Multi-omics approaches reveal that diffuse midline gliomas present altered DNA replication and are susceptible to replication stress therapy.

Background: The fatal diffuse midline gliomas (DMG) are characterized by an undruggable H3K27M mutation in H3.1 or H3.3.

FDFT1 maintains glioblastoma stem cells through activation of the Akt pathway.

Background: Cancer stem cells (CSCs) have unique metabolic characteristics and are hypothesized to contribute significantly to the recurrence and drug resistance of glioblastoma multiforme (GBM). However, the reliance on mitochondrial metabolism and the underlying mechanism of glioblastoma stem cells (GSCs) remains to be elucidated.

Methods: To quantify differential mitochondrial protein expression between GSCs and differentiated cells, a mass spectrum screen was applied by the Stable Isotope Labeling with Amino Acids in Cell Culture (SILAC) technique.

Reliability of high-quantity human brain organoids for modeling microcephaly, glioma invasion and drug screening.

Brain organoids offer unprecedented insights into brain development and disease modeling and hold promise for drug screening. Significant hindrances, however, are morphological and cellular heterogeneity, inter-organoid size differences, cellular stress, and poor reproducibility. Here, we describe a method that reproducibly generates thousands of organoids across multiple hiPSC lines.

Give me a sign(ature): Converging on the CSC of glioblastoma.

The identification of stem cells in glioblastomas has been controversial. In this issue of Neuron, Xie et al. establish gene signatures for cellular states and a quiescent cancer stem cell (qCSC) and demonstrate that the qCSC population expands in recurrence.

Prion protein regulates invasiveness in glioblastoma stem cells.

Background: Glioblastoma (GBM) is an aggressive brain tumor driven by glioblastoma stem cells (GSCs), which represent an appealing target for therapeutic interventions. The cellular prion protein (PrP), a scaffold protein involved in diverse cellular processes, interacts with various membrane and extracellular matrix molecules, influencing tumor biology. Herein, we investigate the impact of PrP expression on GBM.

The Value of Diffusion Tensor Imaging in Differential Diagnosis of Embryonal Tumors Occurring in the Brainstem and Brainstem Gliomas in Pediatric Patients.

Background: There are no apparent distinctions in clinical presentation or conventional imaging findings between brainstem gliomas and embryonal tumors occurring in the brainstem. Our aim was to study the role of diffusion tensor imaging in differentiating embryonal tumors from gliomas of the brainstem.

Methods: Three cases of embryonal tumors occurring in the brainstem and 19 cases of brainstem gliomas were analyzed retrospectively.

Epidemiology and clinical outcomes of childhood central nervous system cancers in a large low-middle income country pediatric oncology center: a report on 5051 kids.

Background: Central nervous system (CNS) tumors are the leading cause of cancer-related deaths in children. While most cases come from low-middle income countries (LMIC) where their prognosis is worse, few epidemiological studies are conducted in these regions.

Methods: We conducted a registry-based cohort study for childhood CNS tumors at Children's Cancer Hospital, Egypt (CCHE) over 15 years.

A High-Throughput Neurosphere-Based Colony Formation Assay to Test Drug and Radiation Sensitivity of Different Patient-Derived Glioblastoma Lines.

The gold standard assay for radiation response is the clonogenic assay, a normalized colony formation assay (CFA) that can capture a broad range of radiation-induced cell death mechanisms. Traditionally, this assay relies on two-dimensional (2D) cell culture conditions with colonies counted by fixing and staining protocols. While some groups have converted these to three-dimensional (3D) conditions, these models still utilize 2D-like media compositions containing serum that are incompatible with stem-like cell models such as brain tumor initiating cells (BTICs) that form self-aggregating spheroids in neural stem cell media.

Clinico-Pathological Features of Diffuse Midline Glioma, H3 K27-Altered in Adults: A Comprehensive Review of the Literature with an Additional Single-Institution Case Series.

