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Glioblastoma multiforme (GBM) is an aggressive brain tumor, posing significant challenges in diagnosis and treatment, particularly in children. Understanding the pathogenesis, molecular biology, symptom presentation, and imaging features of GBM is vital for effective therapy. This review summarizes current knowledge on pediatric GBM, focusing on diagnosis and treatment. GBM typically arises from the cerebral hemispheres, with gross features marked by heterogeneous morphology and aggressive cell populations. Recent advances in genomic research have shed light on distinct molecular pathways associated with primary and secondary GBMs. Clinical symptoms vary widely, but commonly include neurological deficits and increased intracranial pressure. Magnetic resonance imaging (MRI), with its excellent soft tissue contrast, is crucial for diagnosing and monitoring GBM. Emerging techniques, such as diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI), provide insights into the tumor's microstructure and vascularity, assisting in the development of therapeutic strategies and response assessment. Despite advances in imaging, challenges remain in accurately diagnosing and managing pediatric GBM due to its molecular heterogeneity and unique biological behavior. New therapeutic approaches, including targeted therapies and immunotherapy, offer hope for improving outcomes in children with GBM. Clinical trials are ongoing to evaluate these treatments alongside standard options, such as surgery, radiotherapy, and chemotherapy, to meet the unmet needs of pediatric oncology. A multidisciplinary approach, tailored to the individual characteristics of both the patient and the tumor, is essential to optimize treatment and outcomes for pediatric GBM patients. This review highlights the role of advanced MRI techniques in diagnosis, treatment, and monitoring, while emphasizing the need for further research and clinical trials to develop more effective therapies for this devastating disease.Glioblastoma multiforme (GBM) is a complex and aggressive brain tumor that presents significant diagnostic and therapeutic challenges in both adults and children. Un-derstanding the pathogenesis, molecular biology, symptom presentation, and imaging fea-tures of GBM is vital for effective therapy. This review summarizes current knowledge on pediatric GBM, specifically Pediatric Diffuse High-Grade Gliomas (pHGG), focusing on diagnosis and treatment. GBM typically arises from the cerebral hemispheres, with gross features marked by heterogeneous morphology and aggressive cell populations. Recent ad-vances in genomic research have shed light on distinct molecular pathways associated with primary and secondary GBMs. Clinical symptoms vary widely but commonly include neu-rological deficits and increased intracranial pressure. Magnetic resonance imaging (MRI), with its excellent soft tissue contrast, is crucial for diagnosing and monitoring GBM. Emerg-ing techniques, such as diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI), provide insights into the tumor's microstructure and vascularity, assisting in the de-velopment of therapeutic strategies and response assessment. Despite advances in imaging, challenges remain in accurately diagnosing and managing pediatric GBM due to its molec-ular heterogeneity and unique biological behavior. New therapeutic approaches, including targeted therapies and immunotherapy, offer hope for improving outcomes in children with GBM. Clinical trials are ongoing to evaluate these treatments alongside standard options, such as surgery, radiotherapy, and chemotherapy, to meet the unmet needs of pediatric on-cology. A multidisciplinary approach, tailored to the individual characteristics of both the patient and the tumor, is essential to optimize treatment and outcomes for pediatric GBM patients. This review highlights the role of advanced MRI techniques in diagnosis, treat-ment, and monitoring while emphasizing the need for further research and clinical trials to develop more effective therapies for this devastating disease. Recent studies indicate a me-dian survival rate of 12-18 months for pediatric GBM, with treatment response varying based on molecular subtypes. Clinical trials show that IDH-wild-type tumors exhibit poorer prognosis, whereas targeted therapies are improving outcomes in select patient groups.
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http://dx.doi.org/10.2174/0115680096365252250618115641 | DOI Listing |
J Immunother Cancer
September 2025
Department of Pediatrics, Center for Childhood Cancer and Blood Disorders, Division of Heme/Onc and Bone Marrow Transplant, Children's Hospital Colorado, University of Colorado School of Medicine, Aurora, Colorado, USA
Background: Diffuse midline glioma (DMG) and glioblastoma (GBM) are aggressive brain tumors with limited treatment options. Macrophage phagocytosis is a complex, tightly regulated process governed by competing pro-phagocytic and anti-phagocytic signals. CD47-SIRPα signaling inhibits macrophage activity, while radiotherapy (RT) can enhance tumor immunogenicity.
View Article and Find Full Text PDFNeuro Oncol
September 2025
Leeds Institute of Medical Research, University of Leeds, Leeds, UK.
Background: Glioblastoma (GBM), the most aggressive adult brain cancer, comprises a complex tumour microenvironment (TME) with diverse cellular interactions that drive progression and pathobiology. The aim of this study was to understand how these spatial patterns and interactions evolve with treatment.
Methods: To explore these relationships, we employed imaging mass cytometry to measure the expression of 34 protein markers, enabling the identification of GBM-specific cell types and their interactions at single-cell protein level in paired primary (pre-treatment) and recurrent (post-treatment) GBM samples from five patients.
Cell Commun Signal
September 2025
CNR Institute of Biochemistry and Cell Biology, Monterotondo, Rome, 00015, Italy.
Background: Connexin (Cx) hemichannels (HCs) contribute to glioblastoma (GBM) progression by facilitating intercellular communication and releasing pro-tumorigenic molecules, including ATP and glutamate.
Methods: The efficacy of abEC1.1, a monoclonal antibody that inhibits Cx26, Cx30, and Cx32 HCs, was assessed in vitro by measuring invasion capability, dye and Ca uptake, glutamate and ATP release in patient-derived GBM cultures or organoids.
Neuro Oncol
August 2025
Department of Pathology, Yale School of Medicine, CT, USA.
Background: Therapies for diffuse glioma induce DNA damage response (DDR), and strategies to exploit DDR defects are active areas of investigation. While global DNA methylation profiling effectively classifies gliomas into subtypes, the epigenetic and gene expression patterns of DDR genes, and their contribution to tumor classification and outcomes, have yet to be fully elucidated. Thus, dissecting the DDR epigenetics, gene expression, and single-cell heterogeneity may reveal key molecular characteristics, refine prognosis, and identify novel treatment strategies and resistance mechanisms.
View Article and Find Full Text PDFNeurotherapeutics
August 2025
Department of Neurosurgery, Rostock University Medical Center, University of Rostock, 18057 Rostock, Germany.
Glioblastoma (GBM) is a highly aggressive brain tumor, associated with hypercoagulability and thrombosis. Tumor Treating Fields (TTFields), a non-invasive therapy that uses low-intensity, alternating electric fields to disrupt cancer cell division, prolongs survival when used concomitantly with radiochemotherapy. TTFields-treated patients often exhibit distinct recurrence patterns, suggesting a local interaction between TTFields and tumor-associated coagulation, underlying mechanisms remain unclear.
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