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Cancer remains the foremost cause of mortality globally, characterized by un-controlled cellular proliferation driven by oncogenic mutations and other factors. These mutations disrupt cellular homeostasis, leading to a spectrum of adverse physiological responses. A key feature of cellular metabolism in cancer is the Warburg effect, in which cancer cells preferentially rely on glycolysis for ATP production, even in the presence of oxygen, to meet their elevated metabolic demands. Traditional interventions have often failed to block this metabolism due to limitations in drug design and administration. The advent of nanomedicine has ushered in new possibilities for cancer treatment, offering precise control over drug release and targeted delivery. By leveraging nanocarriers, it is possible to specifically target the altered metabolic pathways in cancer cells, thereby presenting a promising therapeutic strategy. This review provides a comprehensive examination of the Warburg effect and the cutting-edge advancements in nanomedicine aimed at reprogramming cancer cell metabolism. Particular attention is given to the potential applications of these nanotechnological interventions in treating cancer, highlighting the promising synergy between nanomedicine and metabolic reprogramming as a viable approach to counteract cancer progression.
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http://dx.doi.org/10.1016/j.critrevonc.2025.104922 | DOI Listing |
Adv Sci (Weinh)
September 2025
Key Laboratory of Emergency and Trauma of Ministry of Education, The First Affiliated Hospital, NHC Key Laboratory of Tropical Disease Control, School of Tropical Medicine & The Second Affiliated Hospital, Hainan Medical University, Haikou, 571199, China.
Circulating tumor cells (CTCs) carry intact tumor molecular information, making them invaluable for personalized cancer monitoring. However, conventional capture methods, relying on passive diffusion, suffer from low efficiency due to insufficient collision frequency, severely limiting clinical utility. Herein, a magnetic micromotor-functionalized DNA-array hunter (MMDA hunter) is developed by integrating enzyme-propelled micromotors, magnetic nanoparticles, and nucleic acid aptamers into distinct functional partitions of a DNA tile self-assembly structure.
View Article and Find Full Text PDFPharmacotherapy
September 2025
Department of Biomedical Informatics, School of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Background: Omeprazole, a widely used proton pump inhibitor, has been associated with rare but serious adverse events such as myopathy. Previous research suggests that concurrent use of omeprazole with fluconazole, a potent cytochrome P450 (CYP) 2C19/3A4 inhibitor, may increase the risk of myopathy. However, the contribution of genetic polymorphisms in CYP enzymes remains unclear.
View Article and Find Full Text PDFGenet Med
September 2025
Division of Genetics and Epidemiology, The Institute of Cancer Research, London, UK; The Royal Marsden NHS Foundation Trust, Fulham Road, London, UK. Electronic address:
Purpose: Hereditary Leiomyomatosis and Renal Cell Cancer (HLRCC) is a rare cancer susceptibility syndrome exclusively attributable to pathogenic variants in FH (HGNC:3700). This paper quantitatively weights the phenotypic context (PP4/PS4) of such very rare variants in FH.
Methods: We collated clinical diagnostic testing data on germline FH variants from 387 individuals with HLRCC and 1,780 individuals with renal cancer, and compared the frequency of 'very rare' variants in each phenotypic cohort against 562,295 population controls.
ESC Heart Fail
September 2025
Department of Clinical and Molecular Medicine, Sapienza University, Rome, Italy.
Heart failure (HF) is a multifactorial and pathophysiological complex syndrome, involving not only neurohormonal activation but also oxidative stress, chronic low-grade inflammation, and metabolic derangements. Central to the cellular defence against oxidative damage is nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor that orchestrates antioxidant and cytoprotective responses. Preclinical in vitro and in vivo studies reveal that Nrf2 signalling is consistently impaired in HF, contributing to the progression of myocardial dysfunction.
View Article and Find Full Text PDFMult Scler
September 2025
Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA.
Background: Tumefactive demyelination (TD) is a rare variant of multiple sclerosis (MS) characterized by tumor-like lesions that often require aggressive management. Genome-wide association studies (GWAS) identified variants associated with MS; similar analyses in TD are lacking.
Objective: A GWAS was performed to identify variants associated with TD.