98%
921
2 minutes
20
Glioma is the most common and malignant primary brain tumor. Patients with malignant glioma usually have a poor prognosis due to drug resistance and disease relapse. Cancer stem cells contribute to glioma initiation, progression, resistance, and relapse. Hence, quick identification and efficient understanding of glioma stem cells (GSCs) are of profound importance for therapeutic strategies and outcomes. Ideally, therapeutic approaches will only kill cancer stem cells without harming normal neural stem cells (NSCs) that can inhibit GSCs and are often beneficial. It is key to identify the differences between cancer stem cells and normal NSCs. However, reports detailing an efficient and uniform protocol are scarce, as are comparisons between normal neural and cancer stem cells. Here, we compared different protocols and developed a fast and efficient approach to obtaining high-purity glioma stem cell by tracking observation and optimizing culture conditions. We examined the proliferative and differentiative properties confirming the identities of the GSCs with relevant markers such as Ki67, SRY-box containing gene 2, an intermediate filament protein member nestin, glial fibrillary acidic protein, and s100 calcium-binding protein (s100-beta). Finally, we identified distinct expression differences between GSCs and normal NSCs including cyclin-dependent kinase 4 and tumor protein p53. This study comprehensively describes the features of GSCs, their properties, and regulatory genes with expression differences between them and normal stem cells. Effective approaches to quickly obtaining high-quality GSCs from patients should have the potential to not only help understand the diseases and the resistances but also enable target drug screening and personalized medicine for brain tumor treatment.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8291338 | PMC |
http://dx.doi.org/10.3389/fgene.2021.639858 | DOI Listing |
Haematologica
September 2025
Division of Medical Oncology, University Hospital Basel, Basel, Switzerland; Laboratory of Translational Immuno-Oncology, Department of Biomedicine, University and University Hospital Basel, Basel.
We previously used a disease-specific B cell receptor (BCR) point mutation (IGLV3-21R110) for selective targeting of a high-risk subset of chronic lymphocytic leukemia (CLL) with chimeric antigen receptor (CAR) T cells. Since CLL is a disease of the elderly and a significant fraction of patients is not able to physically tolerate CAR T cell treatment, we explored bispecific antibodies as an alternative for precision targeting of this tumor mutation. Heterodimeric IgG1-based antibodies consisting of a fragment crystallizable region (Fc) attached to both an anti-IGLV3-21R110 Fab and an anti-CD3 (UCHT1) single chain variable fragment (R110-bsAb) selectively killed cell lines engineered to express high levels of the neoepitope as well as primary CLL cells using healthy donor and CLL patient-derived T cells as effectors.
View Article and Find Full Text PDFLiver Int
October 2025
Division of Gastroenterology, Acireale Hospital, Azienda Sanitaria Provinciale di Catania, Catania, Italy.
Background And Aims: Gut-liver axis has been implicated in the pathophysiology of cirrhosis due to metabolic dysfunction-associated steatotic liver disease (MASLD), an in vitro model for studying epithelial gut dysfunction in MASLD is lacking. In this study, we aimed to characterise intestinal organoids derived from subjects with MASLD.
Materials And Methods: Intestinal organoids were obtained from duodenal samples of individuals with non-fibrotic MASLD and with MASLD-cirrhosis.
Adv Healthc Mater
September 2025
Epigenetics Research Laboratory, Institute of Nano Science and Technology, Knowledge City, Sector 81, Mohali, Punjab, 140306, India.
Acute Myeloid Leukemia (AML) is a heterogeneous hematological malignancy with an altered bone marrow microenvironment sheltering leukemic stem cells (LSCs). LSCs are characterized as self-renewing and highly proliferative cancer stem cells and accumulate abnormal genetic and epigenetic factors contributing to their uncontrolled proliferation. Chromosomal translocation t(9;11)(p22;q23) forms fusion oncoprotein, MLL-AF9, and regulates the transcription factor, C-Myb, which is highly expressed in AML.
View Article and Find Full Text PDFBiophys J
September 2025
Laboratory for Multiscale Mechanics and Medical Science, State Key Laboratory for Strength and Vibration of Mechanical Structures, School of Aerospace Engineering, Xi'an Jiaotong University, Xi'an, 710049, China. Electronic address:
The mechanical properties of cells are crucial for elucidating various physiological and pathological processes. Cells are found to exhibit a universal power-law rheological behavior at low frequencies. While they behave in a different manner at high frequency regimes, which leaves the transition region largely unexplored.
View Article and Find Full Text PDFMol Ther
September 2025
Center for Single-Cell Omics, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China; State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Pancreatic Cancer Heterogeneity, Candiolo Cancer Institute
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with poor prognosis, partly due to cancer stem cells (CSCs) that drive progression and treatment resistance. We explored the therapeutic potential of inducing cuproptosis, a copper-dependent regulated cell death, in CSC-enriched PDAC models. Using human and murine PDAC models, we evaluated elesclomol, a copper transport enhancer.
View Article and Find Full Text PDF