cancers-logo

Journal Browser

Journal Browser

Cellular and Molecular Mechanisms of Malignant Nervous System Cancers

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 31 March 2026 | Viewed by 1384

Special Issue Editor


E-Mail Website
Guest Editor
Department of Biology, Middle Tennessee State University, Murfreesboro, TN 37132, USA
Interests: biology; medulloblastoma

Special Issue Information

Dear Colleagues,

Cancers of the central and peripheral nervous system commonly affect children, adolescents, and young adults. While some may be benign and lead to favorable outcomes, others are aggressive, difficult to treat, and can lead to death. The majority of cancers that arise within the central nervous system are gliomas and medulloblastomas, while the most common extracranial nervous system cancer is neuroblastoma. Significant strides have been made over the last ten years to rigorously characterize these three nervous system cancers, paving the way for the identification of new and improved therapies. However, given the complex and heterogeneous nature of these malignancies, more work is needed to close the survival gap.

This Special Issue aims to improve our understanding of malignant nervous system cancers by combining contemporary research that illuminates current and emerging mechanisms of tumorigenesis, progression, maintenance, and treatment. Research on the cellular and molecular mechanisms of gliomas, medulloblastomas, and neuroblastomas is the key to identifying novel therapeutic avenues to explore, making current therapies less toxic and with fewer side effects, and overcoming resistance associated with high-risk diseases.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following range of topics relevant to malignant nervous system cancers: diagnostic and prognostic marker identification, tumor microenvironment and heterogeneity, resistance mechanisms, targeted therapies, epigenetics, and fundamental biology related to the genetic risk factors associated with the disease.

I look forward to receiving your contributions,

Dr. April Weissmiller
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 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. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • medulloblastoma
  • pediatric glioma
  • neuroblastoma
  • diagnosis and prognostic markers
  • IDH, TERT, and EGFR mutations
  • DNA methylation
  • treatment approaches and strategies (chemotherapy, radiation therapy, immunotherapy, and targeted therapy)
  • resistance mechanisms
  • tumor microenvironment
  • molecular characteristics of tumor heterogeneity

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

16 pages, 6405 KB  
Article
Striking at Survivin: YM-155 Inhibits High-Risk Neuroblastoma Growth and Enhances Chemosensitivity
by Danielle C. Rouse, Rameswari Chilamakuri and Saurabh Agarwal
Cancers 2025, 17(19), 3221; https://doi.org/10.3390/cancers17193221 - 2 Oct 2025
Viewed by 493
Abstract
Background/Objectives: Neuroblastoma (NB) is an aggressive pediatric malignancy that accounts for nearly 15% of all childhood cancer-related deaths, with high-risk cases showing a poor 20% prognosis and limited response to current therapies. Survivin, encoded by the BIRC5 gene, is an anti-apoptotic protein frequently [...] Read more.
Background/Objectives: Neuroblastoma (NB) is an aggressive pediatric malignancy that accounts for nearly 15% of all childhood cancer-related deaths, with high-risk cases showing a poor 20% prognosis and limited response to current therapies. Survivin, encoded by the BIRC5 gene, is an anti-apoptotic protein frequently overexpressed in NB and linked to treatment resistance and unfavorable clinical outcomes. Methods and Results: An analysis of 1235 NB patient datasets revealed a significant association between elevated BIRC5 expression and reduced overall and event-free survival, highlighting survivin as an important therapeutic target in NB. To explore this strategy, we evaluated the efficacy of YM-155, a small-molecule survivin inhibitor, across multiple NB cell lines. YM-155 displayed potent cytotoxic activity in six NB cell lines with IC50 values ranging from 8 to 212 nM and significantly inhibited colony formation and 3D spheroid growth in a dose-dependent manner. Mechanistic analyses revealed that YM-155 downregulated survivin at both mRNA and protein levels, induced apoptosis by about 2–7-fold, and caused G0/G1 phase cell cycle arrest. Moreover, YM-155 treatment enhanced p53 expression, suggesting reactivation of tumor suppressor pathways. Notably, combining YM-155 and the chemotherapeutic agent etoposide resulted in synergistic inhibition of NB growth with ED75 values ranging from 0.17 to 1, compared to either agent alone. In the xenograft mouse model, YM-155 inhibited tumor burden in contrast to controls by about 3-fold, and without any notable toxic effects in vivo. Conclusion: Overall, our findings identify YM-155 as a promising therapeutic agent for high-risk NB by directly targeting survivin and enhancing chemosensitivity. These results support continued preclinical development of survivin inhibitors as part of rational combination strategies in pediatric cancer treatment. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Malignant Nervous System Cancers)
Show Figures

Graphical abstract

15 pages, 2893 KB  
Article
NRP1 and GFAP Expression in the Medulloblastoma Microenvironment: Implications for Angiogenesis and Tumor Progression
by Margarita Belem Santana-Bejarano, María Paulina Reyes-Mata, José de Jesús Guerrero-García, Daniel Ortuño-Sahagún and Marisol Godínez-Rubí
Cancers 2025, 17(15), 2417; https://doi.org/10.3390/cancers17152417 - 22 Jul 2025
Viewed by 642
Abstract
Background/Objectives: Medulloblastoma (MB) is the second leading cause of cancer-related death in children. Its tumor microenvironment (TME) includes endothelial, glial, and immune cells that influence tumor architecture and progression. Neuropilin-1 (NRP1), a co-receptor for semaphorins and vascular endothelial growth factor (VEGF), is [...] Read more.
Background/Objectives: Medulloblastoma (MB) is the second leading cause of cancer-related death in children. Its tumor microenvironment (TME) includes endothelial, glial, and immune cells that influence tumor architecture and progression. Neuropilin-1 (NRP1), a co-receptor for semaphorins and vascular endothelial growth factor (VEGF), is expressed in various cell types during oncogenesis, yet its role in MB progression remains unclear. This study aimed to evaluate the expression and localization of NRP1 and glial fibrillary acidic protein (GFAP) in MB tissue. Methods: We analyzed MB tissue samples using immunohistochemistry, immunofluorescence, and quantitative PCR. Samples were stratified by molecular subgroup (WNT, SHH, non-WNT/non-SHH). We assessed NRP1 expression in tumor-associated microglia/macrophages (TAMs) and endothelial cells, as well as GFAP expression in astrocytes and tumor cells. Histopathological correlations and survival analyses were also conducted. Results: NRP1 was consistently expressed by TAMs across all MB molecular subgroups. Tumor vasculature showed strong endothelial NRP1 expression, while perivascular astrocytic coverage was frequently absent. Astrocytic processes exhibited spatial differences according to tumor histology. In SHH-MBs, a subset of tumor cells showed aberrant GFAP expression, which correlated with tumor recurrence or progression. Conclusions: NRP1 and GFAP display distinct expression patterns within the MB microenvironment, reflecting subgroup-specific biological behavior. Endothelial NRP1 positivity combined with limited vascular-astrocytic interaction and aberrant GFAP expression in SHH-MB may contribute to dysregulated angiogenesis and tumor progression. These findings warrant further investigation to explore their prognostic and therapeutic implications. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Malignant Nervous System Cancers)
Show Figures

Graphical abstract

Back to TopTop