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Neuroglia
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Glioblastoma (GBM) Brain Tumor Invasion and Consequences on Diagnosis, Clinical...
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Glioblastoma (GBM) Brain Tumor Invasion and Consequences on Diagnosis, Clinical Strategies and Therapy

A special issue of Neuroglia (ISSN 2571-6980).

Deadline for manuscript submissions: 31 December 2024 | Viewed by 9120

Special Issue Editors

Dr. Mauro Palmieri

E-Mail Website
Guest Editor
Department of Human Neurosciences, Neurosurgery Division, Università “La Sapienza” di Roma, Viale del Policlinico 155, 00161 Rome, Italy
Interests: neuro-oncology; spine tumors
Special Issues, Collections and Topics in MDPI journals
Dr. Alessandro Pesce

E-Mail Website
Guest Editor
Neurosurgery Division, A.O. “Santa Maria Goretti”, 04100 Latina, Italy
Interests: neuroanatomy; neuroncology; glioblastoma; neurosurgery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Glioblastoma is one of the most common primary brain tumors in adulthood and the most frequent glioma. To date, the best treatment for glioblastoma is surgery, followed by radiation therapy and chemotherapy with Temozolomide, however, considering the dismal prognosis related to its high malignancy even after this gold standard treatment, there are still many features to further clarify regarding the progression and recurrence of this disease. More specifically, recent fields of research regard the molecular behavior of Glioblastoma and the mechanism of healthy brain invasion and how the findings in this field affect clinical strategies.

The aim of this Special Issue of Neuroglia is to present a collection of articles that provides a current snapshot of the research in the Glioblastoma field. Manuscripts covering all aspects of research relating to Glioblastoma and the interaction between Glioblastoma and healthy brain tissues are welcome, including work from an applied perspective—such as novel diagnostics, use of new technologies, and innovations in the treatment of Glioblastoma—through to more fundamental questions relating to the biology of the disease and its pathogenesis, diffusion to surrounding tissues, and treatment.

Dr. Mauro Palmieri
Dr. Alessandro Pesce
Guest Editors

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. Neuroglia is an international peer-reviewed open access quarterly 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 1000 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

  • glioblastoma
  • primary brain tumor
  • brain tumor invasion
  • neurosurgery
  • high-grade glioma
  • molecular analytic in neuro-oncology
  • advanced neuroimaging in neuro-oncology

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Published Papers (4 papers)

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Research

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9 pages, 1926 KiB  
Communication
Metformin Reduces Viability and Inhibits the Immunoinflammatory Profile of Human Glioblastoma Multiforme Cells
by Daewoo Hong, Regina Ambe, Jose Barragan, Kristina Marie Reyes and Jorge Cervantes
Neuroglia 2024, 5(2), 80-88; https://doi.org/10.3390/neuroglia5020006 - 31 Mar 2024
Viewed by 1581
Abstract
Glioblastoma (GBM) is the predominant primary malignant brain tumor. Metformin, a well-known antidiabetic medication, has emerged as a potential therapeutic candidate in the treatment of GBM. We have herein investigated two aspects of the effect of MTF on GBM cells: the effect of [...] Read more.
Glioblastoma (GBM) is the predominant primary malignant brain tumor. Metformin, a well-known antidiabetic medication, has emerged as a potential therapeutic candidate in the treatment of GBM. We have herein investigated two aspects of the effect of MTF on GBM cells: the effect of MTF on GBM cell viability, as previous studies have shown that MTF can selectively affect human GBM tumors; and the immunomodulatory effect of MTF on GBM, as there is evidence that inflammation is associated with GBM growth and progression. The human GBM cell line (U87) was exposed to various doses of MTF (1 mM, 20 mM, and 50 mM), followed by examination of cell viability and inflammatory mediator secretion at various time points. We observed that MTF treatment exerted a dose-response effect on glioblastoma multiforme cell viability. It also had an immunomodulatory effect on GBM cells. Our study identified several mechanisms that led to the overall inhibitory effect of MTF on human GBM. Further inquiry is necessary to gain a better understanding of how these in vitro findings would translate into successful in vivo approaches. Full article
(This article belongs to the Special Issue Glioblastoma (GBM) Brain Tumor Invasion and Consequences on Diagnosis, Clinical Strategies and Therapy)
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Review

