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Current Developments in Glioblastoma Research and Therapy: 2nd Edition

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

Deadline for manuscript submissions: 30 June 2026 | Viewed by 8436

Special Issue Editor

Dr. Aleksandra Majchrzak-Celińska

E-Mail Website
Guest Editor
Department of Pharmaceutical Biochemistry, Poznan University of Medical Sciences, 60-806 Poznan, Poland
Interests: brain tumors; glioblastoma; epigenetics; pharmacoepigenetics; biomarkers; Wnt/β-catenin pathway; phytocompounds
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Glioblastoma remains one of the most aggressive and incurable malignancies. Even after standard treatment, consisting of surgery, radiotherapy, and chemotherapy, tumor recurrence is often inevitable, and the prognosis for glioblastoma patients is still very poor. Therefore, rapid progress is urgently needing in developing a better understanding of glioblastoma pathogenesis and recurrence, as well as novel methods of improving patient outcomes.

Fortunately, research into glioblastoma is thriving, and new approaches involving more precise diagnosis and effective therapy for this deadly disease are constantly being evaluated. The implementation of combinatorial therapies, immunotherapy, and nanomedicine are examples of the strategies being tested to surpass current obstacles in glioblastoma treatment.

The aim of this Special Issue is to collect the most recent research findings in glioblastoma research, ranging from molecular mechanisms to therapeutic approaches. All advancements in characterizing GBM pathogenesis, including genomic, epigenomic, transcriptomic, and proteomic analyses of GBM cells, are of interest for this Special Issue. Moreover, we welcome the evaluation of innovative therapeutic agents and new treatment approaches.

We invite authors to submit their original preclinical, translational, and clinical works, as well as review articles regarding the above-mentioned cutting-edge topics, to this Special Issue of International Journal of Molecular Sciences.

We are looking forward to your contributions.

Dr. Aleksandra Majchrzak-Celińska
Guest Editor

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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.

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Keywords

  • diagnostic, prognostic and predictive biomarkers of glioblastoma
  • ways to target glioma stem cells
  • targeting glioblastoma-related signaling pathways
  • epigenetics of glioblastoma
  • treatment resistance mechanisms
  • novel treatment options for glioblastoma
  • combinatorial therapies
  • immunotherapy
  • nanotherapy
  • the application of CRISPR/Cas9 in glioma research
  • molecular testing of long-term glioblastoma survivors

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Related Special Issue

Published Papers (6 papers)

