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Journal articles on the topic 'Non GBM human brain cells'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Cheng, Jiying, Min Li, Charlotte Flüh, et al. "TMIC-76. HUMANIN RELEASE FROM TUMOR ASSOCIATED MYELOID CELLS PROMOTES GLIOMA CHEMORESISTANCE." Neuro-Oncology 24, Supplement_7 (2022): vii288. http://dx.doi.org/10.1093/neuonc/noac209.1119.

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Abstract Transcriptomic screens of brain tumor (glioblastoma; GBM) parenchymal cells indicated tumor supporting traits of the GBM microenvironment, but largely excluded mitochondrially enriched gene-sets. Here, we show that a mitochondrial transcript of GBM parenchymal cells contributes to therapy resistance. We inspected the non-coding transcriptome of human GBM associated myeloid cells (GAM) and observed an upregulation of the mitochondrial ribosomal subunit MT-RNR2, which contains an open reading frame for the signaling peptide humanin. Immunohistology disclosed that humanin was preponderan

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Jiang, Michael Q., Shan Ping Yu, Takira Estaba, et al. "Reprogramming Glioblastoma Cells into Non-Cancerous Neuronal Cells as a Novel Anti-Cancer Strategy." Cells 13, no. 11 (2024): 897. http://dx.doi.org/10.3390/cells13110897.

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Glioblastoma Multiforme (GBM) is an aggressive brain tumor with a high mortality rate. Direct reprogramming of glial cells to different cell lineages, such as induced neural stem cells (iNSCs) and induced neurons (iNeurons), provides genetic tools to manipulate a cell’s fate as a potential therapy for neurological diseases. NeuroD1 (ND1) is a master transcriptional factor for neurogenesis and it promotes neuronal differentiation. In the present study, we tested the hypothesis that the expression of ND1 in GBM cells can force them to differentiate toward post-mitotic neurons and halt GBM tumor

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3

Wang, Mary, Arin N. Graner, Bryne Knowles, et al. "Differential Effects of Extracellular Vesicles from Two Different Glioblastomas on Normal Human Brain Cells." Neurology International 16, no. 6 (2024): 1355–84. http://dx.doi.org/10.3390/neurolint16060103.

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Background/Objectives: Glioblastomas (GBMs) are dreadful brain tumors with abysmal survival outcomes. GBM extracellular vesicles (EVs) dramatically affect normal brain cells (largely astrocytes) constituting the tumor microenvironment (TME). We asked if EVs from different GBM patient-derived spheroid lines would differentially alter recipient brain cell phenotypes. This turned out to be the case, with the net outcome of treatment with GBM EVs nonetheless converging on increased tumorigenicity. Methods: GBM spheroids and brain slices were derived from neurosurgical patient tissues following inf

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4

Yadav, Poonam, Raghupathy Vengoji, David Doss, Maneesh Jain, Surinder Batra, and Nicole Shonka. "EXTH-65. EXPLORING ANTIHISTAMINES TO TREAT GLIOBLASTOMA." Neuro-Oncology 26, Supplement_8 (2024): viii251. http://dx.doi.org/10.1093/neuonc/noae165.0995.

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Abstract BACKGROUND Glioblastoma (GBM) is an aggressive and lethal primary malignant brain tumor with a 5-year survival of 6.8%. Interestingly, people with allergies, atopy, or asthma are less likely to develop GBM. A recent study recognized that high histamine receptor 1 (HRH1) expression is inversely related to overall and progression-free survival. METHODS We used a bioinformatics tool, iLINCS, which, after analyzing 99 GBM and 38 healthy samples, identified 36 drugs that can reverse GBM signatures. Based on the concordance score and blood-brain barrier permeability, we selected bromphenira

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5

Takei, Jun, Ken Furudate, Opeyemi Iwaloye, et al. "TMOD-31. SINGLE-CELL PROFILING AND CHARACTERIZATION OF PATIENT-DERIVED XENOGRAFT GLIOBLASTOMA MODEL IN HUMANIZED MICE." Neuro-Oncology 26, Supplement_8 (2024): viii326. http://dx.doi.org/10.1093/neuonc/noae165.1295.

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Abstract Glioblastoma (GBM) is the most common and aggressive malignant brain tumor in adults, and the current standard therapy has limited efficacy. To develop effective therapies, it is desirable to develop an animal model that can replicate the tumor heterogeneity and immune microenvironment of human GBM. Here, we describe a novel GBM mouse model established with a patient-derived xenograft (PDX) in humanized mice harboring a nearly complete human immune environment. Humanized mice were generated by engrafting human CD34+ hematopoietic stem cells from umbilical cord blood into immunocomprom

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Kanji, Suman, Nozomi Tomimatsu, Luis Fernando Macedo Di Cristofaro, et al. "DNAR-12. ATR INHIBITION AS A NOVEL RADIOSENSITIZATION STRATEGY FOR GLIOBLASTOMA." Neuro-Oncology 25, Supplement_5 (2023): v100—v101. http://dx.doi.org/10.1093/neuonc/noad179.0378.

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Abstract Glioblastomas (GBM) are lethal brain tumors for which surgical resection followed by ionizing radiation (IR) with concurrent and adjuvant Temozolomide (TMZ) remains the mainstay of therapy. GBMs are extremely radioresistant, and radiosensitization approaches are desperately needed for these tumors. IR induces DNA double-strand breaks (DSBs), and these lesions can be repaired either by error-prone non-homologous end joining (NHEJ) or the error-free homologous recombination (HR) pathway. Research in our and other laboratories has shown that the ATR kinase promotes the HR pathway. We the

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7

Lee, Hyeji, Kanghye Bae, Ah-Rum Baek, et al. "Glioblastoma-Derived Exosomes as Nanopharmaceutics for Improved Glioma Treatment." Pharmaceutics 14, no. 5 (2022): 1002. http://dx.doi.org/10.3390/pharmaceutics14051002.

