bims-malgli Biomed News
on Biology of malignant gliomas
Issue of 2025–04–06
twelve papers selected by
Oltea Sampetrean, Keio University
  1. Differential Phagocytosis induces Diverse Macrophage Activation States in Malignant Gliomas.
  2. Lipid peroxidation and immune activation: TRAF3's double-edged strategy against glioblastoma.
  3. IL-6 underlies microenvironment immunosuppression and resistance to therapy in glioblastoma.
  4. Response to anti-angiogenic therapy is affected by AIMP protein family activity in glioblastoma and lower-grade gliomas.
  5. Multi-omic landscape of human gliomas from diagnosis to treatment and recurrence.
  6. Lysine-arginine imbalance overcomes therapeutic tolerance governed by the transcription factor E3-lysosome axis in glioblastoma.
  7. Interstitial fluid transport dynamics predict glioblastoma invasion and progression.
  8. Antibody-Free Immunopeptide Nano-Conjugates for Brain-Targeted Drug Delivery in Glioblastoma Multiforme.
  9. Advancing Clinical Response Against Glioblastoma: Evaluating SHP1705 CRY2 Activator Efficacy in Preclinical Models and Safety in Phase I Trials.
  10. Engineering sonogenetic EchoBack-CAR T cells.
  11. Targeting CHEK2-YBX1&YBX3 regulatory hub to potentiate immune checkpoint blockade response in gliomas.
  12. Targeting gut microbiota: a potential therapeutic approach for tumor microenvironment in glioma.
  1. bioRxiv. 2025 Mar 17. pii: 2025.03.15.642920. [Epub ahead of print]
    Differential Phagocytosis induces Diverse Macrophage Activation States in Malignant Gliomas.
    Senthilnath Lakshmanachetty, Kent Riemondy, Bridget Sanford, Andrew Donson, Ilango Balakrishnan, Eric Prince, Todd Hankinson, Nathan Dahl, Rajeev Vibhakar, Nicholas K Foreman, Sujatha Venkataraman, Siddhartha S Mitra.
      Diffuse midline glioma (DMG) and Glioblastoma are malignant brain tumors in pediatric and adult patients. The current standard-of-care treatment for DMG is radiotherapy (RT), whereas GBM treatment includes surgery, followed by RT and chemotherapy. Although RT is known to modulate immune responses in cancer and enhance the effectiveness of myeloid checkpoint blockade, the downstream macrophage responses to differential phagocytosis induction remain poorly understood. This study examined macrophage-mediated phagocytosis caused by either RT, anti-CD47 checkpoint blockade, or their combination. We found that RT increased the expression of several damage-associated molecular patterns on the surface of glioma cell lines. Furthermore, RT enhanced anti-CD47-mediated macrophage phagocytosis of glioma cell lines in vitro . Single-cell RNA-sequencing revealed the diverse transcriptional and functional signatures of human macrophage subsets that either promoted or inhibited phagocytosis of glioma cells pretreated with RT, anti-CD47 therapy, or both. Consistent with these results, the combination therapy significantly reduced tumor growth, prolonged survival in glioma-bearing mice, and induced distinct macrophage activation states in vivo compared to either treatment alone. These findings highlight the plasticity and heterogeneity of macrophage responses during phagocytosis and provide compelling evidence for combining RT with anti-CD47 therapy as a promising therapeutic strategy for glioma treatment.
    DOI:  https://doi.org/10.1101/2025.03.15.642920
  2. J Clin Invest. 2025 Apr 01. pii: e190471. [Epub ahead of print]135(7):
    Lipid peroxidation and immune activation: TRAF3's double-edged strategy against glioblastoma.
    Tzu-Yi Chia, Nishanth S Sadagopan, Jason Miska.
      Glioblastoma (GBM), the most aggressive type of primary brain tumor, continues to defy therapeutic advances with its metabolic adaptability and resistance to treatment. In this issue of the JCI, Zeng et al. delve into a pivotal mechanism underpinning this adaptability. They identified an important role for TNF receptor-associated factor 3 (TRAF3) in regulating lipid metabolism through its interaction with enoyl-CoA hydratase 1 (ECH1). These findings elucidate a unique signaling axis that shields GBM cells from lipid peroxidation and antitumor immunity, advancing therapeutic strategies for GBM that may also carry over to other cancers with similar metabolic vulnerabilities.
