bims-malgli Biomed News
on Biology of malignant gliomas
Issue of 2024–12–08
nine papers selected by
Oltea Sampetrean, Keio University



  1. Proc Natl Acad Sci U S A. 2024 Dec 10. 121(50): e2417420121
      Gliomas are the most common malignant primary brain tumor and are often associated with severe neurological deficits and mortality. Unlike many cancers, gliomas rarely metastasize outside the brain, indicating a possible dependency on unique features of brain microenvironment. Synapses between neurons and glioma cells exist, suggesting that glioma cells rely on neuronal inputs and synaptic signaling for proliferation. Yet, the locations and properties of neurons that innervate gliomas have remained elusive. In this study, we utilized transsynaptic tracing with an EnvA-pseudotyped, glycoprotein-deleted rabies virus to specifically infect TVA and glycoprotein-expressing human glioblastoma cells in an orthotopic xenograft mouse model, allowing us to identify the neurons that form synapses onto the gliomas. Comprehensive whole-brain mapping revealed that these glioma-innervating neurons (GINs) from brain regions, including diverse neuromodulatory centers and specific cortical layers, known to project to the glioma locations. Molecular profiling revealed that long-range cortical GINs are predominantly glutamatergic, and subsets express both glutamatergic and GABAergic markers, whereas local striatal GINs are largely GABAergic. Electrophysiological studies demonstrate that while GINs share passive intrinsic properties with cortex-innervating neurons, their action potential waveforms are altered. Our study introduces a method for identifying and mapping GINs and reveals their consistent integration into existing location-dependent neuronal networks involving diverse neurotransmitters and neuromodulators. The observed intrinsic electrophysiological differences in GINs lay the groundwork for future investigations into how these alterations relate to the postsynaptic characteristics of glioma cells.
    Keywords:  GABAergic; gliomas; glutamatergic; monosynaptic tracing; neuron-glioma synapse
    DOI:  https://doi.org/10.1073/pnas.2417420121
  2. Cancer Res. 2024 Dec 02. 84(23): 4017-4030
      Glioblastoma (GBM) is a highly aggressive brain tumor with poor prognosis and high recurrence rates. The complex immune microenvironment of GBM is highly infiltrated by tumor-associated microglia and macrophages (TAM). TAMs are known to be heterogeneous in their functional and metabolic states and can transmit either protumoral or antitumoral signals to glioma cells. Here, we performed bulk RNA sequencing and single-cell RNA sequencing on samples from patients with GBM, which revealed increased ATP synthase expression and oxidative phosphorylation activity in TAMs located in the tumor core relative to the tumor periphery. Both in vitro and in vivo models displayed similar trends of augmented TAM mitochondrial activity, along with elevated mitochondrial fission, glucose uptake, mitochondrial membrane potential, and extracellular ATP (eATP) production by TAMs in the presence of GBM cells. Tumor-secreted factors, including GM-CSF, induced the increase in TAM eATP production. Elevated eATP in the GBM microenvironment promoted glioma growth and invasion by activating the P2X purinoceptor 7 (P2X7R) on glioma cells. Inhibition of the eATP-P2X7R axis attenuated tumor cell viability in vitro and reduced tumor size and prolonged survival in glioma-bearing mouse models. Overall, this study revealed elevated TAM-derived eATP in GBM and provided the basis for targeting the eATP-P2X7R signaling axis as a therapeutic strategy in GBM. Significance: Glioblastoma-mediated metabolic reprogramming in tumor-associated microglia increases ATP secretion that supports cancer cell proliferation and invasion by activating P2X7R, which can be inhibited to attenuate tumor growth.
