Pathophysiology of Central Nervous System Tumors

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 15 March 2025 | Viewed by 4919

Special Issue Editor


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Guest Editor
Princess Máxima Center for Pediatric Oncology, Heidelberglaan 25, 3584 CS Utrecht, The Netherlands
Interests: pediatric neuro-oncology; neuropathology; multi-omics; immunotherapy; targeted therapy

Special Issue Information

Dear Colleagues,

The tremendous increase in knowledge of the molecular characteristics of central nervous system (CNS)  tumors over the last decade has created a fundamental change in the basic concepts and experimental practices of CNS tumors. Epigenetic profiling has allowed for classification and re-classification of CNS tumors with many ‘new’ CNS tumor entities, all with characteristics molecular profiles. This has led us to realize the complexity and heterogeneity among the distinct CNS tumor entities, necessitating in-depth profiling of these tumors in order to provide proper treatment for the distinctive CNS tumors. In order to grasp the diversity and relevance of the cell populations within each CNS tumor, it is crucial to conduct synchronized assessments that connect the genetic makeup and its epigenetic control to the expression of genes and proteins at the individual cell level. Extensive multiomic profiling (e.g. single-cell RNA sequencing, transcriptomics, proteomics) will have a strong impact on the understanding of tumor-intrinsic neuropathophysiology. Simultaneously, extrinsic microenvironmental factors, including the interplay between neoplastic cells and neurons or cells of the tumor immune micro environment (TIME), will regulate and modulate the pathophysiology of CNS tumors. More in-depth knowledge of this interplay may allow for tailored (immune) therapy.

The purpose of this Special Issue is to highlight recent findings regarding in-depth profiling of either the neoplastic compartment or the extrinsic microenvironmental  compartment of  CNS tumors, both for adult- and pediatric-type CNS tumors. The goal of this issue is to provide a broad scope that includes research papers and reviews related to in-depth (multiomic) profiling of CNS tumors, directly or indirectly affecting pathogenesis and disease.

Dr. Mariëtte E.G. Kranendonk
Guest Editor

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Keywords

  • CNS tumor
  • pediatric
  • adult
  • molecular profiling
  • multiomics
  • microenvironment

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Published Papers (2 papers)

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Research

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13 pages, 6106 KiB  
Article
Non-Immune-Mediated, p27-Associated, Growth Inhibition of Glioblastoma by Class-II-Transactivator (CIITA)
by A Katherine Tan, Aurelie Henry, Nicolas Goffart, Christophe Poulet, Jacqueline A. Sluijs, Elly M. Hol, Vincent Bours and Pierre A. Robe
Cells 2024, 13(22), 1883; https://doi.org/10.3390/cells13221883 - 14 Nov 2024
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Abstract
Background: Previous works have shown that the expression of Class-II-Transactivator (CIITA) in tumor cells reduces the growth of glioblastoma (GB) in animal models, but immune effects cannot solely explain this. Here, we searched for immune-independent effects of CIITA on the proliferation of GB. [...] Read more.
Background: Previous works have shown that the expression of Class-II-Transactivator (CIITA) in tumor cells reduces the growth of glioblastoma (GB) in animal models, but immune effects cannot solely explain this. Here, we searched for immune-independent effects of CIITA on the proliferation of GB. Methods: Murine GL261 and human U87, GM2 and GM3 malignant glioma cells were transfected with CIITA. NSG (immunodeficient) and nude (athymic) mice were injected in the striatum with GL261-wildtype (-WT) and -CIITA, and tumor growth was assessed by immunohistology and luminescence reporter genes. Clonogenic, sphere-formation, and 3D Matrigel-based in vitro growth assays were performed to compare the growth of WT versus CIITA-expressing murine and human cells. Bulk RNA sequencing and RT2 qRT-PCR profiler arrays were performed on these four cell lines to assess RNA expression changes following CIITA transfection. Western blot analysis on several proliferation-associated proteins was performed. Results: The intracerebral growth of murine GL261-CIITA cells was drastically reduced both in immunodeficient and athymic mice. Tumor growth was reduced in vitro in three of the four cell types. RNA sequencing and RT2 profiler array experiments revealed a modulation of gene expression in the PI3-Akt, MAPK- and cell-cycle regulation pathways following CIITA overexpression. Western blot analysis showed an upregulation of p27 in the growth-inhibited cells following this treatment. PDGFR-beta was downregulated in all cells. We did not find consistent regulation of other proteins involved in GB proliferation. Conclusions: Proliferation is drastically reduced by CIITA in GB, both in vivo and in vitro, notably in association with p27-mediated inhibition of cell-cycle pathways. Full article
(This article belongs to the Special Issue Pathophysiology of Central Nervous System Tumors)
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Review

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21 pages, 3924 KiB  
Review
Dissecting the Natural Patterns of Progression and Senescence in Pediatric Low-Grade Glioma: From Cellular Mechanisms to Clinical Implications
by David Gorodezki, Martin U. Schuhmann, Martin Ebinger and Jens Schittenhelm
Cells 2024, 13(14), 1215; https://doi.org/10.3390/cells13141215 - 19 Jul 2024
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Abstract
Pediatric low-grade gliomas (PLGGs) comprise a heterogeneous set of low-grade glial and glioneuronal tumors, collectively representing the most frequent CNS tumors of childhood and adolescence. Despite excellent overall survival rates, the chronic nature of the disease bears a high risk of long-term disease- [...] Read more.
Pediatric low-grade gliomas (PLGGs) comprise a heterogeneous set of low-grade glial and glioneuronal tumors, collectively representing the most frequent CNS tumors of childhood and adolescence. Despite excellent overall survival rates, the chronic nature of the disease bears a high risk of long-term disease- and therapy-related morbidity in affected patients. Recent in-depth molecular profiling and studies of the genetic landscape of PLGGs led to the discovery of the paramount role of frequent upregulation of RAS/MAPK and mTOR signaling in tumorigenesis and progression of these tumors. Beyond, the subsequent unveiling of RAS/MAPK-driven oncogene-induced senescence in these tumors may shape the understanding of the molecular mechanisms determining the versatile progression patterns of PLGGs, potentially providing a promising target for novel therapies. Recent in vitro and in vivo studies moreover indicate a strong dependence of PLGG formation and growth on the tumor microenvironment. In this work, we provide an overview of the current understanding of the multilayered cellular mechanisms and clinical factors determining the natural progression patterns and the characteristic biological behavior of these tumors, aiming to provide a foundation for advanced stratification for the management of these tumors within a multimodal treatment approach. Full article
(This article belongs to the Special Issue Pathophysiology of Central Nervous System Tumors)
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