Search Results (596)

Previous in vitro studies have shown the therapeutic potential of bee venom (BV) against different types of glioblastoma cells. Our aim was to evaluate the cytotoxic effect of BV on glioma in the zebrafish model. First, safe concentrations of BV and melittin were determined by determining the LD₅₀ for each substance. Two human glioma cell lines, 8MGBA and LN-229, were used in this study. After staining the tested cells for visualization under UV light, they were then implanted into 2-day-old zebrafish embryos. Zebrafish were incubated for 3 days with crude BV and melittin at concentrations of 1.5 and 2.5 µg/mL vs. control group. Tumor growth was assessed with a stereo microscope. We found differential proliferative responses of two human glioma lines in a zebrafish model. The 8MGBA cell line, but not LN-229, showed proliferative potential when implanted into 2-day-old zebrafish embryos. This study showed a dose-dependent cytotoxic effect only for BV against 8MGBA cells. The observed cytotoxic effect is not dependent on the presence of the peptide melittin—the main BV component with the greatest cytotoxic potential. Simultaneously, a slight increase in LN-229 cell proliferation was observed after 3 days of incubation with melittin at a concentration of 2.5 µg/mL. This indicates that any consideration of bee venom as a therapeutic substance must take into account the type of glioblastoma. Full article

Glioma is a type of neoplasia that spontaneously arises from the glial cells of the brain in humans and dogs, and its prognosis is grave. Current treatment options for glioma include surgery, radiation therapy, chemotherapy, or symptomatic treatment. Evidence has shown that cannabidiol (CBD) may have anticancer, anti-angiogenic, and anti-inflammatory properties in both in vitro and in vivo studies. In this in vivo murine experiment, the canine glioma cell line J3TBG was injected into the frontoparietal cortex of immunodeficient mice using xenogeneic tissue transplantation. A total of 20 mice were randomly assigned to one of four treatment groups—Control group (C), CBD group (CBD), Radiation Therapy group (RT), and CBD plus Radiation Therapy group (CBD + RT). After transplantation of J3TBG, a single fraction of 5.5 Gy RT was administered to the RT and CBD + RT groups, and CBD was administered daily to the CBD and CBD + RT groups. Necropsies were performed to collect blood and brain tissue. Although there was not a statistically significant difference, the survival time among mice were longer in the CBD + RT group than the RT group. These results indicate that CBD may be used as an adjunctive therapy to enhance RT treatment. Larger cohort studies are required to substantiate the hypothesis. Full article

Extracellular vesicles (EVs), nanoscale membrane-enclosed particles, are natural carriers of proteins and nucleic acids. Microalgae are widely used as a source of bioactive substances in the food and cosmetic industries and definitely have a potential to be used as the producers of EVs for biomedical applications. In this study, the extracellular vesicles isolated from the culture medium of two unicellular microalgae, Chlamydomonas reinhardtii (Chlamy-EVs) and Parachlorella kessleri (Chlore-EVs), were characterized by atomic force microscopy (AFM), cryo-electronic microscopy (cryo-EM), and nanoparticle tracking analysis (NTA). The biocompatibility with human cells in vitro (HEK-293T, DF-2 and A172) and biodistribution in mouse organs and tissues in vivo were tested for both microalgal EVs. An exogenous therapeutic protein, human heat shock protein 70 (HSP70), was successfully loaded to Chlamy- and Chlore-EVs, and its efficient delivery to human glioma and colon carcinoma cell lines has been confirmed. Additionally, in order to search for potential therapeutic biomolecules within the EVs, their proteomes have been characterized. A total of 105 proteins were identified for Chlamy-EVs and 33 for Chlore-EVs. The presence of superoxide dismutase and catalase in the Chlamy-EV constituents allows for considering them as antioxidant agents. The effective delivery of exogenous cargo to human cells and the possibility of the particle yield optimization by varying the microalgae growth conditions make them favorable producers of EVs for biotechnology and biomedical application. Full article

Using neural networks has become the standard technique for medical diagnostics, especially in cancer detection and classification. This work evaluates the performance of Vision Transformer architectures, including Swin Transformer and MaxViT, for several datasets of magnetic resonance imaging (MRI) and computed tomography (CT) scans. We used three training sets of images with brain, lung, and kidney tumors. Each dataset included different classification labels, from brain gliomas and meningiomas to benign and malignant lung conditions and kidney anomalies such as cysts and cancers. This work aims to analyze the behavior of the neural networks in each dataset and the benefits of combining different image modalities and tumor classes. We designed several experiments by fine-tuning the models on combined and individual datasets. The results revealed that the Swin Transformer achieved the highest accuracy, with an average of 99.0% on single datasets and reaching 99.43% on the combined dataset. This research highlights the adaptability of Transformer-based models to various human organs and image modalities. The main contribution lies in evaluating multiple ViT architectures across multi-organ tumor datasets, demonstrating their generalization to multi-organ classification. Integrating these models across diverse datasets could mark a significant advance in precision medicine, paving the way for more efficient healthcare solutions. Full article