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The use of cancer-derived exosomes has been studied in several cancer types, but the cancer-targeting efficacy of glioma-derived exosomes has not been investigated in depth for malignant glioblastoma (GBM) cells. In this study, exosomes were derived from U87MG human glioblastoma cells, and selumetinib, a new anticancer drug, was loaded into the exosomes. We observed the tropism of GBM-derived exosomes in vitro and in vivo. We found that the tropism of GBM-derived exosomes is in contrast to the behavior of non-exosome-enveloped drugs and non-GBM-specific exosomes in vitro and in vivo in an anim

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8

Zhai, Lijie, Galina Gritsina, Brenda Nyugen, et al. "IMMU-32. NON-METABOLIC IDO ACTIVITY INCREASES COMPLEMENT FACTOR H LEVELS WHICH ENHANCES IMMUNOSUPPRESSION IN HUMAN GLIOBLASTOMA." Neuro-Oncology 22, Supplement_2 (2020): ii111. http://dx.doi.org/10.1093/neuonc/noaa215.462.

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Abstract Indoleamine 2,3 dioxygenase 1 (IDO) is an immunosuppressive factor expressed in ≥90% of patient resected glioblastoma (GBM). Canonically, IDO suppresses the immune response by metabolizing the essential amino acid, tryptophan, into the downstream metabolite, kynurenine. Based on the in vivo finding that the genetic knockout of tumor cell IDO does not change brain tumor tryptophan and kynurenine levels in syngeneic mice, we recently questioned the mechanistic role of IDO in GBM. To determine whether tumor cell tryptophan metabolism is responsible for the pathogenic effects of IDO, we c

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9

El-Ayoubi, Ali, Moritz Klawitter, Jakob Rüttinger, et al. "Intranasal Delivery of Oncolytic Adenovirus XVir-N-31 via Optimized Shuttle Cells Significantly Extends Survival of Glioblastoma-Bearing Mice." Cancers 15, no. 20 (2023): 4912. http://dx.doi.org/10.3390/cancers15204912.

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A glioblastoma (GBM) is an aggressive and lethal primary brain tumor with restricted treatment options and a dismal prognosis. Oncolytic virotherapy (OVT) has developed as a promising approach for GBM treatment. However, reaching invasive GBM cells may be hindered by tumor-surrounding, non-neoplastic cells when the oncolytic virus (OV) is applied intratumorally. Using two xenograft GBM mouse models and immunofluorescence analyses, we investigated the intranasal delivery of the oncolytic adenovirus (OAV) XVir-N-31 via virus-loaded, optimized shuttle cells. Intranasal administration (INA) was se

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10

Yoon, Seon-Jin, Ran Joo Choi, Yoojung Oh, et al. "STEM-12. DISCOVERY THE ORIGIN-CELLS FOR HUMAN GLIOBLASTOMA GENESIS IN SUBVENTRICULAR ZONE." Neuro-Oncology 24, Supplement_7 (2022): vii33. http://dx.doi.org/10.1093/neuonc/noac209.129.

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Abstract Human glioblastoma (GBM), originating from the subventricular zone (SVZ), occurs due to molecular disruptions in chromosomes. Most GBM tissues exhibit definitive chromosomal patterns: copy-number-variations (CNV) in chromosome 7 (gain) and 10 (loss), known as the earliest molecular events. Herein, we hypothesised that the origin-cells in SVZ of GBM patients can provide clues regarding these chromosomal alterations. We compared bulk RNA sequencing (RNAseq) data of GBM tumor tissue (n=126), tumour free GBM SVZ (n=40), and tumor-free control SVZ of non-glial tumor (n=9). Paired single-ce

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Binder, Zev, Sarah Hyun Ji Kim, Pei-Hsun Wu та ін. "TMOD-12. THE ROLE OF INTEGRIN α V AND CD44 IN GBM MIGRATION USING HUMAN ORGANOTYPIC SLICES". Neuro-Oncology 21, Supplement_6 (2019): vi265. http://dx.doi.org/10.1093/neuonc/noz175.1111.

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Abstract Current model systems used for GBM research include traditional in vitro cell line-based assays and in vivo animal studies. In vitro model systems offer the advantages of being easy to use, relatively inexpensive, and fast growing. However, these models lack key elements of the pathology they are attempting to model, including the biochemical and biophysical microenvironment and three-dimensional structure inherent to human brain tissue. In vivo model systems address these limitations, but have restrictions of their own. Species differences may result in non-applicable results and ani

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Tong, Tong, Kirstine Juul Elbæk, Jens Eschen, et al. "CNSC-22. GLIOBLASTOMA CELLS EXHIBIT NEURON-LIKE EXCITABILITY IN BOTH ACUTE AND ORGANOTYPIC HUMAN BRAIN SLICES." Neuro-Oncology 26, Supplement_8 (2024): viii45. http://dx.doi.org/10.1093/neuonc/noae165.0178.

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Abstract Glioblastomas (GBM) are known for their significant intratumor heterogeneity, featuring a variety of plastic cell types that make effective treatment challenging. Recent studies have shown that neuronal-progenitor-like transcriptomic cell states at the leading edge of the tumor receive synaptic input from nearby neurons, which drives disease proliferation. However, the excitability of GBM cells remains controversial, with observations ranging from non-excitable to neuron-like excitability, complicating our understanding of their pathophysiology. In this study, we developed a novel exp

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Sarnow, K., G. Kanli, O. Keunen та R. Bjerkvig. "OS06.6A Inhibition of GBM invasion by the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor antagonist Perampanel". Neuro-Oncology 23, Supplement_2 (2021): ii10. http://dx.doi.org/10.1093/neuonc/noab180.030.

