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Advanced Molecular Research in Brain Tumors
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Advanced Molecular Research in Brain Tumors

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 February 2026 | Viewed by 2611

Special Issue Editor

Dr. Shiv K. Gupta

E-Mail Website
Guest Editor
Mayo Clinic, Rochester, MN 55905, USA
Interests: DNA repair; replicative stress; PDX models

Special Issue Information

Dear Colleagues,

Treating brain tumors remains a major challenge due to therapy resistance, restrictive blood–brain and blood–glioma barriers, and immunosuppressive tumor microenvironments. Despite advances in drug development, prognosis remains poor, emphasizing the need for innovative solutions. Recent molecular insights into brain tumor biology have driven the development of targeted therapies, including tyrosine kinase, angiogenesis inhibitors, gene therapies, viro-therapies, and immuno-therapies. There is an ongoing effort for the development of sensitization strategies to enhance chemo- and radiotherapy efficacy. To foster active discussion and accelerate progress in this field, we invite the submission of original research articles and comprehensive reviews for our Special Issue "Advanced Molecular Research in Brain Tumors". This Special Issue aims to highlight cutting-edge discoveries revealing molecular mechanisms underlying brain tumor initiation, progression, and therapeutic resistance.

We welcome submissions exploring various aspects of brain tumor biology, including, but not limited, to the following: tumor pathogenesis, molecularly targeted therapies and resistance mechanisms, and the molecular basis of responses to DNA damage response (DDR)-targeted therapeutics. We also encourage the submission of studies on radio-sensitization strategies, immunotherapy, and tumor microenvironment modulation. Additionally, we invite articles utilizing single-cell and spatial multi-omics approaches, and research focused on liquid biopsy and biomarker discovery. We look forward to your contributions, which will advance the molecular understanding of critical factors that shape brain tumor progression and treatment outcomes.

Dr. Shiv K. Gupta
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 250 words) can be sent to the Editorial Office for assessment.

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

  • targeted therapy
  • blood–brain barrier
  • GBM
  • glioma
  • immune checkpoint blockers
  • TME

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Published Papers (3 papers)

