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New Insights into Glioblastoma: Cellular and Molecular (2nd Edition)
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New Insights into Glioblastoma: Cellular and Molecular (2nd Edition)

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 November 2024) | Viewed by 5074

Special Issue Editor

Prof. Dr. Giuseppe Lombardi

E-Mail Website
Guest Editor
Department of Oncology, Oncology 1, Veneto Institute of Oncology-IRCCS, 35128 Padua, Italy
Interests: neuro-oncology; glioblastoma; gliomas; targeted therapy; brain tumors; immunotherapy; quality of life
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Glioblastoma is the most common and aggressive primary malignant brain tumor in adult patients. Despite multimodal treatment with maximal safe surgical resection followed by concurrent radio-chemotherapy and adjuvant chemotherapy with temozolomide, prognosis remains poor with a median survival of 1 year. Because glioblastoma treatment remains a highly unmet clinical need, deeper mechanistic insight into the molecular changes present in these tumors is required.

In recent years, a multitude of novel therapies have shown promising signs of efficacy in glioblastoma patients. Precision medicine such as the combination of dabrafenib and trametinib in BRAF-V600E-mutated gliomas, or other tyrosine kinase inhibitors such as regorafenib or NTRK inhibitors, may be used in certain patients. However, in the longer term, an enhanced understanding of the underlying molecular characteristics and genetic landscape of glioblastoma is required to identify novel therapies such as targeted therapies and combination regimens.

This Special Issue is the continuation of our previous Special Issue "New Insights into Glioblastoma: Cellular and Molecular” and will cover all molecular aspects of glioblastoma, including original research on current and experimental treatment options with molecular research and translational work on this cancer’s molecular characteristics. Full reviews and novel communications on these topics are also welcome.

Prof. Dr. Giuseppe Lombardi
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
  • brain tumors
  • targeted therapy

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Related Special Issue

Published Papers (3 papers)