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Abstract BACKGROUND Extensive tumor cell invasion within the brain represents a major problem for effective treatment of glioblastomas (GBMs). The invasive processes can be divided into three types: Collective cell invasion, perivascular infiltration and single-cell invasion into the brain parenchyma. It has recently been shown that GBM cells have the ability to form synapses with neural cells pointing at an extensive communication network between brain cells GBM cells. This communication network can be mediated via the metabolites glutamine and glutamate both needed for GBM cell proliferation

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Turchi, Laurent, Nathalie Sakakini, Gaelle Saviane, et al. "CELF2 Sustains a Proliferating/OLIG2+ Glioblastoma Cell Phenotype via the Epigenetic Repression of SOX3." Cancers 15, no. 20 (2023): 5038. http://dx.doi.org/10.3390/cancers15205038.

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Glioblastomas (GBs) are incurable brain tumors. The persistence of aggressive stem-like tumor cells after cytotoxic treatments compromises therapeutic efficacy, leading to GBM recurrence. Forcing the GBM cells to irreversibly abandon their aggressive stem-like phenotype may offer an alternative to conventional cytotoxic treatments. Here, we show that the RNA binding protein CELF2 is strongly expressed in mitotic and OLIG2-positive GBM cells, while it is downregulated in differentiated and non-mitotic cells by miR-199a-3p, exemplifying GBM intra-tumor heterogeneity. Using patient-derived cells

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Sarnow, Katharina, Georgia Kanli, Olivier Keunen та Rolf Bjerkvig. "TAMI-24. INHIBITION OF GBM INVASION BY THE Α-AMINO-3-HYDROXY-5-METHYL-4-ISOXAZOLEPROPIONIC ACID (AMPA) GLUTAMATE RECEPTOR ANTAGONIST PERAMPANEL". Neuro-Oncology 23, Supplement_6 (2021): vi203. http://dx.doi.org/10.1093/neuonc/noab196.808.

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Abstract BACKGROUND Extensive tumor cell invasion within the brain represents a major problem for effective treatment of glioblastomas (GBMs). The invasive processes can be divided into three types: Collective cell invasion, perivascular infiltration, and single-cell invasion into the brain parenchyma. GBM cells can form synapses with neural cells pointing at an extensive communication network between brain and GBM cells which can be mediated via the metabolites Glutamine and Glutamate both needed for GBM cell proliferation. In this context, it has been shown in preclinical models that Perampa

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Wang, Lin, Karin Shamardani, Husam Babikir, et al. "EPCO-10. CHANGES IN ALTERNATIVE SPLICING AND ASSOCIATED NEOANTIGENS DUE TO THERAPY." Neuro-Oncology 22, Supplement_2 (2020): ii71. http://dx.doi.org/10.1093/neuonc/noaa215.289.

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Abstract Recent studies have identified alternative splicing (AS) as a novel source of neoantigens for immunotherapy. Surprisingly little is known about the AS milieu in recurrent glioblastoma (GBM), despite this being the venue for most clinical trials. We profiled 29 primary-recurrent paired human GBM specimens via RNA sequencing and re-analyzed RNA-sequencing data from non-malignant human brain tissues. From these data, we reconstructed the landscape of AS in GBM through recurrence and contrasted that to isoforms observed in non-malignant brain. The AS events we identified were cross-refere

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Karwacinski, Victor, Tatiana Carneiro-Lobo, Cheryl Olson, et al. "TMIC-26. TAMS AND HYPOXIA ENHANCE GLIOBLASTOMA STEM-LIKE CELL ENRICHMENT AND MAY IMPACT RADIORESISTANCE." Neuro-Oncology 25, Supplement_5 (2023): v283—v284. http://dx.doi.org/10.1093/neuonc/noad179.1092.

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Abstract The dismal survival rates of glioblastoma (GBM) patients are due, at least in part, to therapeutic resistance of GBM stem-like cells (GSCs) and their ability to repopulate recurrent tumors. Our goal was to determine if tumor-associated macrophages (TAMs) or hypoxia enhance the enrichment of GSCs in a manner that could impact radioresistance. First, we established GBM-brain cortical organoids (GBM-BCOs) to model human GBM. We co-cultured GFP-labeled GBM neurospheres with BCOs for 14 days and observed a tumor take rate of 100%. Next, we evaluated whether hypoxia enhanced TAM migration i

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Bollu, Lakshmi, Prashant Bommi, Derek Wainwright, et al. "DDRE-11. SECOND GENERATION IDO INHIBITORS FOR IMPROVING IMMUNOTHERAPEUTIC EFFICACY IN PATIENTS WITH GLIOBLASTOMA." Neuro-Oncology 23, Supplement_6 (2021): vi76. http://dx.doi.org/10.1093/neuonc/noab196.295.

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Abstract INTRODUCTION Indoleamine 2,3-dioxygenase 1 (IDO; IDO1) is a rate-limiting enzyme that metabolizes tryptophan and is expressed in &gt;90% of patient-resected glioblastoma (GBM). IDO-mediated tryptophan metabolism has been the proposed mechanism for suppressing the immune response in GBM. Recently, we discovered that IDO also possesses non-enzymic functions that contribute to suppress the anti-GBM immune response. This finding motivated us to develop IDO-Proteolysis Targeting Chimeras (IDO-PROTACs) to degrade IDO protein rather than simply inhibiting IDO enzyme activity. METHODS Wes

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Virtuoso, Assunta, Giuseppa D’Amico, Federica Scalia, et al. "The Interplay between Glioblastoma Cells and Tumor Microenvironment: New Perspectives for Early Diagnosis and Targeted Cancer Therapy." Brain Sciences 14, no. 4 (2024): 331. http://dx.doi.org/10.3390/brainsci14040331.

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Glioblastoma multiforme (GBM) stands out as the most tremendous brain tumor, constituting 60% of primary brain cancers, accompanied by dismal survival rates. Despite advancements in research, therapeutic options remain limited to chemotherapy and surgery. GBM molecular heterogeneity, the intricate interaction with the tumor microenvironment (TME), and non-selective treatments contribute to the neoplastic relapse. Diagnostic challenges arise from GBM advanced-stage detection, necessitating the exploration of novel biomarkers for early diagnosis. Using data from the literature and a bioinformati

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Mendanha, Daniel, Joana Vieira de Castro, Joana Moreira, et al. "A New Chalcone Derivative with Promising Antiproliferative and Anti-Invasion Activities in Glioblastoma Cells." Molecules 26, no. 11 (2021): 3383. http://dx.doi.org/10.3390/molecules26113383.

