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Biomedicines
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Mechanisms and Novel Therapeutic Approaches for Gliomas: 2nd Edition
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Mechanisms and Novel Therapeutic Approaches for Gliomas: 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: 30 January 2027 | Viewed by 5463

Editor

Dr. Maria V. Chatziathanasiadou

E-Mail Website
Guest Editor
Honorary Research Associate, Department of Brain Sciences, Faculty of Medicine, Imperial College London, London, UK
Interests: glioblastoma; metabolic therapies; immunotherapies; tumour microenvironment; cancer drug discovery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Gliomas, the most common type of primary malignant brain tumour, present significant clinical challenges. This is mainly due to their invasive nature, intratumour heterogeneity, immunosuppressive microenvironment, and the presence of the blood–brain barrier. Little progress has been achieved in glioma treatment over the last few decades, while the main therapeutic options are surgery, radiotherapy, and chemotherapy. Thus, there is an imperative need to deepen our current understanding of glioma mechanisms and develop cutting-edge therapeutic strategies.

This Special Issue aims to cover molecular and cellular glioma mechanisms, including molecular markers, signaling, tumour landscape, cell crosstalk, and immunity, as well as novel therapeutic approaches, such as metabolic therapies, immunotherapies, newly designed and repurposed drugs, and combination treatments.

We also welcome review manuscripts that present recently discovered molecular markers, therapeutic targets, tumour landscape characteristics, or innovative therapies from preclinical studies and clinical trials.

Dr. Maria V. Chatziathanasiadou
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • glioma
  • molecular mechanisms
  • tumour immunity
  • tumour metabolism
  • tumour microenvironment
  • metabolic therapies
  • immunotherapies
  • combination treatment

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Related Special Issue

Published Papers (5 papers)

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Editorial

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3 pages, 132 KB  
Editorial
Mechanisms and Novel Therapeutic Approaches for Gliomas
by Maria V. Chatziathanasiadou
Biomedicines 2026, 14(8), 1704; https://doi.org/10.3390/biomedicines14081704 - 29 Jul 2026
Viewed by 174
Abstract
Gliomas are a broad category of primary brain tumours accounting for 80% of all malignant central nervous system (CNS) tumours [...] Full article
(This article belongs to the Special Issue Mechanisms and Novel Therapeutic Approaches for Gliomas: 2nd Edition)

