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Biomedicines
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Glioma Metabolism, Epigenetics, and Microenvironment
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Glioma Metabolism, Epigenetics, and Microenvironment

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 22787

Special Issue Editors

Dr. L. Eric Huang

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Guest Editor
Department of Neurosurgery, University of Utah, Salt Lake City, UT, USA
Interests: brain tumor; cancer biology/metabolism; tumor hypoxia; prognosis
Prof. Dr. Shi-Yuan Cheng

E-Mail Website
Guest Editor
Department of Neurology, Northwestern Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center University of Northwestern Feinberg School of Medicine, 303 East Superior, Lurie 7-119, Chicago, IL 60026, USA
Interests: oncogenic signaling; glioblastomas; breast cancers; cancer biology; molecular mechanisms of human cancer tumorigenesis; progression; invasion/metastasis and angiogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Malignant gliomas represent the most common primary malignancy of the central nervous system and cause significant morbidity and mortality. Extensive characterization at the genetic level has led to the adoption of molecular parameters, for the first time, in addition to the traditional histology features in the 2016 World Health Organization (WHO) classification of the central nervous system tumors. The inclusion of molecular parameters, including hotspot mutations in IDH1 and H3F3A, genetic alterations in TP53 and ATRX, and chromosomal 1p/19q codeletion, in the WHO classification considerably improves the classification of gliomas and the prediction of patient outcome. Although the knowledge has yet to significantly improve patient outcome, recent discoveries in glioma metabolism, epigenetics, and the microenvironmental influence including immune microenvironment on cellular states and plasticity have identified tumor vulnerability and heterogeneity but have also revealed tumor complexity. This Special Issue is to collect novel contributions in research articles or reviews to these topics and aims to generate opportunities for future research where the advanced knowledge can be translated into potential therapeutic approaches for better treatment.

Dr. L. Eric Huang
Prof. Dr. Shi-Yuan Cheng
Guest Editors

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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • DNA methylation
  • epigenetics
  • glioma
  • histone modification
  • isocitrate dehydrogenase
  • metabolism
  • microenvironment

Published Papers (7 papers)

