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Glioblastoma (GBM) is a malignant tumor of the central nervous system with high mortality rates. Gene expression profiling may determine the chemosensitivity of GBMs. However, the molecular mechanisms underlying GBM remain to be determined. To screen the novel key genes in its occurrence and development, two glioma databases, GSE122498 and GSE104291, were analyzed in the present study. Bioinformatics analyses were performed using the Database for Annotation, Visualization and Integrated Discovery, the Search Tool for the Retrieval of Interacting Genes, Cytoscape, cBioPortal, and Gene Expression Profiling Interactive Analysis softwares. Patients with recurrent GBM showed worse overall survival rate. Overall, 341 differentially expressed genes (DEGs) were authenticated based on two microarray datasets, which were primarily enriched in 'cell division', 'mitotic nuclear division', 'DNA replication', 'nucleoplasm', 'cytosol, nucleus', 'protein binding', 'ATP binding', 'protein C-terminus binding', 'the cell cycle', 'DNA replication', 'oocyte meiosis' and 'valine'. The protein-protein interaction network was composed of 1,799 edges and 237 nodes. Its significant module had 10 hub genes, and and were significantly associated with carcinogenesis and the development of GBM. The present study indicated that the DEGs and hub genes, identified based on bioinformatics analyses, had significant diagnostic value for patients with GBM.
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http://dx.doi.org/10.3892/ol.2019.10804 | DOI Listing |
Nanotoxicology
September 2025
Department of Biophysics of Environmental Pollution, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
The effect of non-functionalized polystyrene nanoparticles (PS-NPs) with diameters of 29, 44, and 72 nm on plasmid DNA integrity and the expression of genes involved in the architecture of chromatin was investigated in human peripheral blood mononuclear cells (PBMCs). The cells were incubated with PS-NPs at concentrations ranging from 0.001 to 100 µg/mL for 24 hours.
View Article and Find Full Text PDFInt J Gen Med
September 2025
Department of Geriatrics, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, People's Republic of China.
Background: Sepsis is characterized by profound immune and metabolic perturbations, with glycolysis serving as a pivotal modulator of immune responses. However, the molecular mechanisms linking glycolytic reprogramming to immune dysfunction remain poorly defined.
Methods: Transcriptomic profiles of sepsis were obtained from the Gene Expression Omnibus.
Mol Ther Methods Clin Dev
June 2025
Université Paris-Saclay, University Evry, Inserm, Genethon, Integrare Research Unit UMR_S951, 91000 Evry, France.
Pompe disease is a glycogen storage disorder caused by mutations in the acid α-glucosidase (GAA) gene, leading to reduced GAA activity and glycogen accumulation in heart and skeletal muscles. Enzyme replacement therapy with recombinant GAA, the standard of care for Pompe disease, is limited by poor skeletal muscle distribution and immune responses after repeated administrations. The expression of GAA in muscle with adeno-associated virus (AAV) vectors has shown limitations, mainly the low targeting efficiency and immune responses to the transgene.
View Article and Find Full Text PDFMol Ther Methods Clin Dev
June 2025
Eisai Co., Ltd., Tsukuba Research Laboratories, 5-1-3, Tokodai, Tsukuba, Ibaraki 300-2635, Japan.
Liver-humanized chimeric mice (PXB-mice) are widely utilized for predicting human pharmacokinetics (PK) and as human disease models. However, residual metabolic activity of mouse hepatocytes in chimeric mice can interfere with accurate human PK estimation. Lipid nanoparticle (LNP)-formulated small interfering RNA (siRNA) treatment makes it possible to eliminate the shortcomings of chimeras and create new models.
View Article and Find Full Text PDFMol Ther Methods Clin Dev
June 2025
Shanghai Vitalgen BioPharma Co., Ltd., Shanghai 201210, China.
Bietti crystalline dystrophy (BCD) is an autosomal recessive disorder caused by loss-of-function mutations in the gene, characterized by crystal-like lipid deposits in the retina, progressive photoreceptor loss, and retinal pigment epithelium (RPE) deterioration. Currently, there are no approved treatments for BCD. VGR-R01, an investigational gene therapy, uses subretinal administration of recombinant adeno-associated virus type 8 (AAV8) vector to deliver the human CYP4V2 gene.
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