    DOI:  https://doi.org/10.1158/0008-5472.CAN-24-0018
  3. Cell Rep. 2024 Dec 03. pii: S2211-1247(24)01365-2. [Epub ahead of print]43(12): 115014
      Glioblastoma represents one of the most aggressive cancers, characterized by severely limited therapeutic options. Despite extensive investigations into this brain malignancy, cellular and molecular components governing its immunosuppressive microenvironment remain incompletely understood. Here, we identify a distinct neutrophil subpopulation, termed disease-specific suppressive granulocytes (DSSGs), present in human glioblastoma and lower-grade gliomas. DSSGs exhibit the concurrent expression of multiple immunosuppressive and immunomodulatory signals, and their abundance strongly correlates with glioma grades and poor clinical outcomes. Genetic disruption of neutrophil recruitment in immunocompetent mouse models of gliomas, achieved through Cxcl1 knockout in glioma cells or host-specific Cxcr2 deletion or diphtheria toxin A-mediated neutrophil depletion, can significantly enhance antitumor immunity and prolong survival. Further, we reveal that the skull bone marrow and meninges can be the primary sources of neutrophils and DSSGs in human and mouse glioma tumors. These findings demonstrate a critical mechanism underlying the establishment of the immunosuppressive microenvironment in gliomas.
    Keywords:  CP: Cancer
    DOI:  https://doi.org/10.1016/j.celrep.2024.115014
  4. Sci Rep. 2024 12 02. 14(1): 29897
      Controlled drug delivery systems have been intensively researched for cancer treatment to increase precision targeting and therapeutic efficacy. In this context, novel magnetic-/pH-sensitive graphene oxide/chitosan/iron oxide magnetic nanocomposite microspheres were synthesized. Fe3O4 (IO) nanoparticles (NPs) were synthesized via the green synthesis method in the presence of Salvia officinalis extract. The graphene oxide (GO) NPs were prepared using the Staudenmaier method, and synthesized materials were characterized. Chitosan (CS) was used to prepare microspheres. GO/CS/IO microspheres were investigated as prospective vehicles for controlled temozolomide delivery in the presence and absence of an external magnetic field. The release percentage of temozolomide molecules in the presence of 100 Hz reached a maximum in 90 min. This is approximately twice the amount of drug release in the absence of a magnetic field and more than that in the presence of a 50 Hz magnetic field. Also, the highest degree of swelling was observed at a pH of 4.5, higher than at a pH of 7.4. Also, the MTT assay results indicated the cytotoxicity of the synthesized microspheres for glioblastoma cells; notably, a significant difference was observed between the groups exposed to the magnetic field and those not, with exposure to the magnetic field further reducing survival. These results indicated that the magnetic microspheres potentially apply to controlled drug delivery systems.
    Keywords:  Controlled drug delivery; Glioblastoma; Magnetic Microspheres; PH-sensitive; Temozolomide
    DOI:  https://doi.org/10.1038/s41598-024-80596-8
  5. Sci Rep. 2024 12 04. 14(1): 30180
      Compounds targeting non-canonical secondary structures of nucleic acids, known as G-quadruplexes, are highly cytotoxic, both for cancer and healthy cells, because of their action mechanism's lack of appropriate selectivity. The targeted delivery of cytotoxic molecules to cancer cells is a valuable strategy to expand the repertoire of potential drugs, especially for cancer types for which new therapeutic tools are urgently needed, like glioblastoma. In this work, we conjugated a cyclic arginyl-glycyl-aspartic acid peptide to a naphthalene diimide, previously described as a highly performing stabilizing ligand for DNA G-quadruplexes, to specifically target glioma cells overexpressing RGD-binding integrin receptors. Our results, including confocal microscopy and cell toxicity assays, demonstrated improved efficacy and selective cellular absorption of the new conjugate without affecting the NDI's ability to interact with the G4 target.
    DOI:  https://doi.org/10.1038/s41598-024-81513-9
  6. J Immunother Cancer. 2024 Dec 02. pii: e009604. [Epub ahead of print]12(12):
       BACKGROUND: Glioblastoma multiforme (GBM) is known for its high antigenic heterogeneity, which undermines the effectiveness of monospecific immunotherapies. Multivalent immunotherapeutic strategies that target multiple tumor antigens simultaneously could enhance clinical outcomes by preventing antigen-driven tumor escape mechanisms.