    DOI:  https://doi.org/10.1172/JCI190471
  3. bioRxiv. 2025 Mar 14. pii: 2025.03.12.642800. [Epub ahead of print]
    IL-6 underlies microenvironment immunosuppression and resistance to therapy in glioblastoma.
    Jacob S Young, Nam Woo Cho, Calixto-Hope G Lucas, Hinda Najem, Kanish Mirchia, William C Chen, Kyounghee Seo, Naomi Zakimi, Vikas Daggubati, Tim Casey-Clyde, Minh P Nguyen, Arya Chen, Joanna J Phillips, Tomoko Ozawa, Manish K Aghi, Jennie W Taylor, Joseph L DeRisi, Aparna Bhaduri, Mitchel S Berger, Amy B Heimberger, Nicholas Butowski, Matthew H Spitzer, David R Raleigh.
      The glioblastoma tumor immune microenvironment (TIME) is an immunosuppressive barrier to therapy that encumbers glioblastoma responses to immune checkpoint inhibition (ICI). Immunosuppressive cytokines, pro-tumor myeloid cells, and exhausted T-cells are hallmarks of the glioblastoma TIME. Here we integrate spatial and single-cell analyses of patient-matched human glioblastoma samples before and after ICI with genetic, immunologic, single-cell, and pharmacologic studies in preclinical models to reveal that interleukin-6 (IL-6) inhibition reprograms the glioblastoma TIME to sensitize mouse glioblastoma to ICI and radiotherapy. Rare human glioblastoma patients who achieve clinical responses to ICI have lower pre-treatment IL-6 levels compared to glioblastomas who do not respond to ICI. Immune stimulatory gene therapy suppresses IL-6 tumor levels in preclinical murine models of glioblastoma. Furthermore, survival was longer in Il-6 knockout mice with orthotopic SB28 glioblastoma relative to wild-type mice. IL-6 blockade with a neutralizing antibody transiently sensitizes mouse glioblastoma to anti-PD-1 by increasing MHCII+ monocytes, CD103+ migratory dendritic cells (DCs), CD11b+ conventional DCs, and effector CD8+ T cells, and decreasing immunosuppressive Tregs. To translate these findings to a combination treatment strategy for recurrent glioblastoma patients, we show that IL-6 blockade plus ICI durably sensitizes mouse glioblastoma to high-dose radiotherapy.
    DOI:  https://doi.org/10.1101/2025.03.12.642800
  4. bioRxiv. 2025 Mar 14. pii: 2025.03.13.643116. [Epub ahead of print]
    Response to anti-angiogenic therapy is affected by AIMP protein family activity in glioblastoma and lower-grade gliomas.
    Humaira Noor, Yuanning Zheng, Haruka Itakura, Olivier Gevaert.
       Background: Glioblastoma (GBM) is a highly vascularized, heterogeneous tumor, yet anti-angiogenic therapies have yielded limited survival benefits. The lack of validated predictive biomarkers for treatment response stratification remains a major challenge. Aminoacyl tRNA synthetase complex-interacting multicomplex proteins (AIMPs) 1/2/3 have been implicated in CNS diseases, but their roles in gliomas remain unexplored. We investigated their association with angiogenesis and their significance as predictive biomarkers for anti-angiogenic treatment response.
    Methods: In this multi-cohort retrospective study we analyzed glioma samples from TCGA, CGGA, Rembrandt, Gravendeel, BELOB and REGOMA trials, and four single-cell transcriptomic datasets. Multi-omic analyses incorporated transcriptomic, epigenetic, and proteomic data. Kaplan-Meier and Cox proportional hazards models were used to assess the prognostic value of AIMPs in heterogeneous and homogeneous treatment-groups. Using single-cell transcriptomics, we explored spatial and cell-type-specific AIMP2 expression in GBM.
    Results: AIMP1/2/3 expressions correlated significantly with angiogenesis across TCGA cancers. In gliomas, AIMPs were upregulated in tumor vs. normal tissues, higher- vs. lower-grade gliomas, and recurrent vs. primary tumors (p<0.05). Upon retrospective analysis of two clinical trials assessing different anti-angiogenic drugs, we found that high-AIMP2 subgroups had improved response to therapies in GBM (REGOMA: HR 4.75 [1.96-11.5], p<0.001; BELOB: HR 2.3 [1.17-4.49], p=0.015). AIMP2-cg04317940 methylation emerged as a clinically applicable stratification marker. Single-cell analysis revealed homogeneous AIMP2 expression in tumor tissues, particularly in AC-like cells, suggesting a mechanistic link to tumor angiogenesis.
