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.

The accelerating global demand for sustainable energy, driven by population growth, industrialization, and environmental concerns, has intensified the search for renewable alternatives to fossil fuels. Biofuels, including bioethanol, biodiesel, biogas, and biohydrogen, offer a viable and practical pathway to reducing net carbon dioxide (CO₂) emissions. Yet, their large-scale production remains constrained by biomass recalcitrance, high pretreatment costs, and the enzyme-intensive nature of conversion processes. Recent advances in enzyme immobilization using magnetic nanoparticles (MNPs), covalent organic frameworks, metal–organic frameworks, and biochar have significantly improved enzyme stability, recyclability, and catalytic efficiency. Complementary strategies such as cross-linked enzyme aggregates, carrier-free immobilization, and site-specific attachment further reduce enzyme leaching and operational costs, particularly in lipase-mediated biodiesel synthesis. In addition to biocatalysis, nanozymes—nanomaterials exhibiting enzyme-like activity—are emerging as robust co-catalysts for biomass degradation and upgrading, although challenges in selectivity and environmental safety persist. Green synthesis approaches employing plant extracts, microbes, and agro-industrial wastes are increasingly adopted to produce eco-friendly nanomaterials and bio-derived supports aligned with circular economy principles. These functionalized materials have demonstrated promising performance in esterification, transesterification, and catalytic routes for biohydrogen generation. Technoeconomic and lifecycle assessments emphasize the need to balance catalyst complexity with environmental and economic sustainability. Multifunctional catalysts, process intensification strategies, and engineered thermostable enzymes are improving productivity. Looking forward, pilot-scale validation of green-synthesized nano- and biomaterials, coupled with appropriate regulatory frameworks, will be critical for real-world deployment.

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.