    METHODS: We describe novel trivalent antibodies, DNA-encoded tri-specific T-cell engagers (DTriTEs), targeting two GBM antigens, epidermal growth factor receptor variant III (EGFRvIII) and IL-13Rα2, and engaging T cells through CD3. We engineered three DTriTE constructs, each with a unique arrangement of the antigen-binding fragments within a single-chain sequence. We assessed the binding efficiency and cytotoxic activity of these DTriTEs in vitro on target cells expressing relevant antigens. In vivo efficacy was tested in immunocompromised mice, including a longitudinal expression study post-administration and a survival analysis in an NOD scid gamma (NSG)-K mouse model under a heterogeneous tumor burden. RNA sequencing of DTriTE-activated T cells was employed to identify the molecular pathways influenced by the treatment. The antitumor cytotoxicity of patient-derived immune cells was evaluated following stimulation by DTriTE to assess its potential effectiveness in a clinical setting.
    RESULTS: All DTriTE constructs demonstrated strong binding to EGFRvIII and IL-13Rα2-expressing cells, induced significant T cell-mediated cytotoxicity, and enhanced cytokine production (interferon-γ, tumor necrosis factor (TNF)-α, and interleukin(IL)-2). The lead construct, DT2035, sustained expression for over 105 days in vivo and exhibited elimination of tumor burden in a heterogeneous intracranial GBM model, outperforming monospecific antibody controls. In extended survival studies using the NSG-K model, DT2035 achieved a 67% survival rate over 120 days. RNA sequencing of DTriTE-activated T cells showed that DT2035 enhances genes linked to cytotoxicity, proliferation, and immunomodulation, reflecting potent immune activation. Finally, DT2035 effectively induced target-specific cytotoxicity in post-treatment peripheral blood mononuclear cells from patients with GBM, highlighting its potential for clinical effectiveness.
    CONCLUSIONS: DTriTEs exhibit potent anti-tumor effects and durable in vivo activity, offering promising therapeutic potential against GBM. These findings support further development of such multivalent therapeutic strategies to improve treatment outcomes in GBM and potentially other antigenically heterogeneous tumors. The opportunity to advance such important therapies either through biologic delivery or direct in vivo nucleic acid production is compelling.
    Keywords:  Bispecific T cell engager - BiTE; Immunotherapy; T cell
    DOI:  https://doi.org/10.1136/jitc-2024-009604
  7. iScience. 2024 Dec 20. 27(12): 111311
      While mitotic spindle inhibitors specifically kill proliferating tumor cells without the toxicities of microtubule poisons, resistance has limited their clinical utility. Treating glioblastomas with the spindle inhibitors ispinesib, alisertib, or volasertib creates a subpopulation of therapy induced senescent cells that resist these drugs by relying upon the anti-apoptotic and metabolic effects of activated STAT3. Furthermore, these senescent cells expand the repertoire of cells resistant to these drugs by secreting an array of factors, including TGFβ, which induce proliferating cells to exit mitosis and become quiescent-a state that also resists spindle inhibitors. Targeting STAT3 restores sensitivity to each of these drugs by depleting the senescent subpopulation and inducing quiescent cells to enter the mitotic cycle. These results support a therapeutic strategy of targeting STAT3-dependent therapy-induced senescence to enhance the efficacy of spindle inhibitors for the treatment of glioblastoma.
