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Cancers
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Signaling Pathways in Gliomas
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Signaling Pathways in Gliomas

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

Deadline for manuscript submissions: closed (20 November 2023) | Viewed by 7455

Special Issue Editor

Dr. Roman Sankowski

E-Mail Website
Guest Editor
Institute of Neuropathology, Faculty of Medicine, University of Freiburg, Freiburg, Germany
Interests: neuroimmunology; neurooncology; transcriptomics

Special Issue Information

Dear Colleagues,

High-grade gliomas are brain tumors derived from glial progenitor cells. These lesions are among the most lethal cancers. Despite aggressive surgery, chemotherapy and radiotherapy, the median survival of glioblastoma, the most common glioma, is 15 months. To date, immune therapies have failed in treating these tumors. Notably, the majority of cells within gliomas are immune cells. Unraveling intra-glioma immunity holds the promise of identifying predictive markers and opening novel therapeutic avenues. We are pleased to invite the submission of original research articles and comprehensive reviews focused on signaling in primary gliomas and glioma models. The Cancers journal publishes high-quality articles including basic, translational and clinical studies on all tumor types. This Special Issue aims to build an understanding of the specifics of the glioma microenvironment in order to facilitate future therapies.

This Special Issue aims to understand the specifics of the glioma microenvironment for future therapy development. To this end, we invite contributions examining signaling pathways in primary gliomas and glioma models. We encourage submissions of original studies and comprehensive reviews focused on the following research areas: (i) cell crosstalk in gliomas; (ii) in situ studies of glioma transcriptomics, epigenomics, proteomics and metabolomics; (iii) comparative studies with other tumor entities; (iv) insights from novel glioma models.

Original research articles and reviews are welcome for submission to this Special Issue. Research areas may include (but are not limited to) the following research areas: (i) cell crosstalk in gliomas; (ii) in situ studies of glioma transcriptomics, epigenomics, proteomics and metabolomics; (iii) comparative studies with other tumor entities; (iv) insights from novel glioma models.

Dr. Roman Sankowski
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. 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

  • glioblastoma
  • glioma
  • immunity
  • immunotherapy
  • cell–cell interaction
  • spatial analysis
  • glioma model
  • multi-omics
  • predictive markers

Published Papers (4 papers)