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Glioblastoma (GBM) is the most common and most deadly primary malignant brain tumor. Current therapies are not effective, the average survival of GBM patients after diagnosis being limited to few months. Therefore, the discovery of new treatments for this highly aggressive brain cancer is urgently needed. Chalcones are synthetic and naturally occurring compounds that have been widely investigated as anticancer agents. In this work, three chalcone derivatives were tested regarding their inhibitory activity and selectivity towards GBM cell lines (human and mouse) and a non-cancerous mouse brain

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Martínez-Escardó, Laura, Montse Alemany, María Sánchez-Osuna, et al. "Gossypol Treatment Restores Insufficient Apoptotic Function of DFF40/CAD in Human Glioblastoma Cells." Cancers 13, no. 21 (2021): 5579. http://dx.doi.org/10.3390/cancers13215579.

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Glioblastoma (GBM) is a highly aggressive brain tumor and almost all patients die because of relapses. GBM-derived cells undergo cell death without nuclear fragmentation upon treatment with different apoptotic agents. Nuclear dismantling determines the point-of-no-return in the apoptotic process. DFF40/CAD is the main endonuclease implicated in apoptotic nuclear disassembly. To be properly activated, DFF40/CAD should reside in the cytosol. However, the endonuclease is poorly expressed in the cytosol and remains cumulated in the nucleus of GBM cells. Here, by employing commercial and non-commer

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Zhang, Minjie, Alice Tsai, Kevin Cottrell, et al. "DDDR-33. TNG908, A BRAIN-PENETRANT MTA-COOPERATIVE PRMT5 INHIBITOR, IS EFFICACIOUS IN PRECLINICAL MTAP-DELETED MODELS INCLUDING GLIOBLASTOMA." Neuro-Oncology 25, Supplement_5 (2023): v113. http://dx.doi.org/10.1093/neuonc/noad179.0426.

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Abstract Glioblastoma multiforme (GBM) is the most common malignant primary brain tumor in adults. The median overall survival (OS) of GBM patients is poor (1-2 years) with standard of care therapies, demonstrating the significant need for the development of novel therapeutics. TNG908 is a clinical stage MTA-cooperative PRMT5 inhibitor that is selectively active in MTAP-deleted cells by leveraging a synthetic lethal interaction. Approximately 40% of GBM tumors have MTAP loss due to a co-deletion event with the proximal tumor suppressor gene, CDKN2A. In preclinical in vitro studies, TNG908 was

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Hazra, Rasmani. "STEM-19. TARGETINGGIHCG LNCRNA IN GLIOBLASTOMA STEM CELLS: A POTENTIAL THERAPEUTIC STRATEGY." Neuro-Oncology 26, Supplement_8 (2024): viii62. http://dx.doi.org/10.1093/neuonc/noae165.0245.

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Abstract Glioblastoma multiforme (GBM) remains the most lethal and prevalent primary brain tumor worldwide. Despite advances in understanding its biology and multimodal therapy options, the overall prognosis for GBM patients remains bleak, primarily due to the high recurrence rate, which is intimately linked to tumor resistance against standard therapeutic interventions. Glioblastoma stem cells (GSCs) contribute to therapeutic resistance and cellular heterogeneity through their self-renewal properties and ability to adapt. Thus, identifying new molecular targets driving GBM progression is cruc

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24

Tomaszewski, William, Jessica Waibl-Polania, Luigi Racioppi, Luis Sanchez-Perez, Gunn Michael, and John Sampson. "IMMU-34. CAMKK2 PROMOTES AN IMMUNOSUPPRESSIVE PROGRAM AND CHECKPOINT BLOCKADE RESISTANCE IN THE GLIOBLASTOMA TUMOR MICROENVIRONMENT." Neuro-Oncology 23, Supplement_6 (2021): vi100. http://dx.doi.org/10.1093/neuonc/noab196.393.

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Abstract BACKGROUND Immunotherapy has demonstrated efficacy in several cancers but has shown only modest effects in Glioblastoma (GBM). This is linked to the anti-inflammatory nature of the tumor microenvironment (TME) and the pro-tumor functions of brain native cells. Targeting stromal cells, such as tumor associated macrophages (TAMs) and neurons, is a promising approach. Re-analysis of human and murine brain single cell-RNAseq (scRNAseq) datasets shows Calmodulin Dependent Kinase Kinase 2 (CaMKK2) is highly expressed in both neurons and TAMs. Loss of CaMKK2 polarizes TAMs to an immunostimul

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Ladomersky, Erik, Lijie Zhai, Kristen Lauing, et al. "IMMU-44. INHIBITING IMMUNOSUPPRESSIVE IDO1 IN ADULTS WITH MALIGNANT GLIOMA – A MOVING TARGET THAT CHANGES WITH TREATMENT, CELL OF ORIGIN, AND AGING." Neuro-Oncology 21, Supplement_6 (2019): vi128. http://dx.doi.org/10.1093/neuonc/noz175.536.

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Abstract We previously demonstrated that glioblastoma (GBM) cell IDO1 increases intratumoral immunosuppressive regulatory T cells (Tregs; CD4+CD25+FoxP3+) and decreases overall survival (OS) in the syngeneic GL261 model. IDO1 is characterized as an enzyme that converts the amino acid, tryptophan, into kynurenine. With the finding that IDO1 expression by GBM cells promotes intratumoral Treg accumulation, it was surprising to find that this process was unaffected by the pharmacological treatment with an IDO1 enzyme inhibitor (IDO1i). This led us to question the optimal therapeutic strategy for l

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Zhou, Wenbo, Daniel Lovasz, Zoë Zizzo, et al. "Phenotype and Neuronal Cytotoxic Function of Glioblastoma Extracellular Vesicles." Biomedicines 10, no. 11 (2022): 2718. http://dx.doi.org/10.3390/biomedicines10112718.