    Conclusions: These findings provide novel insights into the role of AIMPs in angiogenesis, offering improved patient stratification and therapeutic outcomes in recurrent GBM.
    Keywords:  AIMP2; Glioblastoma; anti-angiogenesis treatment; bevacizumab response
    DOI:  https://doi.org/10.1101/2025.03.13.643116
  5. bioRxiv. 2025 Mar 14. pii: 2025.03.12.642624. [Epub ahead of print]
    Multi-omic landscape of human gliomas from diagnosis to treatment and recurrence.
    Hadeesha Piyadasa, Benjamin Oberlton, Mikaela Ribi, Jolene S Ranek, Inna Averbukh, Ke Leow, Meelad Amouzgar, Candace C Liu, Noah F Greenwald, Erin F McCaffrey, Rashmi Kumar, Selena Ferrian, Albert G Tsai, Ferda Filiz, Christine Camacho Fullaway, Marc Bosse, Sricharan Reddy Varra, Alex Kong, Cameron Sowers, Melanie Hayden Gephart, Pablo Nuñez-Perez, EnJun Yang, Mike Travers, Michael J Schachter, Samantha Liang, Maria R Santi, Samantha Bucktrout, Pier Federico Gherardini, Kristina Cole, Michael E Barish, Christine E Brown, Derek A Oldridge, Richard R Drake, Joanna J Phillips, Hideho Okada, Robert Prins, Sean C Bendall, Michael Angelo.
      Gliomas are among the most lethal cancers, with limited treatment options. To uncover hallmarks of therapeutic escape and tumor microenvironment (TME) evolution, we applied spatial proteomics, transcriptomics, and glycomics to 670 lesions from 310 adult and pediatric patients. Single-cell analysis shows high B7H3+ tumor cell prevalence in glioblastoma (GBM) and pleomorphic xanthoastrocytoma (PXA), while most gliomas, including pediatric cases, express targetable tumor antigens in less than 50% of tumor cells, potentially explaining trial failures. Longitudinal samples of isocitrate dehydrogenase (IDH)-mutant gliomas reveal recurrence driven by tumor-immune spatial reorganization, shifting from T-cell and vasculature-associated myeloid cell-enriched niches to microglia and CD206+ macrophage-dominated tumors. Multi-omic integration identified N-glycosylation as the best classifier of grade, while the immune transcriptome best predicted GBM survival. Provided as a community resource, this study opens new avenues for glioma targeting, classification, outcome prediction, and a baseline of TME composition across all stages.
    DOI:  https://doi.org/10.1101/2025.03.12.642624
  6. Nat Commun. 2025 Apr 01. 16(1): 2876
    Lysine-arginine imbalance overcomes therapeutic tolerance governed by the transcription factor E3-lysosome axis in glioblastoma.
    Yongwei Jing, Masahiko Kobayashi, Mahmoud I Shoulkamy, Meiqi Zhou, Ha Thi Vu, Hiroshi Arakawa, Hemragul Sabit, Sadahiro Iwabuchi, Cong Quang Vu, Atsuko Kasahara, Masaya Ueno, Yuko Tadokoro, Kenta Kurayoshi, Xi Chen, Yuhang Yan, Satoshi Arai, Shinichi Hashimoto, Tomoyoshi Soga, Tomoki Todo, Mitsutoshi Nakada, Atsushi Hirao.
      Recent advances in cancer therapy have underscored the importance of targeting specific metabolic pathways. In this study, we propose a precision nutrition approach aimed at lysosomal function in glioblastoma multiforme (GBM). Using patient-derived GBM cells, we identify lysosomal activity as a unique metabolic biomarker of tumorigenesis, controlling the efficacy of temozolomide (TMZ), a standard GBM therapy. Employing combined analyses of clinical patient samples and xenograft models, we further elucidate the pivotal role of Transcription Factor Binding To IGHM Enhancer 3 (TFE3), a master regulator of lysosomal biogenesis, in modulating malignant properties, particularly TMZ tolerance, by regulating peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC1α)-mediated mitochondrial activity. Notably, we find that lysine protects GBM cells from lysosomal stress by counteracting arginine's effects on nitric oxide production. The lysine restriction mimetic, homoarginine administration, significantly enhances the efficacy of anticancer therapies through lysosomal dysfunction. This study underscores the critical role of lysosomal function modulated by amino acid metabolism in GBM pathogenesis and treatment.