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Research

23 pages, 7459 KiB  
Article
Photophysical Characterization and In Vitro Evaluation of α-Mangostin-Loaded HDL Mimetic Nano-Complex in LN-229 Glioblastoma Spheroid Model
by Ammar Kapic, Nirupama Sabnis, Akpedje S. Dossou, Jose Chavez, Luca Ceresa, Zygmunt Gryczynski, Rafal Fudala, Rob Dickerman, Bruce A. Bunnell and Andras G. Lacko
Int. J. Mol. Sci. 2024, 25(13), 7378; https://doi.org/10.3390/ijms25137378 - 5 Jul 2024
Viewed by 1288
Abstract
Cytotoxic activity has been reported for the xanthone α-mangostin (AMN) against Glioblastoma multiforme (GBM), an aggressive malignant brain cancer with a poor prognosis. Recognizing that AMN’s high degree of hydrophobicity is likely to limit its systemic administration, we formulated AMN using reconstituted high-density [...] Read more.
Cytotoxic activity has been reported for the xanthone α-mangostin (AMN) against Glioblastoma multiforme (GBM), an aggressive malignant brain cancer with a poor prognosis. Recognizing that AMN’s high degree of hydrophobicity is likely to limit its systemic administration, we formulated AMN using reconstituted high-density lipoprotein (rHDL) nanoparticles. The photophysical characteristics of the formulation, including fluorescence lifetime and steady-state anisotropy, indicated that AMN was successfully incorporated into the rHDL nanoparticles. To our knowledge, this is the first report on the fluorescent characteristics of AMN with an HDL-based drug carrier. Cytotoxicity studies in a 2D culture and 3D spheroid model of LN-229 GBM cells and normal human astrocytes showed an enhanced therapeutic index with the rHDL-AMN formulation compared to the unincorporated AMN and Temozolomide, a standard GBM chemotherapy agent. Furthermore, treatment with the rHDL-AMN facilitated a dose-dependent upregulation of autophagy and reactive oxygen species generation to a greater extent in LN-229 cells compared to astrocytes, indicating the reduced off-target toxicity of this novel formulation. These studies indicate the potential therapeutic benefits to GBM patients via selective targeting using the rHDL-AMN formulation. Full article
(This article belongs to the Special Issue New Insights into Glioblastoma: Cellular and Molecular (2nd Edition))
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16 pages, 4500 KiB  
Article
DKK3 Expression in Glioblastoma: Correlations with Biomolecular Markers
by Maria Caffo, Giovanna Casili, Gerardo Caruso, Valeria Barresi, Michela Campolo, Irene Paterniti, Letteria Minutoli, Tamara Ius and Emanuela Esposito
Int. J. Mol. Sci. 2024, 25(7), 4091; https://doi.org/10.3390/ijms25074091 - 7 Apr 2024
Cited by 1 | Viewed by 1292
Abstract
Glioblastoma is the most common malignant primary tumor of the CNS. The prognosis is dismal, with a median survival of 15 months. Surgical treatment followed by adjuvant therapies such as radiotherapy and chemotherapy characterize the classical strategy. The WNT pathway plays a key [...] Read more.
Glioblastoma is the most common malignant primary tumor of the CNS. The prognosis is dismal, with a median survival of 15 months. Surgical treatment followed by adjuvant therapies such as radiotherapy and chemotherapy characterize the classical strategy. The WNT pathway plays a key role in cellular proliferation, differentiation, and invasion. The DKK3 protein, capable of acting as a tumor suppressor, also appears to be able to modulate the WNT pathway. We performed, in a series of 40 patients, immunohistochemical and Western blot evaluations of DKK3 to better understand how the expression of this protein can influence clinical behavior. We used a statistical analysis, with correlations between the expression of DKK3 and overall survival, age, sex, Ki-67, p53, and MGMT and IDH status. We also correlated our data with information included in the cBioPortal database. In our analyses, DKK3 expression, in both immunohistochemistry and Western blot analyses, was reduced or absent in many cases, showing downregulation. To date, no clinical study exists in the literature that reports a potential correlation between IDH and MGMT status and the WNT pathway through the expression of DKK3. Modulation of this pathway through the expression of DKK3 could represent a new tailored therapeutic strategy in the treatment of glioblastoma. Full article
(This article belongs to the Special Issue New Insights into Glioblastoma: Cellular and Molecular (2nd Edition))
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18 pages, 2619 KiB  
Article
Glut-3 Gene Knockdown as a Potential Strategy to Overcome Glioblastoma Radioresistance
by Gaia Pucci, Luigi Minafra, Valentina Bravatà, Marco Calvaruso, Giuseppina Turturici, Francesco P. Cammarata, Gaetano Savoca, Boris Abbate, Giorgio Russo, Vincenzo Cavalieri and Giusi I. Forte
Int. J. Mol. Sci. 2024, 25(4), 2079; https://doi.org/10.3390/ijms25042079 - 8 Feb 2024
Cited by 2 | Viewed by 1839
Abstract
The hypoxic pattern of glioblastoma (GBM) is known to be a primary cause of radioresistance. Our study explored the possibility of using gene knockdown of key factors involved in the molecular response to hypoxia, to overcome GBM radioresistance. We used the U87 cell [...] Read more.
The hypoxic pattern of glioblastoma (GBM) is known to be a primary cause of radioresistance. Our study explored the possibility of using gene knockdown of key factors involved in the molecular response to hypoxia, to overcome GBM radioresistance. We used the U87 cell line subjected to chemical hypoxia generated by CoCl2 and exposed to 2 Gy of X-rays, as single or combined treatments, and evaluated gene expression changes of biomarkers involved in the Warburg effect, cell cycle control, and survival to identify the best molecular targets to be knocked-down, among those directly activated by the HIF-1α transcription factor. By this approach, glut-3 and pdk-1 genes were chosen, and the effects of their morpholino-induced gene silencing were evaluated by exploring the proliferative rates and the molecular modifications of the above-mentioned biomarkers. We found that, after combined treatments, glut-3 gene knockdown induced a greater decrease in cell proliferation, compared to pdk-1 gene knockdown and strong upregulation of glut-1 and ldha, as a sign of cell response to restore the anaerobic glycolysis pathway. Overall, glut-3 gene knockdown offered a better chance of controlling the anaerobic use of pyruvate and a better proliferation rate reduction, suggesting it is a suitable silencing target to overcome radioresistance. Full article
(This article belongs to the Special Issue New Insights into Glioblastoma: Cellular and Molecular (2nd Edition))
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