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Glioblastoma (GBM) is the most aggressive and lethal form of brain tumor. Extracellular vesicles (EVs) released by tumor cells play a critical role in cellular communication in the tumor microenvironment promoting tumor progression and invasion. We hypothesized that GBM EVs possess unique characteristics which exert effects on endogenous CNS cells including neurons, producing dose-dependent neuronal cytotoxicity. We purified EVs from the plasma of 20 GBM patients, 20 meningioma patients, and 21 healthy controls, and characterized EV phenotypes by electron microscopy, nanoparticle tracking anal

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Watson, Dionysios C., Defne Bayik, Simon Storevik, et al. "Abstract 331: Mitochondrial transfer from astrocytes drives glioblastoma tumorigenicity." Cancer Research 83, no. 7_Supplement (2023): 331. http://dx.doi.org/10.1158/1538-7445.am2023-331.

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Abstract Mitochondrial transfer in the central nervous system occurs from astrocytes to neurons in stroke. Mitochondrial exchange has also been reported among tumor cells in glioblastoma (GBM), the most common primary brain tumor. However, the role of mitochondrial transfer from non-neoplastic cells in the surrounding microenvironment to GBM remains poorly understood. We hypothesized that mitochondrial transfer from these non-neoplastic to GBM cells supports tumor metabolism and growth. Using transgenic mice expressing fluorophore-tagged mitochondria, we found that ~50% of orthotopically-impla

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Fuentes-Fayos, Antonio C., Miguel E. G-García, Jesús M. Pérez-Gómez, et al. "Somatostatin Receptor Splicing Variant sst5TMD4 Overexpression in Glioblastoma Is Associated with Poor Survival, Increased Aggressiveness Features, and Somatostatin Analogs Resistance." International Journal of Molecular Sciences 23, no. 3 (2022): 1143. http://dx.doi.org/10.3390/ijms23031143.

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Glioblastoma (GBM) is the most malignant and lethal brain tumor. Current standard treatment consists of surgery followed by radiotherapy/chemotherapy; however, this is only a palliative approach with a mean post-operative survival of scarcely ~12–15 months. Thus, the identification of novel therapeutic targets to treat this devastating pathology is urgently needed. In this context, the truncated splicing variant of the somatostatin receptor subtype 5 (sst5TMD4), which is produced by aberrant alternative splicing, has been demonstrated to be overexpressed and associated with increased aggressiv

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Ferreira, Rodolfo Sanches, Bruno H. S. Araujo, and Oswaldo Okamoto. "MODL-06. ASSESSMENT OF ONCOLYTIC VIRUS SPECIFICITY AND CYTOTOXICITY IN A HYBRID GLIOBLASTOMA-CEREBRAL ORGANOID MODEL." Neuro-Oncology 24, Supplement_7 (2022): vii292. http://dx.doi.org/10.1093/neuonc/noac209.1134.

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Abstract Recent studies have demonstrated potent oncolytic effects of wild-type Zika virus (ZIKV) against primary central nervous system (CNS) tumors, including Medulloblastoma, Atypical Teratoid/Rhabdoid Tumor (AT/RT), and Glioblastoma (GBM). However, the neurotropism of ZIKV urges further evaluation of specific tumor-targeting properties and comparative toxicity to non-neoplastic neural cells in order to address its therapeutic potential. We have developed a hybrid organoid model by co-culturing GBM cells with mature human cerebral organoids and assessed cytotoxicity of the Brazilian ZIKV is

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Yusuf, D., AD Singh, R. Shaykhutdinov, et al. "07 Identifying and prognosticating malignant brain tumors non-invasively using unique metabolomic signatures derived from patient serum and urine samples." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, S3 (2018): S14. http://dx.doi.org/10.1017/cjn.2018.299.

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BACKGROUND: Metabolomics technology has the potential to revolutionize how we screen, diagnose, and treat cancer, as well as improve upon existing cancer molecular tests that may not sufficiently capture the complexity of most malignancies. In this study, we explore the clinical potential of metabolomics analysis in the diagnosis and risk-stratification of brain tumors. METHODS: To test the hypothesis that brain tumor type and survival could be predicted with metabolomics, we analyzed the pre-operative serum and urine samples of patients with glioblastoma (GBM), oligoastrocytoma (OA2), meningi

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Szeliga, Monika, and Radosław Rola. "Menadione Potentiates Auranofin-Induced Glioblastoma Cell Death." International Journal of Molecular Sciences 23, no. 24 (2022): 15712. http://dx.doi.org/10.3390/ijms232415712.

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Glioblastoma (GBM) is the most aggressive primary brain tumor. Recently, agents increasing the level of oxidative stress have been proposed as anticancer drugs. However, their efficacy may be lowered by the cytoprotective activity of antioxidant enzymes, often upregulated in neoplastic cells. Here, we assessed the mRNA and protein expression of thioredoxin reductase 1 (TrxR1), a master regulator of cellular redox homeostasis, in GBM and non-tumor brain tissues. Next, we examined the influence of an inhibitor of TrxR1, auranofin (AF), alone or in combination with a prooxidant menadione (MEN), o

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Carneiro-Lobo, Tatiana, Cheryl Olson, Steven Markwell, Pinar Mesci, Alysson Muotri, and Daniel Brat. "TMIC-35. CROSSTALK BETWEEN TAMS AND GLIOBLASTOMA STEM-LIKE CELLS IN A HYPOXIC MICROENVIRONMENT INDUCES SENESCENCE ARREST AND ENHANCED RADIORESISTANCE." Neuro-Oncology 24, Supplement_7 (2022): vii279. http://dx.doi.org/10.1093/neuonc/noac209.1079.

