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Molecular Research Progress on Glioblastoma
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Molecular Research Progress on Glioblastoma

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 May 2024 | Viewed by 6595

Special Issue Editor

Prof. Dr. Pierluigi Navarra

E-Mail Website
Guest Editor
Department of Healthcare Surveillance and Bioethics, Section of Pharmacology, Università Cattolica del Sacro Cuore-Fondazione Policlinico Universitario A. Gemelli IRCCS, 00168 Rome, Italy
Interests: neuro-immunology; neuro-oncology; neuro-inflammation; glial pathophysiology; pharmacokinetics; drug development; trial design; regulatory pharmacology

Special Issue Information

Dear Colleagues,

Glioblastoma multiforme (GBM) is the most frequent and aggressive form of primary CNS tumor in humans. GBM remains a high-grade unmet medical need, since recurrence normally occurs within 12–14 months from the standard-of-care therapy, which is currently based on surgery associated with radiotherapy (± chemotherapy). Once GBM progression occurs, therapeutic options are very poor.

In this frustrating scenario, basic research is engaged in a big effort to find out molecular and cellular mechanisms that might translate into druggable targets and novel therapeutic options. Research is spans the areas of epigenetics, cell therapy and tumor microenvironment, to name a few novel approaches. Special focus should be given to studies on the interaction between tumor cells and the immune system, since the CNS is characterized by a peculiar larger contribution from the cells of the innate immune system.

Basic and translational research contributions are welcome, presenting data on molecular mechanisms of pathology and on preclinical evidence of efficacy for novel pharmacological tools. Further, reviews and meta-analyses providing critical overviews on these topics are also of interest. 

Prof. Dr. Pierluigi Navarra
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • glioma stem cells
  • signaling pathways
  • tumor heterogeneity
  • tumor microenvironment
  • microglia
  • molecular pathways
  • immunotherapies

Published Papers (5 papers)

