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Defined human primary cell model systems with growth dependence on oncogenes are highly requested to investigate tumor pathogenesis and to validate pharmacological inhibitors that specifically target oncoproteins and their executing protein complex partners. In acute myeloid leukemia (AML), transcription factors such as RUNX1 and MLL1, which are important for normal blood cell development, frequently harbor mutations including chromosomal translocations with other coding genes, resulting in tumor-promoting gain-of-function fusion proteins. These oncoproteins completely modify transcriptional programs, thereby inducing malignant cell phenotypes. A common theme of the chimeric gene products is their physical interaction with a variety of chromatin-modifying effector molecules, including histone acetyltransferases (HATs) and histone deacetylases (HDACs). These aberrant multiprotein machineries disturb gene expression and promote malignant cell growth. In this chapter, we briefly summarize the current understanding regarding AML-associated oncogene-driven human CD34+ blood progenitor cell expansion in ex vivo liquid cultures. We provide a step-by-step protocol to establish oncogene-induced human CD34+ blood progenitor cell cultures suitable to analyze the impact of transcriptional repressor/HDAC activity in these human AML cell models.
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http://dx.doi.org/10.1007/978-1-0716-2788-4_3 | DOI Listing |
Stem Cell Rev Rep
September 2025
Department of Medical Genetics and Prenatal Diagnostics, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
The emergence of organoid models has significantly bridged the gap between traditional cell cultures/animal models and authentic human disease states, particularly for genetic disorders, where their inherent genetic fidelity enables more biologically relevant research directions and enhances translational validity. This review systematically analyzes established organoid models of genetic diseases across organs (e.g.
View Article and Find Full Text PDFHypertens Res
September 2025
Cardiovascular, Renal, Metabolism Epidemiology, BioPharmaceuticals Medical, AstraZeneca, Cambridge, UK.
This study examined trends in the proportion of adults with self-reported hypertension and in antihypertensive medication use among community-dwelling Australian adults. We analysed data from a longitudinal panel study, covering four waves: 2009 (n = 8023), 2013 (n = 11,475), 2017 (n = 12,843), and 2021 (n = 14,571) for adults aged 18-74 years. Hypertension and antihypertensive medication use were self-reported.
View Article and Find Full Text PDFNat Nanotechnol
September 2025
Department of Bioengineering, Rice University, Houston, TX, USA.
Maintaining safe and potent drug levels in vivo is challenging. Multidomain peptides assemble into supramolecular hydrogels with a well-defined, highly porous nanostructure that makes them attractive for drug delivery. However, their ability to extend release is typically limited by rapid drug diffusion.
View Article and Find Full Text PDFCommun Med (Lond)
September 2025
Department of Microbiology and Immunology, Bio21 Institute and The Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC, Australia.
Background: Mixed-species, mixed-strain plasmodia infections are known to occur in humans in malaria endemic areas. It may be surprising that to date, the extent of this complexity has not been systematically explored in high-burden countries of sub-Saharan Africa, especially in the reservoir of asymptomatic infections in all ages, which sustains transmission.
Methods: Here we take a metagenomic lens to these infections by sampling variable blood volumes from 188 afebrile residents living in high, seasonal transmission in Northern Sahelian Ghana.
Nat Commun
September 2025
Institute of Computational Biology, German Research Center for Environmental Health, Helmholtz Zentrum München, Neuherberg, Germany.
Atherosclerosis, a major cause of cardiovascular diseases, is characterized by the buildup of lipids and chronic inflammation in the arteries, leading to plaque formation and potential rupture. Despite recent advances in single-cell transcriptomics (scRNA-seq), the underlying immune mechanisms and transformations in structural cells driving plaque progression remain incompletely defined. Existing datasets often lack comprehensive coverage and consistent annotations, limiting the utility of downstream analyses.
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