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17 pages, 7593 KiB  
Review
Ketogenic Diet in the Management of Glioblastomas: A Bibliometric Analysis
by Alexandros G. Brotis, Christina Arvaniti, Marina Kontou, Alexandros Tsekouras and Kostas N. Fountas
Neuroglia 2024, 5(2), 63-79; https://doi.org/10.3390/neuroglia5020005 - 22 Mar 2024
Viewed by 2967
Abstract
Glioblastoma is a highly aggressive brain tumor that has a poor prognosis despite various treatments like surgery, chemotherapy, and irradiation. However, a restricted ketogenic diet (RKD), which has been proven to be effective in treating drug-resistant epilepsy, could be a potential adjunct in [...] Read more.
Glioblastoma is a highly aggressive brain tumor that has a poor prognosis despite various treatments like surgery, chemotherapy, and irradiation. However, a restricted ketogenic diet (RKD), which has been proven to be effective in treating drug-resistant epilepsy, could be a potential adjunct in the treatment of certain GBM cases. Our study aimed to highlight the existing knowledge, identify collaboration networks, and emphasize the ongoing research based on highly cited studies. During the literature search, we found 119 relevant articles written between 2010 and 2023. Among the top 20 most cited articles, there were seven laboratory and five clinical studies. The works of Olson LK, Chang HT, Schwartz KA, and Nikolai M from the Michigan State University, followed by Seyfried TN and Mukherjee P from Boston College, and Olieman JF, and Catsman-Berrevoets CE from the University Medical Center of Rotterdam, were significant contributions. The laboratory studies showed that RKD had a significant antitumor effect and could prolong survival in mouse glioblastoma models. The clinical studies verified the tolerability, efficacy, and safety of RKD in patients with GBM, but raised concerns about whether it could be used as a single therapy. The current research interest is focused on the efficacy of using RKD as an adjunct in selected chemotherapy regimens and demonstrates that it could provide GBM patients with better treatment options. Full article
(This article belongs to the Special Issue Glioblastoma (GBM) Brain Tumor Invasion and Consequences on Diagnosis, Clinical Strategies and Therapy)
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22 pages, 3003 KiB  
Review
The Signaling of Neuregulin-Epidermal Growth Factor Receptors and Its Impact on the Nervous System
by Marzia Tagliaferro and Donatella Ponti
Neuroglia 2023, 4(4), 253-274; https://doi.org/10.3390/neuroglia4040018 - 13 Oct 2023
Cited by 1 | Viewed by 2416
Abstract
The activation of members of the Epidermal Growth Factor Receptor (EGFR) family (including ErbB) triggers pathways that have significant effects on cellular processes and have profound consequences both in physiological and pathological conditions. Within the nervous system, the neuregulin (NRG)/ErbB3 signaling plays a [...] Read more.
The activation of members of the Epidermal Growth Factor Receptor (EGFR) family (including ErbB) triggers pathways that have significant effects on cellular processes and have profound consequences both in physiological and pathological conditions. Within the nervous system, the neuregulin (NRG)/ErbB3 signaling plays a crucial role in promoting the formation and maturation of excitatory synapses. Noteworthy is ErbB3, which is actively involved in the process of cerebellar lamination and myelination. All members of the ErbB-family, in particular ErbB3, have been observed within the nuclei of various cell types, including both full-length receptors and alternative variants. One of these variants was detected in Schwann cells and in glioblastoma primary cells where it showed a neuregulin-dependent expression. It binds to promoters’ chromatin associated with genes, like ezrin, involved in the formation of Ranvier’s node. Its nucleolar localization suggests that it may play a role in ribosome biogenesis and in cell proliferation. The regulation of ErbB3 expression is a complex and dynamic process that can be influenced by different factors, including miRNAs. This mechanism appears to play a significant role in glioblastoma and is often associated with a poor prognosis. Altogether, the targeting of ErbB3 has emerged as an active area of research in glioblastoma treatment. These findings highlight the underappreciated role of ErbB3 as a significant receptor that can potentially play a pivotal role in diverse pathologies, implying the existence of a shared and intricate mechanism that warrants further investigation. Full article
(This article belongs to the Special Issue Glioblastoma (GBM) Brain Tumor Invasion and Consequences on Diagnosis, Clinical Strategies and Therapy)
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Other

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11 pages, 936 KiB  
Opinion
Reducing Brain Edema Using Berotralstat, an Inhibitor of Bradykinin, Repurposed as Treatment Adjunct in Glioblastoma
by Richard E. Kast
Neuroglia 2024, 5(3), 223-233; https://doi.org/10.3390/neuroglia5030016 - 2 Jul 2024
Viewed by 1297
Abstract
Glioblastomas synthesize, bear receptors for, and respond to bradykinin, triggering migration and proliferation. Since centrifugal migration into uninvolved surrounding brain tissue occurs early in the course of glioblastoma, this attribute defeats local treatment attempts and is the primary reason current treatments almost always [...] Read more.
Glioblastomas synthesize, bear receptors for, and respond to bradykinin, triggering migration and proliferation. Since centrifugal migration into uninvolved surrounding brain tissue occurs early in the course of glioblastoma, this attribute defeats local treatment attempts and is the primary reason current treatments almost always fail. Stopping bradykinin-triggered migration would be a step closer to control of this disease. The recent approval and marketing of an oral plasma kallikrein inhibitor, berotralstat (Orladeyo™), and pending FDA approval of a similar drug, sebetralstat, now offers a potential method for reducing local bradykinin production at sites of bradykinin-mediated glioblastoma migration. Both drugs are approved for treating hereditary angioedema. They are ideal for repurposing as a treatment adjunct in glioblastoma. Furthermore, it has been established that peritumoral edema, a common problem during the clinical course of glioblastoma, is generated in large part by locally produced bradykinin via kallikrein action. Both brain edema and the consequent use of corticosteroids both shorten survival in glioblastoma. Therefore, by (i) migration inhibition, (ii) growth inhibition, (iii) edema reduction, and (iv) the potential for less use of corticosteroids, berotralstat may be of service in treatment of glioblastoma, slowing disease progression. This paper recounts the details and past research on bradykinin in glioblastoma and the rationale of treating it with berotralstat. Full article
(This article belongs to the Special Issue Glioblastoma (GBM) Brain Tumor Invasion and Consequences on Diagnosis, Clinical Strategies and Therapy)
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