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Research

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17 pages, 3063 KiB  
Article
ABCG2 Expression as a Potential Survival Predictor in Human Gliomas
by Marina Raguž, Marko Tarle, Danko Müller, Čedna Tomasović-Lončarić, Hana Chudy, Tonko Marinović and Darko Chudy
Int. J. Mol. Sci. 2024, 25(6), 3116; https://doi.org/10.3390/ijms25063116 - 8 Mar 2024
Viewed by 670
Abstract
Gliomas are notably challenging to treat due to their invasive nature and resistance to conventional therapies. The ABCG2 protein has attracted attention for its role in multidrug resistance, complicating treatment effectiveness. This study scrutinized the relationship between ABCG2 expression and glioma grade and [...] Read more.
Gliomas are notably challenging to treat due to their invasive nature and resistance to conventional therapies. The ABCG2 protein has attracted attention for its role in multidrug resistance, complicating treatment effectiveness. This study scrutinized the relationship between ABCG2 expression and glioma grade and the role of ABCG2 in the process of glioma progression, aiming to evaluate ABCG2 expression as a predictive factor of tumor progression and patient survival. Conducted at Dubrava University Hospital, Zagreb, Croatia, the study analyzed 152 glioma specimens from 2013 to 2022, assessing ABCG2 expression alongside standard clinical markers. A significant association was found between patients’ survival and the ABCG2 profile (p = 0.003, r = 0.24), separately for patients who underwent chemotherapy (p = 0.0004, r = 0.32) and radiotherapy (p = 0.003, r = 0.29). Furthermore, the ABCG2 profile was significantly associated with disease progression (p = 0.007, r = 0.23), tumor grade (p = 0.0002, r = 0.31), and Ki67 expression (p = 0.0004, r = 0.31). ABCG2-positive tumor cells only showed association with Ki67 expression (p = 0.002, r = 0.28). The ABCG2 profile was found to affect the overall patient survival (p = 0.02) and represent a moderate indicator of tumor progression (p = 0.01), unlike the percentage of ABCG2-positive tumor cells. ABCG2 may serve as a marker of angiogenesis and vascular abnormalities within tumors, predicting glioma progression and treatment response. Targeting ABCG2 could enhance chemoradiotherapy efficacy and improve patient outcomes, which highlights its value in assessing tumor aggressiveness and designing treatment strategies. Full article
(This article belongs to the Special Issue Molecular Research Progress on Glioblastoma)
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14 pages, 5941 KiB  
Article
Hyponatremia Promotes Cancer Growth in a Murine Xenograft Model of Neuroblastoma
by Giada Marroncini, Laura Naldi, Benedetta Fibbi, Alice Errico, Simone Polvani, Marco Brogi, Alessandra Fanelli, Mario Maggi and Alessandro Peri
Int. J. Mol. Sci. 2023, 24(23), 16680; https://doi.org/10.3390/ijms242316680 - 23 Nov 2023
Cited by 1 | Viewed by 891
Abstract
In cancer patients, hyponatremia is detected in about 40% of cases at hospital admission and has been associated to a worse outcome. We have previously observed that cancer cells from different tissues show a significantly increased proliferation rate and invasion potential, when cultured [...] Read more.
In cancer patients, hyponatremia is detected in about 40% of cases at hospital admission and has been associated to a worse outcome. We have previously observed that cancer cells from different tissues show a significantly increased proliferation rate and invasion potential, when cultured in low extracellular [Na+]. We have recently developed an animal model of hyponatremia using Foxn1nu/nu mice. The aim of the present study was to compare tumor growth and invasivity of the neuroblastoma cell line SK-N-AS in hyponatremic vs. normonatremic mice. Animals were subcutaneously implanted with luciferase-expressing SK-N-AS cells. When masses reached about 100 mm3, hyponatremia was induced in a subgroup of animals via desmopressin infusion. Tumor masses were significantly greater in hyponatremic mice, starting from day 14 and until the day of sacrifice (day 28). Immunohistochemical analysis showed a more intense vascularization and higher levels of expression of the proliferating cell nuclear antigen, chromogranin A and heme oxigenase-1 gene in hyponatremic mice. Finally, metalloproteases were also more abundantly expressed in hyponatremic animals compared to control ones. To our knowledge, this is the first demonstration in an experimental animal model that hyponatremia is associated to increased cancer growth by activating molecular mechanisms that promote proliferation, angiogenesis and invasivity. Full article
(This article belongs to the Special Issue Molecular Research Progress on Glioblastoma)
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17 pages, 3695 KiB  
Article
mTOR Inhibition Is Effective against Growth, Survival and Migration, but Not against Microglia Activation in Preclinical Glioma Models
by Lucia Lisi, Michela Pizzoferrato, Gabriella Maria Pia Ciotti, Maria Martire and Pierluigi Navarra
Int. J. Mol. Sci. 2023, 24(12), 9834; https://doi.org/10.3390/ijms24129834 - 7 Jun 2023
Cited by 1 | Viewed by 1452
Abstract
Initially introduced in therapy as immunosuppressants, the selective inhibitors of mTORC1 have been approved for the treatment of solid tumors. Novel non-selective inhibitors of mTOR are currently under preclinical and clinical developments in oncology, attempting to overcome some limitations associated with selective inhibitors, [...] Read more.
Initially introduced in therapy as immunosuppressants, the selective inhibitors of mTORC1 have been approved for the treatment of solid tumors. Novel non-selective inhibitors of mTOR are currently under preclinical and clinical developments in oncology, attempting to overcome some limitations associated with selective inhibitors, such as the development of tumor resistance. Looking at the possible clinical exploitation in the treatment of glioblastoma multiforme, in this study we used the human glioblastoma cell lines U87MG, T98G and microglia (CHME-5) to compare the effects of a non-selective mTOR inhibitor, sapanisertib, with those of rapamycin in a large array of experimental paradigms, including (i) the expression of factors involved in the mTOR signaling cascade, (ii) cell viability and mortality, (iii) cell migration and autophagy, and (iv) the profile of activation in tumor-associated microglia. We could distinguish between effects of the two compounds that were overlapping or similar, although with differences in potency and or/time-course, and effects that were diverging or even opposite. Among the latter, especially relevant is the difference in the profile of microglia activation, with rapamycin being an overall inhibitor of microglia activation, whereas sapanisertib was found to induce an M2-profile, which is usually associated with poor clinical outcomes. Full article
(This article belongs to the Special Issue Molecular Research Progress on Glioblastoma)
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Review