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Research

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19 pages, 4290 KB  
Article
ADAM10 Knockout from Human Glioblastoma and Colon Cancer Cells Modulates Diverse Signalling Networks and Inhibits Tumour Growth In Vivo
by Hengkang Yan, Sakshi Arora, Linda Hii, Carmen Llerena, Mary E. Vail, Amr Allam, James R. W. Conway, Joel R. Steele, Han-Chung Lee, Ralf B. Schittenhelm, Andrew M. Scott and Peter W. Janes
Int. J. Mol. Sci. 2025, 26(21), 10684; https://doi.org/10.3390/ijms262110684 - 3 Nov 2025
Viewed by 630
Abstract
ADAM10 is a transmembrane metalloprotease that regulates diverse signalling functions via the shedding of membrane protein ectodomains, and is implicated in tumour development, including glioblastoma multiforme (GBM) and gastrointestinal (GI) cancers, where high ADAM10 expression is associated with poor prognosis. We assessed the [...] Read more.
ADAM10 is a transmembrane metalloprotease that regulates diverse signalling functions via the shedding of membrane protein ectodomains, and is implicated in tumour development, including glioblastoma multiforme (GBM) and gastrointestinal (GI) cancers, where high ADAM10 expression is associated with poor prognosis. We assessed the role of ADAM10 by gene knockout (KO) in U251 GBM cells, and its effects on protein shedding and protein expression on cell proliferation and on the growth of tumour xenografts in mice. The growth of tumours was severely delayed, relative to modest effects on proliferation in vitro, suggesting roles particularly in the context of the tumour microenvironment (TME). Proteomics analysis of KO cell-conditioned medium showed decreased levels of known ADAM10 targets such as Notch and Eph receptors and ligands, as well as other proteins involved in cell–cell adhesion, migration, signalling, metabolism, differentiation, and development, including angiogenesis. KO cell and tumour lysate analysis also showed modulation of proteins associated with metabolic and catalytic activity, cell–matrix organisation and differentiation. Similar effects were also observed in the SW620 colon cancer model, indicating broader significance. Furthermore, expression of the associated protein sets also correlated with ADAM10 expression in human GBM and colon cancer specimens (TCGA datasets), indicating clinical relevance. Collagens and proteins associated with matrix deposition and fibril organisation were notably reduced in ADAM10 KO GBM tumours, and histology confirmed decreased collagen fibrils and blood vessels. Unexpectedly, increased chondrocyte differentiation was evident in ADAM10 KO U251 tumours, suggesting a role for ADAM10 in maintaining an undifferentiated phenotype in vivo. Together, our data indicate the importance of ADAM10 in diverse signalling mechanisms in tumours and the TME that promote tumour development. Full article
(This article belongs to the Special Issue Advanced Molecular Research in Brain Tumors)
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18 pages, 3816 KB  
Article
The HMGB1-RAGE Axis Drives the Proneural-to-Mesenchymal Transition and Aggressiveness in Glioblastoma
by Hao-Chien Yang, Yu-Kai Su, Vijesh Kumar Yadav, Iat-Hang Fong, Heng-Wei Liu and Chien-Min Lin
Int. J. Mol. Sci. 2025, 26(19), 9352; https://doi.org/10.3390/ijms26199352 - 25 Sep 2025
Viewed by 873
Abstract
Glioblastoma (GBM) remains the most lethal primary brain tumor, owing to profound intratumoral heterogeneity and the limited efficacy of standard treatments. The mesenchymal (MES) molecular subtype is particularly aggressive, exhibiting heightened invasiveness, therapy resistance, and dismal patient survival compared with the proneural (PN) [...] Read more.
Glioblastoma (GBM) remains the most lethal primary brain tumor, owing to profound intratumoral heterogeneity and the limited efficacy of standard treatments. The mesenchymal (MES) molecular subtype is particularly aggressive, exhibiting heightened invasiveness, therapy resistance, and dismal patient survival compared with the proneural (PN) subtype. Emerging evidence implicates the High Mobility Group Box 1 (HMGB1) protein and its cognate receptor, the Receptor for Advanced Glycation End Products (RAGE), as drivers of malignant progression, yet their contribution to the PN-to-MES transition is incompletely defined. We integrated transcriptomic analyses of TCGA-GBM and TCGA-LGG cohorts with immunohistochemistry on in-house patient specimens. Functional studies in patient-derived and established GBM cell lines included migration and invasion assays, tumorsphere formation assays, shRNA knockdowns, and Seahorse XF metabolic profiling to interrogate the HMGB1-RAGE axis. HMGB1 and RAGE expression was markedly elevated in MES GBM tissues and cell lines. Importantly, higher HMGB1 expression correlated with shortened overall survival (p < 0.009). HMGB1 silencing curtailed cell motility and downregulated core epithelial-to-mesenchymal transition markers (N-cadherin, Snail). RAGE knockdown diminished tumorsphere formation efficiency and reduced transcription of stemness genes (OCT4), underscoring its role in sustaining tumor-initiating capacity. Metabolically, HMGB1/RAGE activation boosted both mitochondrial respiration and glycolysis, conferring the bioenergetic flexibility characteristic of MES GBM. The HMGB1-RAGE signaling axis orchestrates mesenchymal identity, invasiveness, stem cell-like properties, and metabolic reprogramming in GBM. Targeting this pathway may disrupt the PN-to-MES transition, mitigate therapeutic resistance, and ultimately improve outcomes for glioblastoma patients. Full article
(This article belongs to the Special Issue Advanced Molecular Research in Brain Tumors)
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Review

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16 pages, 1517 KB  
Review
Von Hippel–Lindau/Hypoxia Inducible Factor Axis in Glioblastoma
by Itamar Flores, Aleli Salazar, Verónica Pérez de la Cruz, Tamara Mena-Guerrero, Javier Angel Navarro Cossio, Rubén Figueroa, Mario Eugenio Cancino-Diaz and Benjamin Pineda
Int. J. Mol. Sci. 2025, 26(20), 9979; https://doi.org/10.3390/ijms26209979 - 14 Oct 2025
Viewed by 772
Abstract
Glioblastoma (GBM) is the most aggressive and lethal primary brain tumor, characterized by rapid proliferation, extensive vascularization, and resistance to conventional therapies. A feature of the GBM microenvironment is hypoxia, which activates a wide range of adaptive responses orchestrated mainly by the hypoxia-inducible [...] Read more.
Glioblastoma (GBM) is the most aggressive and lethal primary brain tumor, characterized by rapid proliferation, extensive vascularization, and resistance to conventional therapies. A feature of the GBM microenvironment is hypoxia, which activates a wide range of adaptive responses orchestrated mainly by the hypoxia-inducible factor (HIF). The Von Hippel–Lindau protein (pVHL) is a central regulator of HIF stability, inducing proteasomal degradation under physiological conditions. However, in GBM, the pVHL is frequently mutated or functionally inactivated by several mechanisms, including microRNA regulation, post-translational modifications, or degradation by specific E3 ubiquitin ligases. This loss of function results in persistent HIF activation, thereby enhancing the oncogenic and pro-angiogenic environment that contributes to the progression and aggressiveness of GBM. This review focuses on the multifaceted roles of the pVHL-HIF axis and proposes it as a key driver of GBM malignancy. Full article
(This article belongs to the Special Issue Advanced Molecular Research in Brain Tumors)
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