Glioblastoma: What Do We Know?

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 25 December 2024 | Viewed by 1829

Special Issue Editor


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Guest Editor
Departments of Anesthesiology, Hematology and Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA
Interests: cell death mechanisms in brain injuries; degenerative diseases; cancer such as glioblastoma (GBM)

Special Issue Information

Dear Colleagues,

Glioblastoma multiforme (GBM) is a common primary astrocytoma and represents the most malignant tumor in the central nervous system. The fast progression of this tumor and short survival time of GBM patients have been a tough challenge in cancer research and clinical treatment. Despite advances in recent years, GBM remains largely incurable. Little is known about the etiology of GBM, although high-dose ionizing radiation is recognized as a risk factor. GBM shows heterogeneous features involving multiple cell types, including cancer stem cells, hemorrhage, necrosis, aggressive invasion, and vascular endothelial hyperplasia, among other malignant features. Primary and secondary GBMs are characterized by molecular correlates, aberrations of signaling pathways, genetic mutations, and altered gene expression. Early detection and accurate monitoring of carcinoma are critical for early diagnosis, effective treatment, and improved patient outcomes. Biomarkers, such as miRNAs, can be valuable in these applications. In the last few years, genetic modifications, such as the reprogramming of cancer cells into non-cancerous phenotypes, provide an exciting opportunity of stopping tumor growth by a gene therapy. Recent advances in imaging techniques, such as MRI and PET, have also helped in evaluating the changes in the hemodynamics, tissue architecture, and cellular metabolism of gliomas. All of these studies raise the hope for improved therapeutics and the development of a new paradigm for the management of GBM. This Special Issue aims to enhance our knowledge about GBM by sharing the most recent advances in basic and clinical investigations. We welcome articles and reviews of cellular/molecular mechanisms and possible pathogenesis. We especially encourage innovative approaches and strategies that show the potential mechanisms of novel treatments or significantly improved GBM therapy.

Prof. Dr. Shan Ping Yu
Guest Editor

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Keywords

  • carcinoma cell
  • diagnoses
  • molecular mechanism
  • cellular mechanism
  • signaling pathways
  • biomarkers
  • therapeutics

Published Papers (2 papers)

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Research

14 pages, 2784 KiB  
Article
Upregulation of the Renin–Angiotensin System Is Associated with Patient Survival and the Tumour Microenvironment in Glioblastoma
by Mathew Lozinski, Eugenie R. Lumbers, Nikola A. Bowden, Jennifer H. Martin, Michael F. Fay, Kirsty G. Pringle and Paul A. Tooney
Cells 2024, 13(7), 634; https://doi.org/10.3390/cells13070634 - 5 Apr 2024
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Abstract
Glioblastoma is a highly aggressive disease with poor survival outcomes. An emerging body of literature links the role of the renin–angiotensin system (RAS), well-known for its function in the cardiovascular system, to the progression of cancers. We studied the expression of RAS-related genes [...] Read more.
Glioblastoma is a highly aggressive disease with poor survival outcomes. An emerging body of literature links the role of the renin–angiotensin system (RAS), well-known for its function in the cardiovascular system, to the progression of cancers. We studied the expression of RAS-related genes (ATP6AP2, AGTR1, AGTR2, ACE, AGT, and REN) in The Cancer Genome Atlas (TCGA) glioblastoma cohort, their relationship to patient survival, and association with tumour microenvironment pathways. The expression of RAS genes was then examined in 12 patient-derived glioblastoma cell lines treated with chemoradiation. In cases of glioblastoma within the TCGA, ATP6AP2, AGTR1, ACE, and AGT had consistent expressions across samples, while AGTR2 and REN were lowly expressed. High expression of AGTR1 was independently associated with lower progression-free survival (PFS) (p = 0.01) and had a non-significant trend for overall survival (OS) after multivariate analysis (p = 0.095). The combined expression of RAS receptors (ATP6AP2, AGTR1, and AGTR2) was positively associated with gene pathways involved in hypoxia, microvasculature, stem cell plasticity, and the molecular characterisation of glioblastoma subtypes. In patient-derived glioblastoma cell lines, ATP6AP2 and AGTR1 were upregulated after chemoradiotherapy and correlated with an increase in HIF1A expression. This data suggests the RAS is correlated with changes in the tumour microenvironment and associated with glioblastoma survival outcomes. Full article
(This article belongs to the Special Issue Glioblastoma: What Do We Know?)
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14 pages, 2852 KiB  
Article
CD99 Expression and Prognostic Impact in Glioblastoma: A Single-Center Cohort Study
by Andrea Rocca, Fabiola Giudici, Carmine Antonio Donofrio, Cristina Bottin, Maurizio Pinamonti, Benvenuto Ferrari, Francesco Schettini, Estela Pineda, Stefano Panni, Marika Cominetti, Patrizia D’Auria, Simonetta Bianchini, Elena Varotti, Marco Ungari, Stefano Ciccarelli, Marzia Filippini, Sarah Brenna, Valentina Fiori, Tomas Di Mambro, Angelo Sparti, Mauro Magnani, Fabrizio Zanconati, Daniele Generali and Antonio Fioravantiadd Show full author list remove Hide full author list
Cells 2024, 13(7), 597; https://doi.org/10.3390/cells13070597 - 29 Mar 2024
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Abstract
Glioblastoma is the most frequent and aggressive brain tumor in adults. This study aims to evaluate the expression and prognostic impact of CD99, a membrane glycoprotein involved in cellular migration and invasion. In a cohort of patients with glioblastoma treated with surgery, radiotherapy [...] Read more.
Glioblastoma is the most frequent and aggressive brain tumor in adults. This study aims to evaluate the expression and prognostic impact of CD99, a membrane glycoprotein involved in cellular migration and invasion. In a cohort of patients with glioblastoma treated with surgery, radiotherapy and temozolomide, we retrospectively analyzed tumor expression of CD99 by immunohistochemistry (IHC) and by quantitative real-time polymerase chain reaction (qRT-PCR) for both the wild type (CD99wt) and the truncated (CD99sh) isoforms. The impact on overall survival (OS) was assessed with the Kaplan–Meier method and log-rank test and by multivariable Cox regression. Forty-six patients with glioblastoma entered this study. Immunohistochemical expression of CD99 was present in 83%. Only the CD99wt isoform was detected by qRT-PCR and was significantly correlated with CD99 expression evaluated by IHC (rho = 0.309, p = 0.037). CD99 expression was not associated with OS, regardless of the assessment methodology used (p = 0.61 for qRT-PCR and p = 0.73 for IHC). In an exploratory analysis of The Cancer Genome Atlas, casuistry of glioblastomas CD99 expression was not associated with OS nor with progression-free survival. This study confirms a high expression of CD99 in glioblastoma but does not show any significant impact on survival. Further preclinical studies are needed to define its role as a therapeutic target in glioblastoma. Full article
(This article belongs to the Special Issue Glioblastoma: What Do We Know?)
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