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Abstract Patients with glioblastoma (GBM) have an overall survival of 15 months. These catastrophic survival rates are correlated with systematic relapses that might arise from remaining glioblastoma stem cells (GSCs) left behind after treatments. Our goal was identifying whether radioresistance of GBM is caused by GSCs and how hypoxia and TAMs affect this process. First, we established a glioblastoma-brain cortical organoid (GBM-BCOs) to model human GBM. We co-cultured GFP-labeled GBM neurosphere with BCOs for 14 days and we observed that tumor take rate was 100% for all GBM neurosphere teste

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Kleist, Sierra A., Shawn C. Musial, Jordan F. Isaacs, Hanna N. Degefu, Alexander G. Skorput, and Pamela C. Rosato. "Investigating the source of viral-specific memory T cells in glioblastoma." Journal of Immunology 210, no. 1_Supplement (2023): 171.03. http://dx.doi.org/10.4049/jimmunol.210.supp.171.03.

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Abstract Glioblastoma (GBM) is an aggressive primary brain tumor that is invariably fatal. Immunotherapies have largely failed and a better understanding of the unique brain tumor immune environment is needed. Being historically thought of as immune-privileged, immune cell populations within the brain and brain tumors have been understudied. One such population is resident memory T cells (T RM). In healthy and malignant peripheral tissues, T RMcan provide long-term protection against reinfections or cancers, however the role of T RMin the context of the brain and brain tumors is not fully unde

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Vaughn-Beaucaire, Philippa, Jorge Luis Jimenez Macias, Edward Miller, Bradley Pentelute, and Sean Lawler. "DDEL-13. ENHANCING THE EFFICACY OF THE BBB-PENETRANT PEPTIDE-DRUG CONJUGATE PT(IV)-M13 WITH THE KINASE INHIBITOR BIA TO IMPROVE INTRA-TUMORAL DELIVERY AND INHIBIT DNA REPAIR." Neuro-Oncology 26, Supplement_8 (2024): viii123—viii124. http://dx.doi.org/10.1093/neuonc/noae165.0479.

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Abstract The blood-brain and blood-tumor barriers (BBB and BTB) constitute major obstacles to effective GBM therapy. These barriers impede the penetration of the great majority of pharmacological agents into brain tumors. This study introduces a dual-modality approach aimed at enhancing drug delivery to GBM through manipulating BTB permeability and facilitating targeted drug delivery through a novel BBB penetrant drug conjugate. First, we investigated the effects of the broad specificity kinase inhibitor 6-bromo-indirubin-3’-acetoxime (BIA), a derivative of the natural medicinal indirubin, on

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Hong, Xin, Kevin K. Nelson, Ana C. deCarvalho, and Steven N. Kalkanis. "Heparanase expression of glioma in human and animal models." Journal of Neurosurgery 113, no. 2 (2010): 261–69. http://dx.doi.org/10.3171/2009.9.jns09682.

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Object Mammalian heparanase has been shown to function in tumor progression, invasion, and angiogenesis. However, heparanase expression in gliomas has not been well analyzed. To clarify its expression in gliomas, human glioma tissues and glioma animal models were investigated. Methods The expression of heparanase mRNA was determined in 33 resected human glioma tissues by semiquantitative real-time polymerase chain reaction. Heparanase expression was verified with a Western blot assay and immunohistochemistry (IHC) staining. Primary neurospheres from human glioblastoma multiforme (GBM) were dev

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Bates, Emily A., Charlotte Lovatt, Alice R. Plein, James A. Davies, Florian A. Siebzehnrubl, and Alan L. Parker. "Engineering Adenoviral Vectors with Improved GBM Selectivity." Viruses 15, no. 5 (2023): 1086. http://dx.doi.org/10.3390/v15051086.

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Glioblastoma (GBM) is the most common and aggressive adult brain cancer with an average survival rate of around 15 months in patients receiving standard treatment. Oncolytic adenovirus expressing therapeutic transgenes represent a promising alternative treatment for GBM. Of the many human adenoviral serotypes described to date, adenovirus 5 (HAdV-C5) has been the most utilised clinically and experimentally. However, the use of Ad5 as an anti-cancer agent may be hampered by naturally high seroprevalence rates to HAdV-C5 coupled with the infection of healthy cells via native receptors. To explor

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Bommi, Prashant, Paige Monsen, Kristen Lauing, et al. "CSIG-33. A 2ND GENERATION IDO1 PROTEIN DEGRADER TO OVERCOME NON-ENZYME-MEDIATED IDO1-DEPENDENT IMMUNE SUPPRESSION FOR GLIOBLASTOMA." Neuro-Oncology 25, Supplement_5 (2023): v47. http://dx.doi.org/10.1093/neuonc/noad179.0189.

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Abstract Indoleamine 2,3-dioxygenase 1 (IDO1) is an immunosuppressive rate-limiting enzyme that metabolizes the essential amino acid, tryptophan (Trp), into the downstream catabolite, kynurenine. IDO1 is expressed in &gt;90% of patient-resected glioblastoma (GBM). We recently validated that IDO1 can suppress the anti-brain tumor immune response and ablate immunotherapeutic treatment efficacy through non-metabolic IDO1 activity. To-date, most IDO1-targeted therapy has focused on inhibiting tryptophan metabolism. This class of drugs has failed to improve the overall survival of patients with

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Zhang, Xiaopei, Denise Dunn, Alain Valdivia, et al. "MODL-14. MODELING THE INTRATUMORAL HETEROGENEITY OF AGGRESSIVE GLIOBLASTOMA ON ORGANOTYPIC BRAIN SLICES TO OPTIMIZE TUMOR-HOMING TUMORICIDAL INSC TREATMENT." Neuro-Oncology 24, Supplement_7 (2022): vii293—vii294. http://dx.doi.org/10.1093/neuonc/noac209.1142.