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Research

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19 pages, 732 KB  
Article
Somatic Mutations in Nuclear and Mitochondrial Genes of Mitochondrial Proteins in Primary and Recurrent Glioblastoma
by Marton Tompa, Bence Galik, Peter Urban, Attila Gyenesei and Bernadette Kalman
Int. J. Mol. Sci. 2026, 27(4), 1773; https://doi.org/10.3390/ijms27041773 - 12 Feb 2026
Viewed by 558
Abstract
The accumulation of somatic mutations contributes to clonal evolution and biological properties of cancers. Acquired mutations in mitochondrial (mt)DNA have been studied, but with the exception of those in isocitrate dehydrogenase genes, no comprehensive assessment of mutations in nuclear mitochondrial genes has been [...] Read more.
The accumulation of somatic mutations contributes to clonal evolution and biological properties of cancers. Acquired mutations in mitochondrial (mt)DNA have been studied, but with the exception of those in isocitrate dehydrogenase genes, no comprehensive assessment of mutations in nuclear mitochondrial genes has been reported in sequential glioblastoma (GBM). We obtained ten pairs of GBM samples at diagnosis (GBM-P) and at recurrence (GBM-R). Extracted DNA was subjected to whole exome and mtDNA sequencing. After filtering out germline variants, bioinformatics analysis was performed using a mitochondrial gene panel of 483 nuclear-encoded, and 37 mtDNA-encoded genes. Variant classification was performed using established clinical- and molecular criteria, integrating population-frequency data, bioinformatic predictions, functional evidence, segregation information, and curated entries from the Mitomap and ClinVar databases. Benign single nucleotide variants in mtDNA-encoded genes of RNR1, RNR2, ATP6, CYB, CO2, TV, ATP8, and ND2 were detected, which changed little over time. However, three variants in TI, ND5 and ND1 with possible or likely pathogenic significance were found in the GBM-R samples. In contrast, pathogenic or likely pathogenic variants in 29 nuclear genes were found in GBM-P and GBM-R samples. Not only the overall number, but also the number of protein-truncating variants in nuclear genes increased over time. Conclusions: This study sheds light on the accumulation of mutations in nuclear genes of mitochondrial proteins in sequential GBM samples. As such variants may influence metabolic, proliferative and invasive properties as well as the necrotic propensity of the tumor, a comprehensive analysis of these genes merits further studies. Full article
(This article belongs to the Special Issue Current Developments in Glioblastoma Research and Therapy: 2nd Edition)
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18 pages, 1827 KB  
Article
A Pharmacologic Approach Against Glioblastoma—A Synergistic Combination of a Quinoxaline-Based and a PI3K/mTOR Dual Inhibitor
by Vitória Santório de São José, Bruno Marques Vieira, Camila Saggioro de Figueiredo, Luis Gabriel Valdivieso Gelves, Vivaldo Moura Neto and Lídia Moreira Lima
Int. J. Mol. Sci. 2025, 26(13), 6392; https://doi.org/10.3390/ijms26136392 - 2 Jul 2025
Cited by 2 | Viewed by 1133
Abstract
Glioblastoma (GB) is the most common malignant primary CNS tumor with a fast-growing and invasive profile. As a result of the poor prognosis and limited therapy available, glioblastoma shows a high mortality rate. Given the scarcity of effective chemotherapy options, multiple studies have [...] Read more.