    DOI:  https://doi.org/10.1038/s41467-025-56946-z
  7. bioRxiv. 2025 Mar 14. pii: 2025.03.12.642840. [Epub ahead of print]
    Interstitial fluid transport dynamics predict glioblastoma invasion and progression.
    Cora M Carman-Esparza, Caleb A Stine, Naciye Atay, Kathryn M Kingsmore, Maosen Wang, Ryan T Woodall, Russell C Rockne, Jessica J Cunningham, Jennifer M Munson.
      Glioblastoma is characterized by aggressive infiltration into surrounding brain tissue, hindering complete surgical resection and contributing to poor patient outcomes. Identifying tumor-specific invasion patterns is essential for advancing our understanding of glioblastoma progression and improving surgical and radiotherapeutic strategies. Here, we leverage in vivo dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) to noninvasively quantify interstitial fluid velocity, direction, and diffusion within and around glioblastomas. We introduce a novel vector-based pathline analysis to trace downstream accumulation of fluid flow originating from the tumor core, providing a spatially explicit perspective on local flow patterns. We find that localized fluid transport metrics predict glioblastoma invasion and progression, offering a new framework to non-invasively identify high-risk regions and guide targeted treatment approaches.
    One sentence summary: Invasion and progression of glioblastoma can be predicted with interstitial fluid flow patterns via magnetic resonance imaging.
    DOI:  https://doi.org/10.1101/2025.03.12.642840
  8. bioRxiv. 2025 Mar 12. pii: 2025.03.07.641755. [Epub ahead of print]
    Antibody-Free Immunopeptide Nano-Conjugates for Brain-Targeted Drug Delivery in Glioblastoma Multiforme.
    Saurabh Sharma, David Lee, Surjendu Maity, Prabhjeet Singh, Jay Chadokiya, Neda Mohaghegh, Alireza Hassani, Hanjun Kim, Ankit Gangarade, Julia Y Ljubimova, Amanda Kirane, Eggehard Holler.
      Glioblastoma Multiforme (GBM) represents a significant clinical challenge amongst central nervous system (CNS) tumors, with a dismal mean survival rate of less than 8 months, a statistic that has remained largely unchanged for decades (National Brain Society, 2022). The specialized intricate anatomical features of the brain, notably the blood-brain barrier (BBB), pose significant challenges to effective therapeutic interventions, limiting the potential reach of modern advancements in immunotherapy to impact these types of tumors. This study introduces an innovative, actively targeted immunotherapeutic nanoconjugate (P12/AP-2/NCs) designed to serve as an immunotherapeutic agent capable of traversing the BBB via LRP-1 receptor-mediated transcytosis. P12/AP-2/NCs exert its immune-modulating effects by inhibiting the PD-1/PD-L1 axis through a small-size PD-L1/PD-L2 antagonist peptide Aurigene NP-12 (P12). P12/AP-2/NCs are synthesized from completely biodegradable, functionalized high molecular weight β-poly(L-malic acid) (PMLA) polymer, conjugated with P12 and Angiopep-2 (AP2) to yield P12/AP-2/NCs. Evaluating nanoconjugates for BBB permeability and 3-D tumor model efficacy using an in vitro BBB-Transwell spheroid based model demonstrating successful crossing of the BBB and internalization in brain 3D tumor environments. In addition, the nanoconjugate mediated T cell's cytotoxicity on 3D tumor region death in a U87 GBM 3-D spheroid model. AP2/P12/NCs is selectively inhibited in PD1/PDL1 interaction on T cells and tumor site, increasing inflammatory cytokine secretion and T cell proliferation. In an in-vivo murine brain environment, rhodamine fluorophore-labeled AP2/P12/NCs displayed significantly increased accumulation in the brain during 2-6 h time intervals post-injection with a prolonged bioavailability over unconjugated peptides. AP2/P12/NCs demonstrated a safety profile at both low and high doses based on major organ histopathology evaluations. Our findings introduce a novel, programmable nanoconjugate platform capable of penetrating the BBB for directed delivery of small peptides and significant immune environment modulation without utilizing antibodies, offering promise for treating challenging brain diseases like glioblastoma multiforme and beyond.