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Abstract BACKGROUND Tumor-homing tumoricidal neural stem cell (tNSC) therapy is a promising new strategy that recently entered human patient testing for glioblastoma (GBM). Developing strategies for tNSC therapy to overcome intratumoral heterogeneity, variable cancer cell invasiveness, and differential drug response of GBM will be essential for efficacious treatment response in the clinical setting. We sought to create novel hybrid tumor models and investigate the impact of GBM heterogeneity on tNSC tumor response and treatment durability. METHODS We utilized organotypic brain slice explants a

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Pudełek, Maciej, Kamila Król, Jessica Catapano, Tomasz Wróbel, Jarosław Czyż, and Damian Ryszawy. "Epidermal Growth Factor (EGF) Augments the Invasive Potential of Human Glioblastoma Multiforme Cells via the Activation of Collaborative EGFR/ROS-Dependent Signaling." International Journal of Molecular Sciences 21, no. 10 (2020): 3605. http://dx.doi.org/10.3390/ijms21103605.

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Abnormal secretion of epidermal growth factor (EGF) by non-neuronal cells (e.g., glioma-associated microglia) establishes a feedback loop between glioblastoma multiforme (GBM) invasion and a functional disruption of brain tissue. Considering the postulated significance of this vicious circle for GBM progression, we scrutinized mechanisms of EGF-dependent pro-invasive signaling in terms of its interrelations with energy metabolism and reactive oxygen species (ROS) production. The effects of EGF on the invasiveness of human glioblastoma T98G cells were estimated using time-lapse video microscopy

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Sen, Shamik, Win Pin Ng, and Sanjay Kumar. "Contributions of talin-1 to glioma cell–matrix tensional homeostasis." Journal of The Royal Society Interface 9, no. 71 (2011): 1311–17. http://dx.doi.org/10.1098/rsif.2011.0567.

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The ability of cells to adapt their mechanical properties to those of the surrounding microenvironment (tensional homeostasis) has been implicated in the progression of a variety of solid tumours, including the brain tumour glioblastoma multiforme (GBM). GBM tumour cells are highly sensitive to extracellular matrix (ECM) stiffness and overexpress a variety of focal adhesion proteins, such as talin. While talin has been shown to play critical early roles in integrin-based force-sensing in non-tumour cells, it remains unclear whether this protein contributes to tensional homeostasis in GBM cells

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Beinat, Corinne, Chirag Patel, Tom Haywood, et al. "BIMG-13. A NOVEL RADIOPHARMACEUTICAL ([18F]DASA-23) TO MONITOR PYRUVATE KINASE M2 INDUCED GLYCOLYTIC REPROGRAMMING IN GLIOBLASTOMA." Neuro-Oncology Advances 3, Supplement_1 (2021): i3—i4. http://dx.doi.org/10.1093/noajnl/vdab024.012.

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Abstract BACKGROUND Pyruvate kinase M2 (PKM2) catalyzes the final step in glycolysis, a key process of cancer metabolism. PKM2 is preferentially expressed by glioblastoma (GBM) cells with minimal expression in healthy brain, making it an important biomarker of cancer glycolytic re-programming. We describe the bench-to-bedside development, validation, and translation of a novel positron emission tomography (PET) tracer to study PKM2 in GBM. Specifically, we evaluated 1-((2-fluoro-6-[18F]fluorophenyl)sulfonyl)-4-((4-methoxyphenyl)sulfonyl)piperazine ([18F]DASA-23) in cell culture, mouse models o

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Bommi, Prashant, Paige Monsen, Lakshmi Bommi, et al. "CNSC-27. AN IDO-PROTAC HIGHLIGHTS A NOVEL TRYPTOPHAN METABOLISM- INDEPENDENT ROLE FOR IMMUNOSUPPRESSIVE IDO IN HUMAN GLIOBLASTOMA." Neuro-Oncology 24, Supplement_7 (2022): vii28. http://dx.doi.org/10.1093/neuonc/noac209.108.

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Abstract INTRODUCTION Indoleamine 2,3-dioxygenase 1 (IDO) is an immunosuppressive enzyme that catabolizes the essential amino acid, tryptophan (Trp), into the metabolite, kynurenine. IDO is expressed in &gt;90% of patient resected GBM. IDO suppresses the anti-brain tumor immune response, in-part, through non-metabolic activities. To determine how IDO non-metabolically suppresses the anti-GBM immune response, IDO-protein degrader (IDO-proteolysis targeting chimera; IDO-PROTAC) effects were studied in multiple human models of GBM. METHODS The IDO-expressing GBM cell lines, U87, U138, as well

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Kawauchi, Daisuke, Masamichi Takahashi, Shun Yamamuro, et al. "ACT-01 THE SECOND GENERATION ANAPLASTIC LYMPHOMA KINASE (ALK) INHIBITOR CERITINIB EFFECTIVELY INDUCES CELL DEATH IN HUMAN GLIOBLASTOMA CELLS." Neuro-Oncology Advances 1, Supplement_2 (2019): ii13. http://dx.doi.org/10.1093/noajnl/vdz039.057.

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Abstract Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase which expresses only in the developmental stage of the brain during embryogenesis of human. On the other hand, a variety of ALK gene alterations, such as oncogenic fusion, activating point mutation, or wild type gene amplification, have been recently discovered as the powerful oncogene in various tumors, and these ALK mutations have also been known as the potential therapeutic targets against tumors harboring these ALK mutations. For example, ALK inhibitors have been already approved and used for the clinical treatment of

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Perez, T., R. Berges, H. Maccario, D. Braguer, and S. Honoré. "P11.06 Non epigenetic effect of vorinostat in glioblastoma cells." Neuro-Oncology 21, Supplement_3 (2019): iii43. http://dx.doi.org/10.1093/neuonc/noz126.152.