Oncolytic virotherapy is a rapidly evolving approach to cancer treatment. Our group previously designed VV-GMCSF-Lact, a recombinant oncolytic vaccinia virus targeting solid tumors including gliomas. In this study, we used single-cell RNA sequencing to compare transcriptional responses in human glioma cells, non-malignant brain cells, and immortalized glioblastoma U87 MG cells following infection with this oncolytic virus. We found that proneural glioblastoma cells and microglia-like cells from patient-derived glioma cultures were the most susceptible to VV-GMCSF-Lact. Increased expressions of histones, translational regulators, and ribosomal proteins positively correlated with viral load at the transcript level. Furthermore, higher viral loads were accompanied by a large-scale downregulation of genes involved in mitochondrial translation, metabolism, and oxidative phosphorylation. Levels of early vaccinia virus transcripts are also positively correlated with infection intensity, suggesting that the fate of cells is determined at the early stage of infection. Full article

Background: BCI and AI-driven image segmentation are revolutionizing precision neurosurgery by enhancing surgical accuracy, reducing human error, and improving patient outcomes. Methods: This systematic review explores the integration of AI techniques—particularly DL and CNNs—with neuroimaging modalities such as MRI, CT, EEG, and ECoG for automated brain mapping and tissue classification. Eligible clinical and computational studies, primarily published between 2015 and 2025, were identified via PubMed, Scopus, and IEEE Xplore. The review follows PRISMA guidelines and is registered with the OSF (registration number: J59CY). Results: AI-based segmentation methods have demonstrated Dice similarity coefficients exceeding 0.91 in glioma boundary delineation and tumor segmentation tasks. Concurrently, BCI systems leveraging EEG and SSVEP paradigms have achieved information transfer rates surpassing 22.5 bits/min, enabling high-speed neural decoding with sub-second latency. We critically evaluate real-time neural signal processing pipelines and AI-guided surgical robotics, emphasizing clinical performance and architectural constraints. Integrated systems improve targeting precision and postoperative recovery across select neurosurgical applications. Conclusions: This review consolidates recent advancements in BCI and AI-driven medical imaging, identifies barriers to clinical adoption—including signal reliability, latency bottlenecks, and ethical uncertainties—and outlines research pathways essential for realizing closed-loop, intelligent neurosurgical platforms. Full article

Chronic inflammation is increasingly recognized as a driver of glioma progression, with tumor necrosis factor-alpha (TNF-α) playing a central role in modulating the tumor microenvironment. This study aimed to investigate the expression profiles and regulatory mechanisms of TNF-α and its downstream mediators—including interleukin-1 beta (IL-1β), Mitogen-Activated Protein Kinase Kinase Kinase 8 (MAP3K8), and Mitogen-activated protein kinase kinase 7 (MAP2K7)—in astrocytic tumors of varying malignancy. We conducted an integrative molecular analysis of 60 human astrocytic tumor samples (20 G2, 12 G3, 28 G4) using transcriptomic microarrays, Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR), Enzyme-Linked Immunosorbent Assay (ELISA), Western blotting, immunohistochemistry, methylation-specific PCR, and miRNA profiling. Prognostic associations were evaluated using Kaplan–Meier survival and Cox regression analyses. TNF-α, IL-1β, and MAP3K8 were significantly upregulated in high-grade tumors, with log₂ fold changes ranging from 5.56 to 8.76 (p < 0.001). High expression of TNF-α (HR = 2.10, 95% CI: 1.27–3.46, p = 0.004), IL-1β (HR = 2.35, 95% CI: 1.45–3.82, p = 0.001), and MAP3K8 (Hazard Ratio; HR = 1.88, 95% confidence interval; 95% CI: 1.12–3.16, p = 0.015) was associated with poorer overall survival. miR-34a-3p and miR-30 family members, predicted to target TNF-α and IL-1β, were markedly downregulated in G3/G4 tumors (e.g., miR-30e-3p fold change: –3.78, p < 0.01). Promoter hypomethylation was observed in G3/G4 tumors, supporting epigenetic activation. Our findings establish a multi-layered regulatory mechanism of TNF-α signaling in astrocytic tumors. These data highlight the TNF-α/IL-1β/MAP3K8 axis as a critical driver of glioma aggressiveness and a potential therapeutic target. Full article