    Keywords:  3D Tumor-BBB Model; Biodistribution; Immunotherapy; Nanoconjugate
    DOI:  https://doi.org/10.1101/2025.03.07.641755
  9. Neuro Oncol. 2025 Apr 01. pii: noaf089. [Epub ahead of print]
    Advancing Clinical Response Against Glioblastoma: Evaluating SHP1705 CRY2 Activator Efficacy in Preclinical Models and Safety in Phase I Trials.
    Priscilla Chan, Yoshiko Nagai, Qiulian Wu, Anahit Hovsepyan, Seda Mkhitaryan, Jiarui Wang, Gevorg Karapetyan, Theodore Kamenecka, Laura A Solt, Jamie Cope, Rex A Moats, Tsuyoshi Hirota, Jeremy N Rich, Steve A Kay.
       BACKGROUND: It has been reported that circadian clock components, Brain and Muscle ARNT-Like 1 (BMAL1) and Circadian Locomotor Output Cycles Kaput (CLOCK), are essential for glioblastoma (GBM) stem cell (GSC) biology and survival. Consequently, we developed a novel Cryptochrome (CRY) activator SHP1705, which inhibits BMAL1-CLOCK transcriptional activity.
    METHODS: We utilized GlioVis to determine which circadian genes are differentially expressed in non-tumor versus GBM tissues. We employed in vitro and in vivo methods to test the efficacy of SHP1705 against patient-derived GSCs and xenografts in comparison to earlier CRY activator scaffolds. We applied a novel REV-ERB agonist SR29065, which inhibits BMAL1 transcription, to determine whether targeting both negative limbs of the circadian transcription-translation feedback loop (TTFL) would yield synergistic effects against various GBM cells.
    RESULTS: SHP1705 is the first circadian clock-modulating compound to be found safe and well-tolerated in Phase I clinical trials. SHP1705 has increased selectivity for the CRY2 isoform and potency against GSC viability compared to previously published CRY activators, making it promising for applications in GBM where CRY2 levels are found to be low. SHP1705 prolonged survival in mice bearing GBM tumors established with GSCs. When combined with novel REV-ERB agonist SR29065, SHP1705 displayed synergy against multiple GSC lines and differentiated GSCs (DGCs).
    CONCLUSIONS: We demonstrate the efficacy of SHP1705 against GSCs, which pose as a major source of chemoradiation resistance leading to poor GBM patient prognosis. Novel circadian clock compounds have high potential for targeting GBM as single agents or in combination with each other or current standard-of-care.
    Keywords:  CRY2; SHP1705; circadian clock; circadian medicine; glioblastoma
    DOI:  https://doi.org/10.1093/neuonc/noaf089
  10. Cell. 2025 Mar 23. pii: S0092-8674(25)00271-5. [Epub ahead of print]
    Engineering sonogenetic EchoBack-CAR T cells.
    Longwei Liu, Peixiang He, Yuxuan Wang, Fengyi Ma, Dulei Li, Zhiliang Bai, Yunjia Qu, Linshan Zhu, Chi Woo Yoon, Xi Yu, Yixuan Huang, Zhengyu Liang, Yiming Zhang, Kunshu Liu, Tianze Guo, Yushun Zeng, Qifa Zhou, H Kay Chung, Rong Fan, Yingxiao Wang.
      Chimeric antigen receptor (CAR) T cell therapy for solid tumors encounters challenges such as on-target off-tumor toxicity, exhaustion, and limited T cell persistence. Here, we engineer sonogenetic EchoBack-CAR T cells using an ultrasensitive heat-shock promoter screened from a library and integrated with a positive feedback loop from CAR signaling, enabling long-lasting CAR expression upon focused-ultrasound (FUS) stimulation. EchoBack-hGD2CAR T cells, targeting disialoganglioside GD2, exhibited potent cytotoxicity and persistence in 3D glioblastoma (GBM) models. In mice, EchoBack-hGD2CAR T cells suppressed GBM without off-tumor toxicity and outperformed their constitutive counterparts. Single-cell RNA sequencing revealed enhanced cytotoxicity and reduced exhaustion in EchoBack-CAR T cells compared with the standard CAR T cells. This EchoBack design was further adapted to target prostate-specific membrane antigen (EchoBack-PSMACAR) for prostate cancer treatment, demonstrating long-lasting tumor suppression with minimal off-tumor toxicity. Thus, the sonogenetic EchoBack-CAR T cells can serve as a versatile, efficient, and safe strategy for solid tumor treatment.