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32 pages, 3617 KiB  
Review
Small Molecule Tyrosine Kinase Inhibitors (TKIs) for Glioblastoma Treatment
by Davide Frumento, Giancarlo Grossi, Marta Falesiedi, Francesca Musumeci, Anna Carbone and Silvia Schenone
Int. J. Mol. Sci. 2024, 25(3), 1398; https://doi.org/10.3390/ijms25031398 - 23 Jan 2024
Cited by 1 | Viewed by 1298
Abstract
In the last decade, many small molecules, usually characterized by heterocyclic scaffolds, have been designed and synthesized as tyrosine kinase inhibitors (TKIs). Among them, several compounds have been tested at preclinical and clinical levels to treat glioblastoma multiforme (GBM). GBM is the most [...] Read more.
In the last decade, many small molecules, usually characterized by heterocyclic scaffolds, have been designed and synthesized as tyrosine kinase inhibitors (TKIs). Among them, several compounds have been tested at preclinical and clinical levels to treat glioblastoma multiforme (GBM). GBM is the most common and aggressive type of cancer originating in the brain and has an unfavorable prognosis, with a median survival of 15–16 months and a 5-year survival rate of 5%. Despite recent advances in treating GBM, it represents an incurable disease associated with treatment resistance and high recurrence rates. For these reasons, there is an urgent need for the development of new pharmacological agents to fight this malignancy. In this review, we reported the compounds published in the last five years, which showed promising activity in GBM preclinical models acting as TKIs. We grouped the compounds based on the targeted kinase: first, we reported receptor TKIs and then, cytoplasmic and peculiar kinase inhibitors. For each small molecule, we included the chemical structure, and we schematized the interaction with the target for some representative compounds with the aim of elucidating the mechanism of action. Finally, we cited the most relevant clinical trials. Full article
(This article belongs to the Special Issue Molecular Research Progress on Glioblastoma)
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19 pages, 2504 KiB  
Review
The Recent Research Progress of NF-κB Signaling on the Proliferation, Migration, Invasion, Immune Escape and Drug Resistance of Glioblastoma
by Pengfei Shi, Jie Xu and Hongjuan Cui
Int. J. Mol. Sci. 2023, 24(12), 10337; https://doi.org/10.3390/ijms241210337 - 19 Jun 2023
Cited by 5 | Viewed by 1738
Abstract
Glioblastoma multiforme (GBM) is the most common and invasive primary central nervous system tumor in humans, accounting for approximately 45–50% of all primary brain tumors. How to conduct early diagnosis, targeted intervention, and prognostic evaluation of GBM, in order to improve the survival [...] Read more.
Glioblastoma multiforme (GBM) is the most common and invasive primary central nervous system tumor in humans, accounting for approximately 45–50% of all primary brain tumors. How to conduct early diagnosis, targeted intervention, and prognostic evaluation of GBM, in order to improve the survival rate of glioblastoma patients, has always been an urgent clinical problem to be solved. Therefore, a deeper understanding of the molecular mechanisms underlying the occurrence and development of GBM is also needed. Like many other cancers, NF-κB signaling plays a crucial role in tumor growth and therapeutic resistance in GBM. However, the molecular mechanism underlying the high activity of NF-κB in GBM remains to be elucidated. This review aims to identify and summarize the NF-κB signaling involved in the recent pathogenesis of GBM, as well as basic therapy for GBM via NF-κB signaling. Full article
(This article belongs to the Special Issue Molecular Research Progress on Glioblastoma)
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