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Research

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19 pages, 5688 KiB  
Article
Haploinsufficiency of Adenomatous Polyposis Coli Coupled with Kirsten Rat Sarcoma Viral Oncogene Homologue Activation and P53 Loss Provokes High-Grade Glioblastoma Formation in Mice
by Kuan-Te Fang, Chuan-Shiang Su, Jhoanna Jane Layos, Nga Yin Sadonna Lau and Kuang-Hung Cheng
Cancers 2024, 16(5), 1046; https://doi.org/10.3390/cancers16051046 - 4 Mar 2024
Viewed by 751
Abstract
Glioblastoma multiforme (GBM) is the most common and deadly type of brain tumor originating from glial cells. Despite decades of clinical trials and research, there has been limited success in improving survival rates. However, molecular pathology studies have provided a detailed understanding of [...] Read more.
Glioblastoma multiforme (GBM) is the most common and deadly type of brain tumor originating from glial cells. Despite decades of clinical trials and research, there has been limited success in improving survival rates. However, molecular pathology studies have provided a detailed understanding of the genetic alterations associated with the formation and progression of glioblastoma—such as Kirsten rat sarcoma viral oncogene homolog (KRAS) signaling activation (5%), P53 mutations (25%), and adenomatous polyposis coli (APC) alterations (2%)—laying the groundwork for further investigation into the biological and biochemical basis of this malignancy. These analyses have been crucial in revealing the sequential appearance of specific genetic lesions at distinct histopathological stages during the development of GBM. To further explore the pathogenesis and progression of glioblastoma, here, we developed the glial-fibrillary-acidic-protein (GFAP)-Cre-driven mouse model and demonstrated that activated KRAS and p53 deficiencies play distinct and cooperative roles in initiating glioma tumorigenesis. Additionally, the combination of APC haploinsufficiency with mutant Kras activation and p53 deletion resulted in the rapid progression of GBM, characterized by perivascular inflammation, large necrotic areas, and multinucleated giant cells. Consequently, our GBM models have proven to be invaluable resources for identifying early disease biomarkers in glioblastoma, as they closely mimic the human disease. The insights gained from these models may pave the way for potential advancements in the diagnosis and treatment of this challenging brain tumor. Full article
(This article belongs to the Special Issue Signaling Pathways in Gliomas)
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29 pages, 8755 KiB  
Article
Integrating Multi-Omics Analysis for Enhanced Diagnosis and Treatment of Glioblastoma: A Comprehensive Data-Driven Approach
by Amir Barzegar Behrooz, Hamid Latifi-Navid, Simone C. da Silva Rosa, Maciej Swiat, Emilia Wiechec, Carla Vitorino, Rui Vitorino, Zahra Jamalpoor and Saeid Ghavami
Cancers 2023, 15(12), 3158; https://doi.org/10.3390/cancers15123158 - 12 Jun 2023
Cited by 6 | Viewed by 2892
Abstract
The most aggressive primary malignant brain tumor in adults is glioblastoma (GBM), which has poor overall survival (OS). There is a high relapse rate among patients with GBM despite maximally safe surgery, radiation therapy, temozolomide (TMZ), and aggressive treatment. Hence, there is an [...] Read more.
The most aggressive primary malignant brain tumor in adults is glioblastoma (GBM), which has poor overall survival (OS). There is a high relapse rate among patients with GBM despite maximally safe surgery, radiation therapy, temozolomide (TMZ), and aggressive treatment. Hence, there is an urgent and unmet clinical need for new approaches to managing GBM. The current study identified modules (MYC, EGFR, PIK3CA, SUZ12, and SPRK2) involved in GBM disease through the NeDRex plugin. Furthermore, hub genes were identified in a comprehensive interaction network containing 7560 proteins related to GBM disease and 3860 proteins associated with signaling pathways involved in GBM. By integrating the results of the analyses mentioned above and again performing centrality analysis, eleven key genes involved in GBM disease were identified. ProteomicsDB and Gliovis databases were used for determining the gene expression in normal and tumor brain tissue. The NetworkAnalyst and the mGWAS-Explorer tools identified miRNAs, SNPs, and metabolites associated with these 11 genes. Moreover, a literature review of recent studies revealed other lists of metabolites related to GBM disease. The enrichment analysis of identified genes, miRNAs, and metabolites associated with GBM disease was performed using ExpressAnalyst, miEAA, and MetaboAnalyst tools. Further investigation of metabolite roles in GBM was performed using pathway, joint pathway, and network analyses. The results of this study allowed us to identify 11 genes (UBC, HDAC1, CTNNB1, TRIM28, CSNK2A1, RBBP4, TP53, APP, DAB1, PINK1, and RELN), five miRNAs (hsa-mir-221-3p, hsa-mir-30a-5p, hsa-mir-15a-5p, hsa-mir-130a-3p, and hsa-let-7b-5p), six metabolites (HDL, N6-acetyl-L-lysine, cholesterol, formate, N, N-dimethylglycine/xylose, and X2. piperidinone) and 15 distinct signaling pathways that play an indispensable role in GBM disease development. The identified top genes, miRNAs, and metabolite signatures can be targeted to establish early diagnostic methods and plan personalized GBM treatment strategies. Full article
(This article belongs to the Special Issue Signaling Pathways in Gliomas)
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18 pages, 6712 KiB  
Article
Transcriptome Analysis Identifies Accumulation of Natural Killer Cells with Enhanced Lymphotoxin-β Expression during Glioblastoma Progression
by Gianni Monaco, Ashkan Khavaran, Adrià Dalmau Gasull, Jonathan Cahueau, Martin Diebold, Chintan Chhatbar, Mirco Friedrich, Dieter Henrik Heiland and Roman Sankowski
Cancers 2022, 14(19), 4915; https://doi.org/10.3390/cancers14194915 - 7 Oct 2022
Cited by 1 | Viewed by 2042
Abstract
Glioblastomas are the most common primary brain tumors. Despite extensive clinical and molecular insights into these tumors, the prognosis remains dismal. While targeted immunotherapies have shown remarkable success across different non-brain tumor entities, they failed to show efficacy in glioblastomas. These failures prompted [...] Read more.
Glioblastomas are the most common primary brain tumors. Despite extensive clinical and molecular insights into these tumors, the prognosis remains dismal. While targeted immunotherapies have shown remarkable success across different non-brain tumor entities, they failed to show efficacy in glioblastomas. These failures prompted the field to reassess the idiosyncrasies of the glioblastoma microenvironment. Several high-dimensional single-cell RNA sequencing studies generated remarkable findings about glioblastoma-associated immune cells. To build on the collective strength of these studies, we integrated several murine and human datasets that profiled glioblastoma-associated immune cells at different time points. We integrated these datasets and utilized state-of-the-art algorithms to investigate them in a hypothesis-free, purely exploratory approach. We identified a robust accumulation of a natural killer cell subset that was characterized by a downregulation of activation-associated genes with a concomitant upregulation of apoptosis genes. In both species, we found a robust upregulation of the Lymphotoxin-β gene, a cytokine from the TNF superfamily and a key factor for the development of adaptive immunity. Further validation analyses uncovered a correlation of lymphotoxin signaling with mesenchymal-like glioblastoma regions in situ and in TCGA and CGGA glioblastoma cohorts. In summary, we identify lymphotoxin signaling as a potential therapeutic target in glioblastoma-associated natural killer cells. Full article
(This article belongs to the Special Issue Signaling Pathways in Gliomas)
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Review

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20 pages, 23746 KiB  
Review
Glioma–Immune Cell Crosstalk in Tumor Progression
by Mahmoud Elguindy, Jacob S. Young, Isha Mondal, Rongze O. Lu and Winson S. Ho
Cancers 2024, 16(2), 308; https://doi.org/10.3390/cancers16020308 - 11 Jan 2024
Viewed by 1307
Abstract
Glioma progression is a complex process controlled by molecular factors that coordinate the crosstalk between tumor cells and components of the tumor microenvironment (TME). Among these, immune cells play a critical role in cancer survival and progression. The complex interplay between cancer cells [...] Read more.
Glioma progression is a complex process controlled by molecular factors that coordinate the crosstalk between tumor cells and components of the tumor microenvironment (TME). Among these, immune cells play a critical role in cancer survival and progression. The complex interplay between cancer cells and the immune TME influences the outcome of immunotherapy and other anti-cancer therapies. Here, we present an updated view of the pro- and anti-tumor activities of the main myeloid and lymphocyte cell populations in the glioma TME. We review the underlying mechanisms involved in crosstalk between cancer cells and immune cells that enable gliomas to evade the immune system and co-opt these cells for tumor growth. Lastly, we discuss the current and experimental therapeutic options being developed to revert the immunosuppressive activity of the glioma TME. Knowledge of the complex interplay that elapses between tumor and immune cells may help develop new combination treatments able to overcome tumor immune evasion mechanisms and enhance response to immunotherapies. Full article
(This article belongs to the Special Issue Signaling Pathways in Gliomas)
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