    Keywords:  CAR T; feedback engineering; immunotherapy; inducible gene expression; promoter library screening; solid tumor; sonogenetics; spatiotemporal CAR regulation; ultrasound controled CAR-T
    DOI:  https://doi.org/10.1016/j.cell.2025.02.035
  11. bioRxiv. 2025 Mar 13. pii: 2025.03.09.642289. [Epub ahead of print]
    Targeting CHEK2-YBX1&YBX3 regulatory hub to potentiate immune checkpoint blockade response in gliomas.
    Heba Ali, Ningjia Zhou, Li Chen, Levi van Hijfte, Vivekanudeep Karri, Yalu Zhou, Karl Habashy, Victor A Arrieta, Kwang-Soo Kim, Joseph Duffy, Ragini Yeeravalli, Deanna M Tiek, Xiao Song, Snehasis Mishra, Catalina Lee-Chang, Atique U Ahmed, Dieter Henrik Heiland, Adam M Sonabend, Crismita Dmello.
      Although GBM's immunosuppressive environment is well known, the tumor's resistance to CD8+ T cell killing is not fully understood. Our previous study identified Checkpoint Kinase 2 (Chek2) as the key driver of CD8+ T cell resistance in mouse glioma through an in vivo CRISPR screen and demonstrated that Chk2 inhibition, combined with PD-1/PD-L1 blockade, significantly enhanced CD8+ T cell-mediated tumor killing and improved survival in preclinical model. Here, we aimed to elucidate the immunosuppressive function of Chek2. Immunoprecipitation (IP) followed by mass spectrometry (MS) and phosphoproteomics identified an association between Chek2 with the DNA/RNA-binding proteins YBX1 and YBX3 that are implicated in transcriptional repression of pro-inflammatory genes. Single-gene knock-out and overexpression studies of CHEK2, YBX1, and YBX3 in multiple glioma cell lines revealed that these proteins positively regulate each other's expression. RNA sequencing coupled with chromatin immunoprecipitation-sequencing (ChIP-seq) analysis demonstrated common inflammatory genes repressed by CHK2-YBX1&YBX3 hub. Targeting one of the hub proteins, YBX1, with the YBX1 inhibitor SU056 led to degradation of CHK2-YBX1&YBX3 hub. Targeting of this hub by SU056 led to enhanced antigen presentation and antigen specific CD8+ T cell proliferation. Further, combination of SU056 with ICB significantly improved survival in multiple glioma models. Collectively, these findings reveal an immunosuppressive mechanism mediated by the CHK2-YBX1&YBX3 hub proteins. Therefore, CHK2-YBX1&YBX3 hub targeting in combination with immune checkpoint blockade therapies in gliomas is warranted.
    DOI:  https://doi.org/10.1101/2025.03.09.642289
  12. Front Neurol. 2025 ;16 1549465
    Targeting gut microbiota: a potential therapeutic approach for tumor microenvironment in glioma.
    Fan Qi, Kaiqiang Meng, Xiaoping Zhao, Jing Lv, Lan Huang, Xiaoxuan Fan, Zhaoqun Feng.
      Glioma, being one of the malignant tumors with the highest mortality rate globally, has an unclear pathogenesis, and the existing treatment effects still have certain limitations. The tumor microenvironment (TME) plays an important role in the occurrence, development, and recurrence of glioma. As one of the important regulatory factors of TME, the gut microbiota can regulate the progression of glioma not only by interacting with the brain through the brain-gut axis but also by influencing the tumor immune microenvironment (TIME) and inflammatory microenvironment. Recent studies have identified the gut microbiota and TME as potential therapeutic targets for glioma. This paper aims to summarize the role of the gut microbiota in TME, the association between them and glioma, and the potential of developing new intervention measures by targeting the gut microbiota. Understanding the involvement process of the gut microbiota in glioma may pave the way for the development of effective treatment methods that can regulate TME and prevent disease progression.
    Keywords:  dysbiosis; glioma; gut microbiota; microbiota-brain-gut axis; tumor microenvironment
    DOI:  https://doi.org/10.3389/fneur.2025.1549465
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