Glioblastoma (GB) is the most common malignant primary CNS tumor with a fast-growing and invasive profile. As a result of the poor prognosis and limited therapy available, glioblastoma shows a high mortality rate. Given the scarcity of effective chemotherapy options, multiple studies have explored the potential of tyrosine kinase inhibitors. To mitigate resistance and improve potency and selectivity, we proposed the combination of a potent irreversible epidermal growth factor receptor inhibitor—LASSBio-1971—and a potent phosphatidylinositol-3-kinase/mammalian target of rapamycin dual inhibitor—Gedatolisib—through an in vitro phenotypic study using five human GB lines. Here, we aimed to establish the cytotoxic potency, selectivity, and effect on proliferation, apoptosis, migration, and the cell cycle. Our data showed the cytotoxic potency of Gedatolisib and LASSBio-1971 and improved selectivity in the GB cell lines. They highlighted the synergistic response from their combination and its impact on migration reduction, G0/G1 cell cycle arrest, GB cytotoxicity, and apoptosis-inducing effects for different GB cell lines. The drug combination studies in phenotypic in vitro models made it possible to suggest a new potential treatment for glioblastoma that justifies further safety in in vivo phases of preclinical trials with the combination. Full article
(This article belongs to the Special Issue Current Developments in Glioblastoma Research and Therapy: 2nd Edition)
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16 pages, 2250 KB  
Article
Oxamate, an LDHA Inhibitor, Inhibits Stemness, Including EMT and High DNA Repair Ability, Induces Senescence, and Exhibits Radiosensitizing Effects in Glioblastoma Cells
by Takuma Hashimoto, Go Ushikubo, Naoya Arao, Khaled Hatabi, Kazuki Tsubota and Yoshio Hosoi
Int. J. Mol. Sci. 2025, 26(12), 5710; https://doi.org/10.3390/ijms26125710 - 14 Jun 2025
Cited by 14 | Viewed by 2936
Abstract
Enhancement of glycolysis has been reported in tumor cells, and it is believed that this enhancement is important for maintaining the stemness of tumor cells and contributes to malignant phenotypes. Here, we investigated the effects of Oxamate, which inhibits glycolysis by blocking the [...] Read more.
Enhancement of glycolysis has been reported in tumor cells, and it is believed that this enhancement is important for maintaining the stemness of tumor cells and contributes to malignant phenotypes. Here, we investigated the effects of Oxamate, which inhibits glycolysis by blocking the conversion of pyruvate to lactate, on radiosensitivity and its molecular mechanisms in T98G glioblastoma cells. Oxamate significantly enhanced radiosensitivity by delaying DNA repair, as indicated by the persistence of γ-H2AX foci up to four days post-irradiation. Mechanistically, Oxamate suppressed the expression and phosphorylation of key DNA repair factors. Furthermore, Oxamate induced apoptosis and promoted cellular senescence, as evidenced by the accumulation of SA-β-gal and the upregulation of pS15-p53 and p21. In addition, Oxamate downregulated EGFR expression, reduced the levels of stem cell markers, and modulated epithelial–mesenchymal transition (EMT) markers, suggesting a potential suppression of EMT-related pathways. Together, these results demonstrate that Oxamate enhances radiosensitivity in glioblastoma cells through multiple mechanisms, including the inhibition of DNA repair, induction of apoptosis and senescence, and suppression of cancer stem cell properties and EMT. Our findings provide new insights into the potential use of Oxamate as a radiosensitizer and warrant further investigation of its clinical application in glioblastoma therapy. Full article
(This article belongs to the Special Issue Current Developments in Glioblastoma Research and Therapy: 2nd Edition)
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Review