Diffuse midline glioma (DMG), H3 K27-altered, is a WHO grade 4 malignant glioma located at midline structures, including the thalamus, brainstem and spinal cord. While H3 K27-altered DMG is more common in pediatric age in which it shows a uniformly aggressive clinical behavior, its occurrence is relatively unusual among adults, and its clinico-pathological and prognostic features are not fully characterized in this age group. In this present paper, a review of the literature, including all cases of adult H3 K27-altered DMG published from January 2010 to December 2023 was performed, and the following clinical parameters were evaluated: sex, age (median and range), anatomic site, median follow-up, leptomeningeal dissemination, local recurrence and treatment.

Role of Podoplanin (PDPN) in Advancing the Progression and Metastasis of Glioblastoma Multiforme (GBM).

Glioblastoma multiforme (GBM) is a malignant primary brain tumor categorized as a Grade 4 astrocytic glioma by the World Health Organization (WHO). Some of the established risk factors of GBM include inherited genetic syndromes, body mass index, alcohol consumption, use of non-steroidal anti-inflammatory drugs (NSAIDs), and therapeutic ionizing radiation. Vascular anomalies, including local and peripheral thrombosis, are common features of GBM.

[Liquid biopsy in diagnosis of central nervous system tumors].

Unlabelled: Tumor tissue samples are necessary for histological diagnosis. Biopsy is associated with certain difficulties, especially in neuro-oncology. An alternative approach (liquid biopsy) is currently being developed.

[Antidepressants as additional drugs for human brain gliomas].

Unlabelled: Glioblastoma (GB) is the most aggressive malignant brain tumor. To date, there is no optimal treatment approach for this disease. Antidepressants with antitumor effects are one of the new therapeutic directions.

PET imaging of the anticancer drug candidate [C]trimebutine in a rat glioma model.

Purpose: Preclinical studies suggest that trimebutine could be a potential treatment for glioblastoma. The aim of this study was to investigate the distribution, kinetics and tumor accumulation of [C]trimebutine.

Method: A proliferation assay and cell scratch healing assay were performed to confirm the antitumor effects of trimebutine on C6 glioma cells in-vitro.

CCN1 Promotes Mesenchymal Phenotype Transition Through Activating NF-κB Signaling Pathway Regulated by S100A8 in Glioma Stem Cells.

Background: The presence of glioma stem cells (GSCs) and the occurrence of mesenchymal phenotype transition contribute to the miserable prognosis of glioblastoma (GBM). Cellular communication network factor 1 (CCN1) is upregulated within various malignancies and associated with cancer development and progression, while the implications of CCN1 in the phenotype transition and tumorigenicity of GSCs remain unclear.

Methods: Data for bioinformatic analysis were obtained from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) databases.

Characterizing and targeting glioblastoma neuron-tumor networks with retrograde tracing.

Glioblastomas are invasive brain tumors with high therapeutic resistance. Neuron-to-glioma synapses have been shown to promote glioblastoma progression. However, a characterization of tumor-connected neurons has been hampered by a lack of technologies.

Clofazimine enhances anti-glioma effect of immunotherapy.

Rationale: Glioblastoma is one of the most aggressive human brain tumors. The prognosis is unfavorable and treatment effects are relatively low. However, temozolomide (TMZ) chemotherapy may prolong patients' survival.

CD97 maintains tumorigenicity of glioblastoma stem cells via mTORC2 signaling and is targeted by CAR Th9 cells.

Glioblastoma (GBM) stem cells (GSCs) contribute to poor prognosis in patients with GBM. Identifying molecular markers is crucial for developing targeted therapies. Here, we identify cluster of differentiation 97 (CD97) as an optimal GSC surface antigen for potential targeting by chimeric antigen receptor (CAR) T cell therapy through in vitro antibody screening.

Nanotherapeutic strategy against glioblastoma using enzyme inhibitors.

Glioblastoma is the most aggressive brain cancer and thus patients with glioblastoma have a severely low 5-year survival rate (<5 %). Glioblastoma damages neural centers, causing severe depression, anxiety, and cognitive disorders. Glioblastoma is highly resistant to most of available anti-tumor medications, due to heterogeneity of glioblastoma as well as the presence of stem-like cells.