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Abstract BACKGROUND Glioblastoma multiform (GBM) is the most frequent primitive brain tumor. GBM has a high recurrence and mortality. Histone deacetylase (HDAC) inhibitors have evoked great interest because they are able to change transcriptomic profiles to promote tumor cell death but also show undesirable side effects due to the lack of selectivity.We show new properties of low dose vorinostat, which inhibits cytoplasmic HDAC6 and display interesting non-epigenetics effects, especially on the microtubular cytoskeleton. MATERIAL AND METHODS We used murine (GL261) and human (U87 and GBM6 stem

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Watson, Dionysios C., Defne Bayik, Matthew Grabowski, Manmeet Ahluwalia, Alireza Mohammadi, and Justin D. Lathia. "OTEH-2. High-dimensional analysis of spatial immune cell heterogeneity in glioblastoma reveals differences between contrast-enhancing and non-contrast-enhancing tumor rims." Neuro-Oncology Advances 3, Supplement_2 (2021): ii10. http://dx.doi.org/10.1093/noajnl/vdab070.041.

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Abstract Background Glioblastoma (GBM) is the most common primary malignant brain tumor in adults. GBM remains an incurable disease, with a median survival ~20 months. Complex intercellular interactions within the tumor microenvironment and spatial heterogeneity have challenged and impeded therapeutic efficacy. The non-contrast-enhancing (by T1-weighted MRI) rim of GBM is not always safely resectable and represents a major source of recurrence. We hypothesized that differential immune infiltration is an underlying factor of spatial heterogeneity in GBM, particularly in the non-contrast-enhanci

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Watson, Dionysios, Defne Bayik, Adam Lauko, et al. "TMIC-69. MITOCHONDRIAL TRANSFER FROM ASTROCYTES ENHANCES METABOLISM AND DRIVES PROLIFERATION OF GLIOBLASTOMA." Neuro-Oncology 24, Supplement_7 (2022): vii286—vii287. http://dx.doi.org/10.1093/neuonc/noac209.1112.

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Abstract Mitochondrial transfer occurs both in stroke (central nervous system) and inflammatory pain (peripheral nerves). However, its role in glioblastoma (GBM) remains poorly understood. We hypothesized that mitochondrial transfer from non-malignant to GBM cells supports tumor metabolism and growth. Using transgenic mice expressing fluorophore-tagged mitochondria, we found that ~50% of orthotopically-implanted mouse GBM cells acquire mitochondria. Brain-resident cells, especially astrocytes, were the primary mitochondrial donors in vitro and in vivo. Mitochondrial transfer also occurred from

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Ganguly, Debolina, Chun Cai, Michelle Sims, et al. "APELA Expression in Glioma, and Its Association with Patient Survival and Tumor Grade." Pharmaceuticals 12, no. 1 (2019): 45. http://dx.doi.org/10.3390/ph12010045.

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Glioblastoma (GBM) is the most common and deadliest primary adult brain tumor. Invasion, resistance to therapy, and tumor recurrence in GBM can be attributed in part to brain tumor-initiating cells (BTICs). BTICs isolated from various patient-derived xenografts showed high expression of the poorly characterized Apelin early ligand A (APELA) gene. Although originally considered to be a non-coding gene, the APELA gene encodes a protein that binds to the Apelin receptor and promotes the growth of human embryonic stem cells and the formation of the embryonic vasculature. We found that both APELA m

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Abdelkareem, Aly O., Katalin Osz, Donna Senger, Jennifer A. Chan, and Sorana Morrissy. "Abstract 6397: Understanding the glioblastoma microenvironment with spatial resolution in PDX models." Cancer Research 82, no. 12_Supplement (2022): 6397. http://dx.doi.org/10.1158/1538-7445.am2022-6397.

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Abstract Glioblastoma multiforme (GBM) is the most common adult brain tumour, and despite aggressive treatment, it recurs fatally. GBM tumours include diverse populations of malignant and non-neoplastic cells with distinct molecular capabilities and with differential levels of sensitivity to treatment. Understanding the cell dynamics that occur during the development of GBM resistance to therapy could reveal key aspects of this process, including how resistance is acquired in time and how the diverse cell types of the tumour microenvironment (TME) contribute to this phenotype. In addition to t

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Azzarelli, Dr Roberta, Dr Laura Morcom, Prof David Rowitch, and Prof Anna Philpott. "INVESTIGATING GLIOBLASTOMA STEM CELL DIFFERENTIATION IN HUMAN BRAIN 3D ORGANOID CO-CULTURES." Neuro-Oncology 26, Supplement_7 (2024): vii4. http://dx.doi.org/10.1093/neuonc/noae158.013.

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Abstract AIMS Glioblastoma (GBM) recurrence is rooted in the ability of residual stem cells to survive treatment and drive relapse. One way to eradicate glioblastoma stem cells (GSCs) is to differentiate them into post-mitotic, non-tumorigenic cell types. Here we aim to differentiate GSCs via genetic manipulation, and test how their response differs in 2D and 3D cultures. METHOD We generated a co-culture model to grow GSC lines with iPSC-derived 3D human brain organoids. Before co-culture, the GSC lines were genetically engineered to overexpress a Doxycycline (Dox) inducible form of the proneu

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Kälin, Roland, Dongxu Zhao, Huabin Zhang, Ramazan Uyar, Jörg-Christian Tonn, and Rainer Glass. "TMOD-12. COMPARING TUMOR CELL INVASION AND MYELOID CELL COMPOSITION IN GENETICALLY IDENTICAL PRIMARY AND RELAPSING GLIOBLASTOMA." Neuro-Oncology 23, Supplement_6 (2021): vi218. http://dx.doi.org/10.1093/neuonc/noab196.873.

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Abstract Glioblastoma (GBM) recurrence after treatment is almost inevitable, but addressing this issue with adequate preclinical models has remained challenging. Here, we introduce a GBM mouse model allowing non-invasive and scalable de-bulking of a tumor mass located deeply in the brain, which can be combined with conventional therapeutic approaches. Towards this aim we genetically engineered mouse GBM cells to stably express the herpes simplex virus thymidine kinase. Strong reduction of the GBM volume is achieved after pharmacologically inducing a tumor-specific cell death mechanism by the p

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