Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
Glioblastoma 2.0
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Glioblastoma 2.0

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 (30 November 2021) | Viewed by 11202

Special Issue Editors

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
Prof. Dr. Ahmed Idbaih

E-Mail Website1 Website2
Co-Guest Editor
1. AP-HP.Sorbonne Université, Groupe Hospitalier Pitié-Salpêtrière, Service de Neurologie 2, 47 Boulevard de l'Hôpital, 75651 Paris Cedex 13, France
2. Brain Institute of Paris (ICM), 47 Boulevard de l'Hôpital, 75651 Paris Cedex 13, France
Interests: glioma; brain cancer; biomarkers; clinical trial; experimental therapeutics

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 radiochemotherapy and adjuvant chemotherapy with temozolomide, the 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 selected 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 will cover all molecular aspects of glioblastoma, including original research on current and experimental treatment options with molecular research, translational works on molecular characteristics of glioblastoma. Full reviews and novel communication on these topics are also welcome.

Prof. Giuseppe Lombardi
Guest Editor
Prof. Dr. Ahmed Idbaih
Co-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
  • brain tumors
  • targeted therapy
  • glioma
  • IDH
  • personalized medicine
  • imaging

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

25 pages, 3621 KiB  
Article
Novel NK1R-Targeted 68Ga-/177Lu-Radioconjugates with Potential Application against Glioblastoma Multiforme: Preliminary Exploration of Structure–Activity Relationships
by Joanna Matalińska, Katarzyna Kosińska, Paweł K. Halik, Przemysław Koźmiński, Piotr F. J. Lipiński, Ewa Gniazdowska and Aleksandra Misicka
Int. J. Mol. Sci. 2022, 23(3), 1214; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031214 - 21 Jan 2022
Cited by 12 | Viewed by 2140
Abstract
Locoregionally administered, NK1 receptor (NK1R) targeted radionuclide therapy is a promising strategy for the treatment of glioblastoma multiforme. So far, the radiopharmaceuticals used in this approach have been based on the endogenous agonist of NK1R, Substance P or on its close analogues. Herein, [...] Read more.
Locoregionally administered, NK1 receptor (NK1R) targeted radionuclide therapy is a promising strategy for the treatment of glioblastoma multiforme. So far, the radiopharmaceuticals used in this approach have been based on the endogenous agonist of NK1R, Substance P or on its close analogues. Herein, we used a well-known, small molecular NK1R antagonist, L732,138, as the basis for the radiopharmaceutical vector. First, 14 analogues of this compound were evaluated to check whether extending the parent structure with linkers of different lengths would not deteriorate the NK1R binding. The tested analogues had affinity similar to or better than the parent compound, and none of the linkers had a negative impact on the binding. Next, five DOTA conjugates were synthesized and used for labelling with 68Ga and 177Lu. The obtained radioconjugates turned out to be fairly lipophilic but showed rather limited stability in human plasma. Evaluation of the receptor affinity of the (radio)conjugates showed that neither the chelator nor the metal negatively impacts the NK1R binding. The 177Lu-radioconjugates exhibited the binding characteristics towards NK1R similar or better than that of the 177Lu-labelled derivative of Substance P, which is in current clinical use. The experimental results presented herein, along with their structural rationalization provided by modelling, give insight for the further molecular design of small molecular NK1R-targeting vectors. Full article
(This article belongs to the Special Issue Glioblastoma 2.0)
►▼ Show Figures

Figure 1

14 pages, 2889 KiB  
Article
Novel Insights into the Role of the Mineralocorticoid Receptor in Human Glioblastoma
by Paula Aldaz, Amaya Fernández-Celis, Natalia López-Andrés and Imanol Arozarena
Int. J. Mol. Sci. 2021, 22(21), 11656; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222111656 - 28 Oct 2021
Cited by 4 | Viewed by 1777
Abstract
The majority of glioblastoma (GBM) patients require the administration of dexamethasone (DEXA) to reduce brain inflammation. DEXA activates the glucocorticoid receptor (GR), which can consequently crosstalk with the mineralocorticoid receptor (MR). However, while GR signaling is well studied in GBM, little is known [...] Read more.
The majority of glioblastoma (GBM) patients require the administration of dexamethasone (DEXA) to reduce brain inflammation. DEXA activates the glucocorticoid receptor (GR), which can consequently crosstalk with the mineralocorticoid receptor (MR). However, while GR signaling is well studied in GBM, little is known about the MR in brain tumors. We examined the implication of the MR in GBM considering its interplay with DEXA. Together with gene expression studies in patient cohorts, we used human GBM cell lines and patient-derived glioma stem cells (GSCs) to assess the impact of MR activation and inhibition on cell proliferation, response to radiotherapy, and self-renewal capacity. We show that in glioma patients, MR expression inversely correlates with tumor grade. Furthermore, low MR expression correlates with poorer survival in low grade glioma while in GBM the same applies to classical and mesenchymal subtypes, but not proneural tumors. MR activation by aldosterone suppresses the growth of some GBM cell lines and GSC self-renewal. In GBM cells, the MR antagonist spironolactone (SPI) can promote proliferation, radioprotection and cooperate with DEXA. In summary, we propose that MR signaling is anti-proliferative in GBM cells and blocks the self-renewal of GSCs. Contrary to previous evidence obtained in other cancer types, our results suggest that SPI has no compelling anti-neoplastic potential in GBM. Full article
(This article belongs to the Special Issue Glioblastoma 2.0)
►▼ Show Figures

Figure 1

Review

Jump to: Research

17 pages, 937 KiB  
Review
Hypoxia: The Cornerstone of Glioblastoma
by Marta Domènech, Ainhoa Hernández, Andrea Plaja, Eva Martínez-Balibrea and Carmen Balañà
Int. J. Mol. Sci. 2021, 22(22), 12608; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222212608 - 22 Nov 2021
Cited by 61 | Viewed by 6065
Abstract
Glioblastoma is the most aggressive form of brain tumor in adults and is characterized by the presence of hypervascularization and necrosis, both caused by a hypoxic microenvironment. In this review, we highlight that hypoxia-induced factor 1 (HIF-1), the main factor activated by hypoxia, [...] Read more.
Glioblastoma is the most aggressive form of brain tumor in adults and is characterized by the presence of hypervascularization and necrosis, both caused by a hypoxic microenvironment. In this review, we highlight that hypoxia-induced factor 1 (HIF-1), the main factor activated by hypoxia, is an important driver of tumor progression in GB patients. HIF-1α is a transcription factor regulated by the presence or absence of O2. The expression of HIF-1 has been related to high-grade gliomas and aggressive tumor behavior. HIF-1 promotes tumor progression via the activation of angiogenesis, immunosuppression, and metabolic reprogramming, promoting cell invasion and survival. Moreover, in GB, HIF-1 is not solely modulated by oxygen but also by oncogenic signaling pathways, such as MAPK/ERK, p53, and PI3K/PTEN. Therefore, the inhibition of the hypoxia pathway could represent an important treatment alternative in a disease with very few therapy options. Here, we review the roles of HIF-1 in GB progression and the inhibitors that have been studied thus far, with the aim of shedding light on this devastating disease. Full article
(This article belongs to the Special Issue Glioblastoma 2.0)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop