Twenty-eight oligodendrogliomas and seven oligoastrocytomas were immunotested by the peroxidase-antiperoxidase (PAP) method with antiglial fibrillary acidic protein (GFAP) serum, anti-Leu 7 monoclonal antibody (Mab), anti-myelin-associated glycoprotein (MAG) Mab, anti-myelin basic protein (MBP) serum, anti-carbonic anhydrase C (CA C) serum and anti-neuron-specific enolase (NSE) serum. The immunoreactivity of their vascular pattern was studied with Ulex europaeus type I lectin (UEA I). According to their morphology and distribution GFAP-positive cells were respectively interpreted as reactive astrocytes, neoplastic astrocytes and neoplastic oligodendrocytes. Reactive astrocytes were found in the tumor, around the tumor and surrounding the supporting blood vessels. Neoplastic astrocytes were mainly found in the oligoastrocytomas and usually closely intermingled with neoplastic oligodendrocytes. GFAP-positive neoplastic oligodendrocytes were found in the typical oligodendrogliomatous areas. They had central nuclei and GFA positivity was mainly found in the perinuclear cytoplasm. They correspond to the "gliofibrillary oligodendrocytes" described by Herpers and Budka. Of the oligodendrogliomas 91% displayed Leu 7 positivity, but anti-Leu 7 cannot be considered as a specific marker for oligodendrogliomas since other neuroepithelial tumors have been reported to react with this antibody. MAG-, CA C- and NSE-positivities were found in a number of tumor cells in a few oligodendrogliomas. All the tumor cells were MBP-negative, but myelin sheaths and fragments of myelin in the infiltrated white matter were clearly demonstrated by this antiserum. UEA I strikingly demonstrated the vascular pattern of the tumors, and its usefulness as a discriminating marker for the supportive endothelial cells was confirmed.
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http://dx.doi.org/10.1007/BF00687942 | DOI Listing |
Redox Biol
December 2024
Department of Health Sciences, School of Medicine, and Center for Translational Research on Autoimmune and Allergic Disease (CAAD), University of Piemonte Orientale, Novara, Italy; Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), University of Piemonte Orientale, Novara, Italy. Electronic address:
Ferroptosis is a recently characterized form of cell death that has gained attention for its roles in both pathological and physiological contexts. The existence of multiple anti-ferroptotic pathways in both neoplastic and healthy cells, along with the critical regulation of iron metabolism involved in lipid peroxides (lipid-ROS) production-the primary mediators of this cell death process-underscores the necessity of precisely controlling or preventing accidental/unwanted ferroptosis. Conversely, dysregulated iron metabolism and alterations in the expression or activity of key anti-ferroptotic components are linked to the development and progression of various human diseases, including multiple sclerosis (MS).
View Article and Find Full Text PDFNat Commun
November 2024
Department of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
Glioblastomas (GBMs) are highly aggressive, infiltrative, and heterogeneous brain tumors driven by complex genetic alterations. The basic-helix-loop-helix (bHLH) transcription factors ASCL1 and OLIG2 are dynamically co-expressed in GBMs; however, their combinatorial roles in regulating the plasticity and heterogeneity of GBM cells are unclear. Here, we show that induction of somatic mutations in subventricular zone (SVZ) progenitor cells leads to the dysregulation of ASCL1 and OLIG2, which then function redundantly and are required for brain tumor formation in a mouse model of GBM.
View Article and Find Full Text PDFSci Adv
November 2024
RNA Institute, Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan University, Wuhan 430072, China.
Comput Biol Med
January 2025
Institute of Molecular Immunology, School of Medicine and Health, Technical University of Munich (TUM), Munich, Germany. Electronic address:
Glioblastoma multiforme (GBM) is the most invasive form of brain tumor, accounting for 5 % of the cases per 100,000 people in various countries. The phosphatase and tensin homolog deleted from chromosome 10 (PTEN) is a well-known tumor suppressor, and its alteration leads to a deleterious effect on GBM progression. The molecular mechanism of tumorigenesis in glial cell types, driven by PTEN status, is yet to be elucidated.
View Article and Find Full Text PDFSci Rep
November 2024
College of Biomedical Engineering, Sichuan University, Chengdu, Sichuan Province, China.
Glioma stem cells have been recognized as key players in glioma recurrence and therapeutic resistance, presenting a promising target for novel treatments. However, the limited understanding of the role glioma stem cells play in the glioma hierarchy has drawn controversy and hindered research translation into therapies. Despite significant advances in our understanding of gene regulatory networks, the dynamics of these networks and their implications for glioma remain elusive.
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