Exploring bio-inspired nanomaterials (BINMs) and incorporating them into micro/nanodevices represent a significant development in biomedical applications. Nanomaterials, engineered to imitate biological structures and processes, exhibit distinctive attributes such as exceptional biocompatibility, multifunctionality, and unparalleled versatility. The utilization of BINMs demonstrates significant potential in diverse domains of biomedical micro/nanodevices, encompassing biosensors, targeted drug delivery systems, and advanced tissue engineering constructs. This article thoroughly examines the development and distinctive attributes of various BINMs, including those originating from proteins, DNA, and biomimetic polymers. Significant attention is directed toward incorporating these entities into micro/nanodevices and the subsequent biomedical ramifications that arise. This review explores biomimicry’s structure–function correlations. Synthesis mosaics include bioprocesses, biomolecules, and natural structures. These nanomaterials’ interfaces use biomimetic functionalization and geometric adaptations, transforming drug delivery, nanobiosensing, bio-inspired organ-on-chip systems, cancer-on-chip models, wound healing dressing mats, and antimicrobial surfaces. It provides an in-depth analysis of the existing challenges and proposes prospective strategies to improve the efficiency, performance, and reliability of these devices. Furthermore, this study offers a forward-thinking viewpoint highlighting potential avenues for future exploration and advancement. The objective is to effectively utilize and maximize the application of BINMs in the progression of biomedical micro/nanodevices, thereby propelling this rapidly developing field toward its promising future.

Cancer remains a leading cause of morbidity and mortality worldwide, necessitating ongoing exploration of effective prevention strategies. Micronutrients, vital for maintaining cellular health, offer promising avenues for cancer prevention. This review delineates the critical roles of micronutrients in cancer prevention, elucidating their mechanisms at the cellular level. Focusing on essential vitamins and minerals like Vitamins A, C, D, E, selenium, and zinc, we explore their profound effects on fundamental cellular processes such as DNA repair, oxidative stress regulation, cellular proliferation, and immune surveillance. These nutrients, characterized by their antioxidative, anti-inflammatory, and immune-enhancing properties, have shown potential in reducing the risk of cancer. The article synthesizes outcomes from a broad spectrum of clinical trials, epidemiological studies, and systematic reviews to evaluate the efficacy of micronutrients in thwarting cancer development. This critical analysis explores significant trials, addresses controversies in nutrient efficacy, and highlights the implications for clinical practice and public health policy. The review underscores the importance of integrating nutritional strategies into comprehensive cancer prevention frameworks and suggests directions for future research to optimize the preventive potentials of micronutrients.

Introduction: Increasing epidemiological evidence suggests that diabetes is associated with a modest but significant elevation in breast cancer risk, as well as poorer clinical outcomes following diagnosis. This integrative review critically synthesizes current epidemiological, biological and clinical evidence to elucidate the role of diabetes in breast cancer development and progression among women. Methods: We conducted a structured literature search (2010–2025) to identify original studies examining the relationship between diabetes and breast cancer risk and outcomes. English‐language human studies were included. Titles, abstracts and full texts were screened against predefined criteria, and relevant data were extracted and synthesized narratively. Results: Studies indicate that women with diabetes experience an increased incidence of breast cancer, with stronger associations observed in postmenopausal populations, and partial attenuation of risk following adjustment for obesity, highlighting both shared and independent metabolic contributions. Mechanistically, chronic hyperinsulinemia, altered insulin‐like growth factor signalling, low‐grade systemic inflammation, oxidative stress and oestrogen‐metabolic crosstalk are frequently proposed as biologically plausible pathways through which diabetes may influence breast carcinogenesis, particularly in hormone‐receptor‐positive tumours. Clinically, diabetes has been linked to delayed diagnosis, increased treatment‐related complications, and higher breast cancer‐specific mortality, underscoring the need for integrated metabolic and oncologic care. Conclusion: Diabetes mellitus, particularly type 2 diabetes, is consistently associated in observational studies with a small increment in breast cancer risk and a more clearly adverse impact on survival. Mechanistic and translational evidence supports biologically plausible pathways linking metabolic dysregulation to tumour initiation, progression and treatment tolerance, but definitive causal effects remain uncertain. Medication and biomarker‐based research and practice should be incorporated in metabolic‐oncologic care and research to enhance prevention and outcomes.