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Biomedicines
Special Issues
Molecular Mechanisms and Therapy of Gliomas
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Molecular Mechanisms and Therapy of Gliomas

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (31 May 2025) | Viewed by 1046

Special Issue Editor

Dr. Valeria Barresi

E-Mail Website
Guest Editor
Department of Diagnostics and Public Health, P.le L.A. Scuro, University of Verona, 37129 Verona, Italy
Interests: cancer biology; colorectal cancer; neuropathology; surgical pathology; prognostic markers; cancer biomarkers; can-cer diagnostics; molecular biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In recent years, knowledge of the molecular landscape of gliomas has greatly expanded. It has been shown that histologically similar tumors display distinct epigenetic, genetic, transcriptomic, and proteomic features and that the clinical outcome of gliomas can be better predicted by integrating histological and molecular data rather than by histology. This has led to the development of novel glioma classification schemes. Indeed, the latest World Health Organization Classification of gliomas, published in 2021, subdivided gliomas not only on their growth pattern, that is, diffuse or circumscribed, on their histopathological features and on their anatomical location, but also on genetic alterations. In addition, the essential diagnostic criterion for some tumor types is a unique DNA methylation profile.

An increasing understanding of the molecular features of gliomas has also led to the identification of novel potential therapeutic targets.

This Special Issue aims to collect papers on recent advances in the molecular mechanisms of glioma pathogenesis and progression and on novel therapeutic strategies for these tumors.

Dr. Valeria Barresi
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 100 words) can be sent to the Editorial Office for announcement on this website.

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-blind 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
  • epigenetic
  • methylome
  • therapy
  • genetic alteration
  • transcriptomic
  • proteomic

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Published Papers (1 paper)

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Research

20 pages, 3490 KiB  
Article
Isocitrate Dehydrogenase-Wildtype Glioma Adapts Toward Mutant Phenotypes and Enhanced Therapy Sensitivity Under D-2-Hydroxyglutarate Exposure
by Geraldine Rocha, Clara Francés-Gómez, Javier Megías, Lisandra Muñoz-Hidalgo, Pilar Casanova, Jose F. Haro-Estevez, Vicent Teruel-Martí, Daniel Monleón and Teresa San-Miguel
Biomedicines 2025, 13(7), 1584; https://doi.org/10.3390/biomedicines13071584 - 28 Jun 2025
Viewed by 401
Abstract
Background/Objectives: Isocitrate dehydrogenase (IDH) mutations are hallmark features in subsets of gliomas, producing the oncometabolite D-2-hydroxyglutarate (2HG). Although IDH mutations are associated with better clinical outcomes, their relationship with tumor progression is complex. This study aimed to investigate, in vitro [...] Read more.
Background/Objectives: Isocitrate dehydrogenase (IDH) mutations are hallmark features in subsets of gliomas, producing the oncometabolite D-2-hydroxyglutarate (2HG). Although IDH mutations are associated with better clinical outcomes, their relationship with tumor progression is complex. This study aimed to investigate, in vitro and in vivo, the phenotypic consequences of IDH mutation and 2HG exposure in glioblastoma (GBM) under normoxic and hypoxic conditions and under temozolomide (TMZ) and radiation exposure. Methods: Experiments were conducted using IDH-wildtype (IDH-wt) and IDH-mutant (IDH-mut) glioma cell lines under controlled oxygen conditions. Functional assays included cell viability, cell cycle analysis, apoptosis profiling, migration, and surface marker expression via flow cytometry. Orthotopic xenografts were established in immunocompromised mice to assess in vivo tumor growth and morphology, followed by MRI and histological analysis. Treatments included TMZ, radiation, and 2HG at varying concentrations. Statistical analyses were performed using SPSS and RStudio. Results:IDH-wt cells exhibited faster proliferation and greater adaptability under hypoxia, while IDH-mut cells showed cell cycle arrest and limited growth. 2HG recapitulated IDH-mut features in IDH-wt cells, including increased apoptosis under TMZ, reduced proliferation, and altered CD24/CD44 expression. In vivo, IDH-wt tumors were larger and more infiltrative, while 2HG administration reduced tumor volume and promoted compact morphology. Notably, migration was initially similar across genotypes but increased in IDH-mut and 2HG-treated IDH-wt cells over time, though suppressed under therapeutic stress. Conclusions: IDH mutation and 2HG modulate glioma cell biology, including cell cycle dynamics, proliferation rates, migration, and apoptosis. While the IDH mutation and its metabolic product confer initial growth advantages, they enhance treatment sensitivity and reduce invasiveness, highlighting potential vulnerabilities for targeted therapy. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapy of Gliomas)
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