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37 pages, 1844 KB  
Review
Advancements in Drug Delivery Systems in Glioblastoma Therapy
by Purusottam Mishra, Payal Gupta, Aleksandra Markowska, Saeid Ghavami, Jarosław Markowski and Marek J. Łos
Int. J. Mol. Sci. 2026, 27(5), 2298; https://doi.org/10.3390/ijms27052298 - 28 Feb 2026
Viewed by 1249
Abstract
Glioblastoma (GB) is one of the most aggressive brain tumours, with a high mortality rate. Tumour heterogeneity, GB’s invasive nature, the blood–brain barrier (BBB) and resistance development offer significant challenges in devising an effective strategy to manage GB. Clinicians rely on tumour resection, [...] Read more.
Glioblastoma (GB) is one of the most aggressive brain tumours, with a high mortality rate. Tumour heterogeneity, GB’s invasive nature, the blood–brain barrier (BBB) and resistance development offer significant challenges in devising an effective strategy to manage GB. Clinicians rely on tumour resection, radiotherapy and temozolomide (TMZ) chemotherapy, but their efficacy is hindered due to poor BBB penetration. EGFR (epidermal growth factor receptor), NF-κB, angiogenic pathways, RAS/RAF/MAPK, PI3K/Akt/mTOR, etc., play an important role in GB progression. Development in nanotechnology, pharmaceutical science and genetic engineering enables the design of drug candidates with superior efficacy and safety profiles. This review delves into recent advancements in nanoparticles, hydrogels, extracellular vesicles, microneedles and other drug delivery platforms used in GB treatment. These novel drug delivery systems achieved superior BBB penetration, tumour targeting, and controlled release and better survival outcomes in preclinical setups. This review also discusses the major translational challenges, including those of large-scale production, tumour heterogeneity, off-target effects and M2 macrophage induction. Innovative strategies focusing on drug delivery as a biological decision-making process, integrating tumour stress responses into drug carrier and system-level design principles, are discussed, outlining future prospects. Full article
(This article belongs to the Special Issue Current Developments in Glioblastoma Research and Therapy: 2nd Edition)
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29 pages, 2203 KB  
Review
Targeting BRD4—A Promising Therapeutic Option for Glioblastoma?
by Maria Lindner, Dagmara Lisińska, Anna Kędzierzyńska and Aleksandra Majchrzak-Celińska
Int. J. Mol. Sci. 2026, 27(5), 2268; https://doi.org/10.3390/ijms27052268 - 28 Feb 2026
Viewed by 968
Abstract
Epigenetic dysregulation is increasingly recognized as a key driver of glioblastoma (GBM), with bromodomain-containing protein 4 (BRD4) emerging as a critical regulator of tumor malignancy. GBM is an aggressive brain tumor marked by diffuse infiltration, a population of stem-like cells and multiple resistance [...] Read more.
Epigenetic dysregulation is increasingly recognized as a key driver of glioblastoma (GBM), with bromodomain-containing protein 4 (BRD4) emerging as a critical regulator of tumor malignancy. GBM is an aggressive brain tumor marked by diffuse infiltration, a population of stem-like cells and multiple resistance mechanisms, which together render it largely incurable. Standard treatment, consisting of surgical resection followed by radiotherapy and temozolomide chemotherapy, confers only limited therapeutic benefit, while a member of the bromodomain and extra-terminal (BET) family, BRD4, regulates transcriptional programs essential for oncogene activation, chromatin stability and glioma cell survival. Its expression is markedly elevated in GBM relative to normal brain tissue, implicating BRD4 in tumor initiation, progression and therapeutic resistance. Recent advances have enabled the development of selective BRD4 inhibitors and degraders capable of penetrating the blood–brain barrier and preferentially targeting glioma cells. Preclinical and early-phase clinical studies indicate that these agents suppress tumor growth and may enhance the efficacy of existing treatments. Although BRD4 clearly influences glioma progression and modulates key oncogenic pathways, the precise mechanisms underlying BRD4-driven gliomagenesis remain only partially understood. Ongoing research continues to advance knowledge of its multifaceted functions. This review summarizes current knowledge on BRD4 in GBM, evaluates emerging BRD4-targeted therapeutic strategies and outlines major challenges and future directions for clinical translation. Full article
(This article belongs to the Special Issue Current Developments in Glioblastoma Research and Therapy: 2nd Edition)
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34 pages, 6520 KB  
Review
The Role of CRISPR and Its Therapeutic Applications in Glioblastoma
by Salma Fayed, Salma Amer, Malak Badawy, Lara Bou Malhab, Nourhan Omran, Ghalia Khoder, Rose Ghemrawi, Mohamed Haider, Rifat Hamoudi and Rania Harati
Int. J. Mol. Sci. 2026, 27(4), 2008; https://doi.org/10.3390/ijms27042008 - 20 Feb 2026
Cited by 1 | Viewed by 902
Abstract
Glioblastoma multiforme (GBM) remains the most aggressive and treatment-refractory form of primary brain tumor in adults, characterized by rapid proliferation, intratumoral heterogeneity and resistance to current therapies. Despite therapeutic advancements in surgical resection, radiotherapy and chemotherapy, clinical outcomes remain poor, underscoring the need [...] Read more.
Glioblastoma multiforme (GBM) remains the most aggressive and treatment-refractory form of primary brain tumor in adults, characterized by rapid proliferation, intratumoral heterogeneity and resistance to current therapies. Despite therapeutic advancements in surgical resection, radiotherapy and chemotherapy, clinical outcomes remain poor, underscoring the need for innovative molecular strategies. This review examines the therapeutic potential of CRISPR/Cas9 genome-editing technologies in GBM, highlighting their ability to model, dissect and potentially correct the genetic alterations that drive GBM tumorigenesis. Key molecular targets, such as EGFR, PTEN, TP53, NF1 and PIK3CA, are discussed within the context of GBM’s mutational and signaling landscape. We further outline emerging CRISPR applications in preclinical models, the current status of CRISPR-based clinical trials and the major barriers hindering translation, including off-target effects, immunogenicity and the challenge of delivering gene-editing systems across the blood–brain barrier. Particular emphasis is placed on delivery technologies, viral and non-viral vectors, including lipid nanoparticles, polymeric systems, inorganic nanocarriers and DNA nanostructures, which are rapidly evolving to improve precision, safety and CNS penetrance. Collectively, this review highlights CRISPR/Cas9 as a powerful tool whose integration with molecular neuro-oncology and precision medicine may ultimately shift GBM treatment toward more personalized and durable therapeutic interventions. Full article
(This article belongs to the Special Issue Current Developments in Glioblastoma Research and Therapy: 2nd Edition)
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