Malignant gliomas, including glioblastoma multiforme (GBM), are highly aggressive brain tumors with a poor prognosis and limited treatment options. This study investigates the antitumor potential of bioactive compounds derived from Cannabis sativa and Piper nigrum using molecular docking, cell viability assays, and transcriptomic and expression analyses from public databases in humans and cell lines. Cannabichromene (CBC), cannabigerol (CBG), cannabidiol (CBD), and Piper nigrum derivates exhibited strong binding affinities relative to glioblastoma-associated targets GPR55 and PINK1. In vitro analyses demonstrated their cytotoxic effects on glioblastoma cell lines (U87MG, T98G, and CCF-STTG1), as well as on neuroblastoma (SH-SY5Y) and oligodendroglial (MO3.13) cell lines, revealing interactions among these compounds. The differential expression of GPR55 and PINK1 in tumor versus normal tissues further supports their potential as biomarkers and therapeutic targets. These findings provide a basis for the development of novel therapies and suggest unexplored molecular pathways for the treatment of malignant glioma. Full article

Diffuse gliomas (DGs) are malignant primary brain tumors originating from glial cells. This study aimed to investigate the role of Receptor-interacting protein kinase 1 (RIPK1) in DG pathology. The RIPK1 mRNA expression was analyzed in DG databases from The Cancer Genome Atlas (TCGA) containing clinical, genomic, and transcriptomic information from 670 patients. Transcriptomic studies were carried out using USC Xena and R, while in vitro assays were performed with the glioblastoma human cell line U251 and the commercial RIPK1 inhibitor GSK2982772. The results showed that high RIPK1 expression was linked to a lower survival probability in patients. Additionally, the RIPK1 expression was higher in the wtIDH samples compared to that in the mIDH samples. Significant differences in the expression of genes related to cellular dedifferentiation, proinflammatory cell death pathways, and tumor-infiltrating immune cells were found between high- and low-RIPK1 expression groups. To further characterize the role of RIPK1 in DG, the effects of the RIPK1 inhibitor were evaluated, alone or combined with cisplatin, on glioblastoma cell proliferation and apoptosis. The combined treatments effectively reduced cell proliferation and increased apoptosis. The overexpression of RIPK1 was associated with a poor prognosis for DG, suggesting that RIPK1 plays a critical role in glioma pathogenesis and should be considered in therapeutic decision-making. Full article

Background and Objectives: Gliomas are characterized by high disability rates, frequent recurrence, and low survival rates, posing a significant threat to human health. Accurate grading of gliomas is crucial for treatment plan selection and prognostic assessment. Previous studies have primarily focused on the binary classification (i.e., high grade vs. low grade) of gliomas. In order to perform the four-grade (grades I, II, III, and IV) glioma classification preoperatively, we constructed an artificial neural network (ANN) model using magnetic resonance imaging data. Materials and Methods: We reviewed and included patients with gliomas who underwent preoperative MRI examinations. Radiomics features were derived from contrast-enhanced T1-weighted images (CE-T₁WI) using Pyradiomics and were selected based on their Spearman’s rank correlation with glioma grades. We developed an ANN model to classify the four pathological grades of glioma, assigning training and validation sets at a 3:1 ratio. A diagnostic confusion matrix was employed to demonstrate the model’s diagnostic performance intuitively. Results: Among the 362-patient cohort, the ANN model’s diagnostic performance plateaued after incorporating the first 19 of the 530 extracted radiomic features. At this point, the average overall diagnostic accuracy ratings for the training and validation sets were 91.28% and 87.04%, respectively, with corresponding coefficients of variation (CVs) of 0.0190 and 0.0272. The diagnostic accuracies for grades I, II, III, and IV in the training set were 91.9%, 89.9%, 92.1%, and 90.7%, respectively. The diagnostic accuracies for grades I, II, III, and IV in the validation set were 88.7%, 87.1%, 86.5%, and 86.9%, respectively. Conclusions: The MRI radiomics-based ANN model shows promising potential for the four-type classification of glioma grading, offering an objective and noninvasive method for more refined glioma grading. This model could aid in clinical decision making regarding the treatment of patients with various grades of gliomas. Full article

