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http://dx.doi.org/10.1002/advs.202305072 | DOI Listing |
Neurogenetics
September 2025
Nur International University, 54600, Lahore, Punjab, Pakistan.
Huntington's disease (HD) is a progressive, autosomal dominant neurodegenerative disorder characterized by motor dysfunction, cognitive decline, and psychiatric disturbances. It is caused by CAG repeat expansions in the HTT gene, resulting in the formation of mutant huntingtin protein that aggregates and disrupts neuronal function. This review outlines the pathogenesis of HD, including genetic, molecular, and environmental factors.
View Article and Find Full Text PDFClin Chim Acta
September 2025
Department of Hematology and Blood Banking, School of Allied Medical Sciences, Iran University of Medical, Tehran, Iran. Electronic address:
Acute myeloid leukemia (AML) represents a genetically heterogeneous malignancy, with mutations in the nucleophosmin-1 (NPM1) gene identified as the most prevalent and clinically significant molecular biomarkers. These mutations play a crucial pivotal role in the realms of diagnosis, prognosis, and therapeutic decision-making. Although an ideal measurable residual disease (MRD) test has yet to be developed, there is increasing acknowledgment of the significance of advanced molecular methodologies for monitoring MRD in NPM1-mutated (NPM1) AML.
View Article and Find Full Text PDFMicrobiol Spectr
September 2025
Shanghai Public Health Clinical Center & Institutes of Biomedical Science, Shanghai Medical College, Fudan University, Shanghai, China.
Influenza A virus (IAV) relies on the host cellular machinery to support its replication. Understanding these host dependencies can inform the development of novel antiviral strategies. In this study, we identified conserved oligomeric Golgi complex subunit 6 (COG6) as a novel host factor critical for IAV replication through a genome-wide clustered regularly interspaced short palindromic repeats/CRISPR-associated protein 9 (CRISPR/Cas9) knockout screen.
View Article and Find Full Text PDFFront Oncol
August 2025
Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taibah University, Madinah, Saudi Arabia.
mutations drive oncogenesis and therapeutic resistance in myelodysplastic syndromes (MDSs) and acute myeloid leukemia (AML), impairing p53-regulated functions such as apoptosis, immune surveillance, and genomic stability, leading to immune evasion and metabolic reprogramming. The tumor microenvironment in -mutated MDS and AML fosters leukemic progression through cytokine dysregulation, altered metabolism, and immune suppression. Current therapies, including chemotherapy and hypomethylating agents, offer limited efficacy, resulting in poor overall survival rates for these high-risk patients.
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