethal cancers, with limited survival benefits from current genetic and molecular-targeted approaches. Emerging evidence reveals that beyond oncogenes and mutations, neuronal plasticity, long-term potentiation, synaptic remodeling, and neurotransmitter-driven signaling play a pivotal role in shaping tumor progression and therapeutic response. This convergence of neuroscience and oncology has given rise to the field of cancer neuroscience, which explores the bidirectional interactions between neurons and malignant cells. In this review, we summarize fundamental principles of neuronal plasticity, contrasting physiological roles with pathological reprogramming in brain tumors. We highlight how tumor cells exploit synaptic input, particularly glutamatergic signaling, to enhance proliferation, invasion, and integration into neural circuits. We further discuss how neuronal-driven feedback loops contribute to therapy resistance, including chemoresistance, radioresistance, and immune evasion, mediated through pathways such as mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), and calcium influx. The tumor microenvironment, including astrocytes, microglia, and oligodendrocyte-lineage cells, emerges as an active participant in reinforcing this neuron-tumor ecosystem. Finally, this review explores therapeutic opportunities targeting neuronal plasticity, spanning pharmacological interventions, neuromodulation approaches (transcranial magnetic stimulation (TMS), deep brain stimulation (DBS), optogenetics), and computational/artificial intelligence frameworks that model neuron tumor networks to predict personalized therapy. Also, we propose future directions integrating connect omics, neuroinformatics, and brain organoid models to refine translational strategies.