Chronic inflammation is a hallmark of brain tumors, especially gliomas, which exhibit elevated levels of pro-inflammatory mediators within the tumor and its microenvironment. Metabolic disturbances triggered by fluoride as a pro-oxidative agent in glioma cells, known for their high aggressiveness and resistance to therapy—remain poorly understood. Therefore, investigating the impact of physiologically elevated fluoride concentrations on oxidative stress and pro-inflammatory responses in glioma cells represents a relevant and timely research objective. Methods: U-87 human glioblastoma cells were subjected to short-term and long-term exposure to physiologically high concentrations of NaF (0.1–10 µM). Both the cells and the culture medium were analyzed. We assessed levels of reactive oxygen species (ROS), antioxidant defenses, and a panel of cytokines and chemokines. Results: Our results demonstrated that oxidative stress and inflammatory conditions in U-87 cells varied with fluoride concentration and exposure time. This led to an increase in ROS levels and key pro-inflammatory cytokines, including IL-6 and TNF-α. Conclusions: Fluoride compounds can generate ROS and disrupt the antioxidant defense system in U-87 human glioblastoma cells, leading to the initiation and progression of inflammatory states. Furthermore, prolonged exposure to NaF may induce adaptive mechanisms in U-87 cells. Full article

The development of an intelligent ultrasonic aspirator controlled by a fiber-optic neoplasm sensor that detects 5-aminolevulinic acid-derived porphyrin fluorescence presents a significant advancement in glioma surgery. By leveraging the fluorescence phenomenon associated with 5-aminolevulinic acid in malignant neoplasms, this device integrates an excitation laser and a high-sensitivity photodiode into the tip of an ultrasonic aspirator handpiece. This setup allows for real-time tumor fluorescence detection, which in turn modulates the aspirator’s power based on fluorescence intensity. Preliminary testing demonstrated high sensitivity, with the device capable of differentiating between weak, strong, and no fluorescence. The sensor sensitivity was comparable to human visual perception, enabling effective tumor differentiation. Tumors with strong fluorescence were effectively crushed, while the aspirator ceased operation in non-fluorescent areas, enabling precise tissue resection. Furthermore, the device functioned efficiently in bright surgical environments and was designed to maintain a clean sensor tip through constant saline irrigation. The system was successfully applied in a surgical case of recurrent glioblastoma, selectively removing tumor tissue while preserving surrounding brain tissue. This innovative approach shows promise for safer, more efficient glioma surgeries and may pave the way for sensor-based robotic surgical systems integrated with navigation technologies. Full article

Brain tumors, in particular gliomas and glioblastoma multiforme (GBM), are thought to originate from different cells facing specific founding insults, a feature that partly justifies the complexity and heterogeneity of these severe forms of cancer. However, gliomas and GBM are usually reproduced in animal models by inducing molecular alterations in mature glial cells, which, though being part of the puzzle, do not represent the whole picture. To fill this conceptual gap, we previously developed a neurogenic model of brain cancer in Drosophila, demonstrating that the loss of cell polarity in neural stem cells (called neuroblasts in the fruit fly) is sufficient to promote the formation of malignant masses that continue to grow in the adult, displaying several phenotypic traits typical of human GBM. Here, we expand on previous work by restricting polarity disruption to Drosophila type II neuroblasts, whose self-renewal is comparable to that of mammalian neural progenitors, with the aim to capture the molecular signature of the resulting cancers in a specific and reproducible context. A comparison of the most deregulated transcripts with those found in human primary GBMs confirmed that our model can be proficiently used to delve into the roots of human brain tumorigenesis. Full article

Background/Objectives: Glioblastoma is an aggressive brain tumor with limited treatment options and significant resistance to conventional therapies. Methods: In this study, we explored the effects of combining curcumin treatment with clusterin inhibition on cell death in glioma cells. Results: We observed that the combination of clusterin silencing and curcumin treatment induces cell death. This combination therapy significantly elevated reactive oxygen species (ROS), triggering oxidative stress, which acted as a key upstream mediator of apoptosis. Elevated ROS levels were found to be associated with caspase activation, suggesting apoptosis as the primary mode of cell death. Furthermore, autophagy was induced as a complementary mechanism, with upregulation of LC3B contributing to the enhanced cytotoxic effects. Conclusions: The synergy between clusterin knockdown-induced senescence and curcumin’s pro-apoptotic and pro-autophagic effects highlights a potential novel therapeutic strategy for gliomas. These findings underscore the potential of this combination therapy in overcoming glioma resistance and improving treatment outcomes through the dual induction of oxidative stress and cell death pathways. Full article