    Keywords:  Cancer; Cell biology; Molecular biology
    DOI:  https://doi.org/10.1016/j.isci.2024.111311
  8. Clin Cancer Res. 2024 Dec 03.
    Audrey-Anne Lamoureux, Michael J Fisher, Lauriane Lemelle, Elke Pfaff, Pouneh Amir-Yazdani, Christof Kramm, Bram De Wilde, Bernarda Kazanowska, Caroline Hutter, Stefan M Pfister, Dominik Sturm, David T W Jones, Daniel Orbach, Gaëlle Pierron, Scott Raskin, Alexander Drilon, Eli L Diamond, Guilherme Harada, Michal Zapotocky, Josef Zamecnik, Lenka Krskova, Benjamin Ellezam, Alexander G Weil, Dominic Venne, Marc Barritault, Pierre Leblond, Hallie Coltin, Rawan Hammad, Uri Tabori, Cynthia Hawkins, Jordan R Hansford, Deborah Meyran, Craig Erker, Kathryn McFadden, Mariko Sato, Nicholas G Gottardo, Hetal Dholaria, Dorte Schou Nørøxe, Hiroaki Goto, David S Ziegler, Frank Y Lin, Donald Williams Parsons, Holly Lindsay, Tai-Tong Wong, Yen-Lin Liu, Kuo-Sheng Wu, Andrea T Franson, Eugene Hwang, Ana Aguilar-Bonilla, Sylvia Cheng, Chantel Cacciotti, Maura Massimino, Elisabetta Schiavello, Paul Wood, Lindsey M Hoffman, Andréa Cappellano, Alvaro Lassaletta, An Van Damme, Anna Llort, Nicolas U Gerber, Mariella Spalato Ceruso, Anne E Bendel, Maggie Skrypek, Dima Hamideh, Naureen Mushtaq, Andrew Walter, Nada Jabado, Aysha Alsahlawi, Jean-Pierre Farmer, Christina Coleman, Sabine Mueller, Claire Mazewski, Dolly Aguilera, Nathan J Robison, Katrina O'Halloran, Samuel Abbou, Pablo Berlanga, Birgit Geoerger, Ingrid Øra, Christopher L Moertel, Evangelia D Razis, Anastasia Vernadou, François Ducray, Charlotte Bronnimann, Romuald Seizeur, Matthew Clarke, Adam C Resnick, Mélanie Alves, Chris Jones, François Doz, Theodore W Laetsch, Sébastien Perreault.
       PURPOSE: TRK fusions are detected in less than 2% of central nervous system tumors. There are limited data on the clinical course of affected patients.
    EXPERIMENTAL DESIGN: We conducted an international retrospective cohort study of patients with TRK fusion-driven CNS tumors.
    RESULTS: 119 patients were identified. The median age at time of diagnosis was 4.5 years. The majority were reported to have a histology consistent with a diagnosis of high-grade glioma (HGG) (57.1%) followed by low-grade glioma (LGG) (27.7%). Pediatric patients had a better prognosis with a median overall survival of 185.5 months compared to 24.8 months in adults (p<.0001). Patients with LGG also had a better outcome when compared to HGG (p=0.0012). The objective response was 68.8% with larotrectinib compared to 38.1% for non-targeted treatment.
    CONCLUSIONS: Children with LGG glioma had a favorable outcome compared to adult and HGG. TRK inhibitors appear to improve tumor control.
    DOI:  https://doi.org/10.1158/1078-0432.CCR-24-0581
  9. ACS Nano. 2024 Dec 03.
      Although dendritic cell (DC)-mediated immunotherapies are effective options for immunotherapy, traditional DC vaccines are hampered by a variety of drawbacks such as insufficient antigen delivery, weak lymph node homing, and the risk of living cell transfusion. To address the above-mentioned issues, we developed a personalized DC-mimicking nanovaccine (HybridDC) that enhances antigen presentation and elicits effective antitumor immunity. The biomimetic nanovaccine contains cell membranes derived from genetically engineered DCs, and several cellular components are simultaneously anchored onto these membranes, including CC-chemokine receptor 7 (CCR7), tumor-associated antigenic (TAA) peptide/tumor-derived exosome (TEX), and relevant costimulatory molecules. Compared with previous vaccines, the HybridDC vaccine showed an increased ability to target lymphoid tissues and reshape the immune landscape in the tumor milieu. HybridDC demonstrated significant therapeutic and prophylactic efficacy in poorly immunogenic, orthotopic models of glioma. Furthermore, the HybridDC vaccine potentiates the therapeutic efficacy of immune checkpoint blockade (ICB) therapy, providing a potential combination strategy to maximize the efficacy of ICB. Specifically, HybridDC can induce long-term protective immunity in memory T cells. Overall, the HybridDC vaccine is a promising platform for personalized cancer vaccines and may offer a combinational modality to improve current immunotherapy.
    Keywords:  cell membrane; dendritic cell; immunotherapy; nanovaccine; tumor microenvironment
    DOI:  https://doi.org/10.1021/acsnano.4c09653