Research

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14 pages, 509 KB  
Article
Circulating Placental Growth Factor as a Prognostic Biomarker in High-Risk Glioblastoma Patients
by Filippo Gagliardi, Francesca Roncelli, Silvia Snider, Pierfrancesco De Domenico, Daniela Boselli, Simona Di Terlizzi, Chiara Villa and Pietro Mortini
Biomedicines 2026, 14(7), 1628; https://doi.org/10.3390/biomedicines14071628 - 20 Jul 2026
Viewed by 297
Abstract
Background/Objectives: Angiogenesis in glioblastoma (GBM) is a multifactorial process, and blood–brain barrier disruption enables the detection of circulating mediators. The clinical relevance of circulating placental growth factor (PlGF) in GBM remains unclear. This study aimed to investigate the role of PlGF in GBM [...] Read more.
Background/Objectives: Angiogenesis in glioblastoma (GBM) is a multifactorial process, and blood–brain barrier disruption enables the detection of circulating mediators. The clinical relevance of circulating placental growth factor (PlGF) in GBM remains unclear. This study aimed to investigate the role of PlGF in GBM and its association with disease characteristics and outcomes. Methods: We conducted a prospective observational study on 54 patients with IDH-wildtype GBM. Plasma samples collected at diagnosis and recurrence were analyzed using a multiplex panel of angiogenesis mediators. Associations with clinical, radiological, molecular, and treatment-related variables were assessed, along with survival outcomes. Statistical analysis was performed with R 4.5.0. Results: At baseline, PlGF correlated with multiple angiogenic mediators, including VEGF, IL-6, angiopoietin-1, EGF, FGF, IL-8, and TNF-α. Higher PlGF levels were associated with radiopathological features of tumor biology, including proliferation markers and the FLAIR/contrast enhancement ratio. In high-risk patients (RPA 3–4; n = 33), low baseline PlGF identified a subgroup with significantly longer overall survival (17.6 vs. 8.5 months; log-rank p = 0.031) and retained a protective association in multivariable models. In the overall cohort, this association was weaker and did not reach statistical significance. Exploratory longitudinal analyses suggested an increase in PlGF at recurrence in selected molecular and treatment-defined subgroups, while no association with bevacizumab exposure was observed. Conclusions: Circulating PlGF may reflect tumor biology in GBM and shows prognostic relevance in high-risk patients, where low baseline levels identify a subgroup with improved survival. These findings support PlGF as a candidate circulating biomarker and warrant validation in larger prospective cohorts. Full article
(This article belongs to the Special Issue Mechanisms and Novel Therapeutic Approaches for Gliomas: 2nd Edition)
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19 pages, 33829 KB  
Article
Identification of RPA3 as a Potential Functional Effector of Chromosome 7 Gain in Glioblastoma
by Yulu Ge, Zhan Hu, Wenbo Wu, Wenbin Ma, Tingyu Liang and Yu Wang
Biomedicines 2026, 14(5), 1014; https://doi.org/10.3390/biomedicines14051014 - 30 Apr 2026
Viewed by 644
Abstract
Background: Chromosome 7 gain (chr7 gain) is a highly prevalent early event in glioblastoma (GBM). Because chr7 gain usually involves broad chromosomal amplification, its biological impact is unlikely to be fully explained by canonical loci such as EGFR and MET. The contribution [...] Read more.
Background: Chromosome 7 gain (chr7 gain) is a highly prevalent early event in glioblastoma (GBM). Because chr7 gain usually involves broad chromosomal amplification, its biological impact is unlikely to be fully explained by canonical loci such as EGFR and MET. The contribution of less-characterized, dosage-sensitive genes on chromosome 7 remains insufficiently defined. This study aimed to identify additional chr7 candidates associated with malignant phenotypes in GBM. Methods: Transcriptomic, copy-number, and clinical data from TCGA-GBM and TCGA-LGG were analyzed to characterize chr7-gain-associated alterations and prioritize candidate genes. Refined GBM and histologic GBM cohorts based on the WHO 2021 framework were used for candidate selection. RPA3-associated pathway features were examined using ssGSEA, PROGENy, WGCNA, and protein–protein interaction analysis, with external validation in the CGGA-693 cohort. Single-cell RNA-seq analysis compared chr7-gain and chr7-normal-copy tumor subclusters. Functional relevance was evaluated by siRNA-mediated knockdown in U87 and U118 cells. Results: Chr7 gain was enriched in high-grade IDH-wildtype gliomas and was associated with cell-cycle- and DNA repair-related programs. RPA3 was prioritized as a dosage-sensitive chromosome 7 candidate based on its upregulation in chr7-gain tumors, association with poor prognosis, and concordance with replication- and repair-related signatures. In vitro, RPA3 knockdown impaired cell growth, proliferation, colony formation, and migration. Single-cell analysis suggested greater transcriptomic and network-level relevance of RPA3 in chr7-gain tumor cells. Conclusions: RPA3 is a dosage-sensitive chromosome 7 candidate associated with aggressive and replication-/repair-related phenotypes in GBM. Increased RPA3 expression may contribute to the selective advantage associated with chr7 gain, which supports further investigation as potential therapeutic target. Full article
(This article belongs to the Special Issue Mechanisms and Novel Therapeutic Approaches for Gliomas: 2nd Edition)
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Review

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23 pages, 1633 KB  
Review
Emerging In Vivo Imaging Modalities for Improved Glioblastoma Surgery and Monitoring
by Oluwagbenga Dada, Shikshita Singh, Francheska Sumadchat, Madison Lather, Benjamin Brooks and JuliAnne E. Allgood
Biomedicines 2026, 14(4), 816; https://doi.org/10.3390/biomedicines14040816 - 2 Apr 2026
Viewed by 1482
Abstract
Glioblastoma (GBM) remains the most aggressive primary malignant brain tumor in adults, with poor survival largely driven by diffuse cellular infiltration, profound heterogeneity, and near-universal recurrence following standard therapy. Although maximizing the extent of resection is a key determinant of patient outcome, current [...] Read more.
Glioblastoma (GBM) remains the most aggressive primary malignant brain tumor in adults, with poor survival largely driven by diffuse cellular infiltration, profound heterogeneity, and near-universal recurrence following standard therapy. Although maximizing the extent of resection is a key determinant of patient outcome, current clinical imaging modalities lack the spatial resolution necessary to detect microscopic tumor invasion and therapy-resistant cell populations. Emerging in vivo imaging technologies capable of cellular and near-single-cell resolution have therefore become a major focus in preclinical neuro-oncology research, with growing relevance for surgical guidance, treatment adaptation, and translational discovery. This review evaluates multiple optical imaging modalities, including multi-photon microscopy, near-infrared II fluorescence imaging, bioluminescence imaging, photoacoustic imaging, optical coherence tomography, confocal laser endomicroscopy, Raman spectroscopy, autofluorescence microscopy, and fluorescence macroscopy with a focus on their ability to detect residual GBM cells. Despite significant advances, these approaches remain constrained by limitations in molecular target availability, probe delivery across the blood–brain barrier, and signal variability within heterogeneous tumor regions. The biological complexity of GBM further challenges detection, as residual tumor cells are spatially dispersed and phenotypically diverse, limiting the effectiveness of single-marker or single-modality strategies. Together, these findings highlight the need for integrated, biologically informed imaging approaches to improve detection of residual disease and guide surgical decision making. Full article
(This article belongs to the Special Issue Mechanisms and Novel Therapeutic Approaches for Gliomas: 2nd Edition)
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27 pages, 2167 KB  
Review
The Extracellular Matrix, the Silent ‘Architect’ of Glioma
by Carmen Rubio, Javier Pérez-Villavicencio, Nadia F. Esteban-Román, Ángel Lee, Gervith Reyes-Soto and Moisés Rubio-Osornio
Biomedicines 2026, 14(1), 205; https://doi.org/10.3390/biomedicines14010205 - 17 Jan 2026
Cited by 3 | Viewed by 2155
Abstract
The brain’s extracellular matrix (ECM) serves as a dynamic and instructive regulator of glioma progression. The ECM provides structural support while integrating pharmacological and mechanical signals that influence glioma initiation, progression, and treatment resistance. Deviant ECM remodeling fosters tumor heterogeneity, invasion, and immune [...] Read more.
The brain’s extracellular matrix (ECM) serves as a dynamic and instructive regulator of glioma progression. The ECM provides structural support while integrating pharmacological and mechanical signals that influence glioma initiation, progression, and treatment resistance. Deviant ECM remodeling fosters tumor heterogeneity, invasion, and immune evasion by altering stiffness, composition, and cellular matrix signaling. We proposed that ECM remodeling in gliomas not only facilitates tumor growth and heterogeneity but also establishes advantageous biophysical and metabolic conditions that foster treatment resistance and recurrence. Our objective is to analyze current findings regarding the structural, biochemical, and mechanical roles of the brain ECM in glioma growth, emphasizing its contribution to tumor heterogeneity, mechanotransduction, immunological modulation, and its potential as a therapeutic target. Method: A comprehensive literature review was conducted using scientific databases including PubMed, Web of Science, and Scopus. Peer-reviewed literature published between 2000 and 2025 was selected for its relevance to ECM composition, stiffness, remodeling enzymes, extracellular vesicles, and mechanobiological processes in gliomas. Results: Recent investigations demonstrate that glioma cells actively alter the ECM by secreting collagens, laminins, and metalloproteinases, establishing a feedback loop that facilitates invasion and resistance. Discussion: Mechanical variables, such as ECM stiffness and solid stress, influence glioma growth, metabolism, and immune exclusion. Moreover, extracellular vesicles facilitate significant extracellular matrix remodeling and improve communication between tumors and stromal cells. The disruption of ependymal and subventricular extracellular matrix niches enhances invasion and cerebrospinal fluid-mediated signaling. The remodeling of the ECM influences glioma growth through interconnected biochemical, mechanical, and immunological mechanisms. Examining ECM stiffness, crosslinking enzymes, and vesicle-mediated signaling represents a potential therapeutic approach. Integrative methodologies that combine mechanobiology, imaging, and multiomics analysis could uncover ECM-related vulnerabilities to improve glioma treatment. Full article
(This article belongs to the Special Issue Mechanisms and Novel Therapeutic Approaches for Gliomas: 2nd Edition)
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