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Research

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11 pages, 3444 KiB  
Article
EGFR Amplification Is a Phenomenon of IDH Wildtype and TERT Mutated High-Grade Glioma: An Integrated Analysis Using Fluorescence In Situ Hybridization and DNA Methylome Profiling
by Dorothee Hölzl, Georg Hutarew, Barbara Zellinger, Beate Alinger-Scharinger, Hans U. Schlicker, Christoph Schwartz, Karl Sotlar and Theo F. J. Kraus
Biomedicines 2022, 10(4), 794; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10040794 - 29 Mar 2022
Cited by 5 | Viewed by 2226
Abstract
Gliomas are the most common intrinsic brain tumors in adults, and in accordance with their clinical behavior and patients’ outcome, they are graded by the World Health Organization (WHO) classification of brain tumors. One very interesting candidate for targeted tumor therapy may be [...] Read more.
Gliomas are the most common intrinsic brain tumors in adults, and in accordance with their clinical behavior and patients’ outcome, they are graded by the World Health Organization (WHO) classification of brain tumors. One very interesting candidate for targeted tumor therapy may be epidermal growth factor receptor (EGFR) amplification. Here, we performed an integrated comparative analysis of EGFR amplification in 34 glioma samples using standard fluorescence in situ hybridization (FISH) and Illumina EPIC Infinium Methylation Bead Chip and correlated results with molecular glioma hallmarks. We found that the EPIC analysis showed the same power of detecting EGFR amplification compared with FISH. EGFR amplification was detectable in high-grade gliomas (25%). Moreover, EGFR amplification was found to be present solely in IDH wildtype gliomas (26%) and TERT mutated gliomas (27%), occurring independently of MGMT promoter methylation status and being mutually exclusive with 1p/19q codeletion (LOH). In summary, EPIC Bead Chip analysis is a reliable tool for detecting EGFR amplification and is comparable with the standard method FISH. EGFR amplification is a phenomenon of IDH wildtype TERT mutated high-grade gliomas. Full article
(This article belongs to the Special Issue Glioma Metabolism, Epigenetics, and Microenvironment)
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14 pages, 2228 KiB  
Article
Purine Synthesis Inhibitor L-Alanosine Impairs Mitochondrial Function and Stemness of Brain Tumor Initiating Cells
by Simranjit X. Singh, Rui Yang, Kristen Roso, Landon J. Hansen, Changzheng Du, Lee H. Chen, Paula K. Greer, Christopher J. Pirozzi and Yiping He
Biomedicines 2022, 10(4), 751; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10040751 - 23 Mar 2022
Cited by 4 | Viewed by 2493
Abstract
Glioblastoma (GBM) is a lethal brain cancer exhibiting high levels of drug resistance, a feature partially imparted by tumor cell stemness. Recent work shows that homozygous MTAP deletion, a genetic alteration occurring in about half of all GBMs, promotes stemness in GBM cells. [...] Read more.
Glioblastoma (GBM) is a lethal brain cancer exhibiting high levels of drug resistance, a feature partially imparted by tumor cell stemness. Recent work shows that homozygous MTAP deletion, a genetic alteration occurring in about half of all GBMs, promotes stemness in GBM cells. Exploiting MTAP loss-conferred deficiency in purine salvage, we demonstrate that purine blockade via treatment with L-Alanosine (ALA), an inhibitor of de novo purine synthesis, attenuates stemness of MTAP-deficient GBM cells. This ALA-induced reduction in stemness is mediated in part by compromised mitochondrial function, highlighted by ALA-induced elimination of mitochondrial spare respiratory capacity. Notably, these effects of ALA are apparent even when the treatment was transient and with a low dose. Finally, in agreement with diminished stemness and compromised mitochondrial function, we show that ALA sensitizes GBM cells to temozolomide (TMZ) in vitro and in an orthotopic GBM model. Collectively, these results identify purine supply as an essential component in maintaining mitochondrial function in GBM cells and highlight a critical role of mitochondrial function in sustaining GBM stemness. We propose that purine synthesis inhibition can be beneficial in combination with the standard of care for MTAP-deficient GBMs, and that it may be feasible to achieve this benefit without inflicting major toxicity. Full article
(This article belongs to the Special Issue Glioma Metabolism, Epigenetics, and Microenvironment)
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18 pages, 4744 KiB  
Article
A Novel 16-Genes Signature Scoring System as Prognostic Model to Evaluate Survival Risk in Patients with Glioblastoma
by Zunpeng Yu, Manqing Du and Long Lu
Biomedicines 2022, 10(2), 317; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10020317 - 29 Jan 2022
Cited by 13 | Viewed by 3277
Abstract
Previous studies have found that gene expression levels are associated with prognosis and some genes can be used to predict the survival risk of glioblastoma (GBM) patients. However, most of them just built the survival-related gene signature, and personal survival risk can be [...] Read more.
Previous studies have found that gene expression levels are associated with prognosis and some genes can be used to predict the survival risk of glioblastoma (GBM) patients. However, most of them just built the survival-related gene signature, and personal survival risk can be evaluated only in group. This study aimed to find the prognostic survival related genes of GBM, and construct survival risk prediction model, which can be used to evaluate survival risk by individual. We collected gene expression data and clinical information from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. Cox regression analysis and LASSO-cox regression analysis were performed to get survival-related genes and establish the overall survival prediction model. The ROC curve and Kaplan Meier analysis were used to evaluate the prediction ability of the model in training set and two independent cohorts. We also analyzed the biological functions of survival-related genes by GO and KEGG enrichment analysis. We identified 99 genes associated with overall survival and selected 16 genes (IGFBP2, GPRASP1, C1R, CHRM3, CLSTN2, NELL1, SEZ6L2, NMB, ICAM5, HPCAL4, SNAP91, PCSK1N, PGBD5, INA, UCHL1 and LHX6) to establish the survival risk prediction model. Multivariate Cox regression analysis indicted that the risk score could predict overall survival independent of age and gender. ROC analyses showed that our model was more robust than four existing signatures. The sixteen genes can also be potential transcriptional biomarkers and the model can assist doctors on clinical decision-making and personalized treatment of GBM patients. Full article
(This article belongs to the Special Issue Glioma Metabolism, Epigenetics, and Microenvironment)
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Review

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24 pages, 735 KiB  
Review
The Role of Non-Coding RNAs in Glioma
by Anshika Goenka, Deanna Marie Tiek, Xiao Song, Rebeca Piatniczka Iglesia, Minghui Lu, Bo Hu and Shi-Yuan Cheng
Biomedicines 2022, 10(8), 2031; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10082031 - 20 Aug 2022
Cited by 9 | Viewed by 3503
Abstract
For decades, research in cancer biology has been focused on the protein-coding fraction of the human genome. However, with the discovery of non-coding RNAs (ncRNAs), it has become known that these entities not only function in numerous fundamental life processes such as growth, [...] Read more.
For decades, research in cancer biology has been focused on the protein-coding fraction of the human genome. However, with the discovery of non-coding RNAs (ncRNAs), it has become known that these entities not only function in numerous fundamental life processes such as growth, differentiation, and development, but also play critical roles in a wide spectrum of human diseases, including cancer. Dysregulated ncRNA expression is found to affect cancer initiation, progression, and therapy resistance, through transcriptional, post-transcriptional, or epigenetic processes in the cell. In this review, we focus on the recent development and advances in ncRNA biology that are pertinent to their role in glioma tumorigenesis and therapy response. Gliomas are common, and are the most aggressive type of primary tumors, which account for ~30% of central nervous system (CNS) tumors. Of these, glioblastoma (GBM), which are grade IV tumors, are the most lethal brain tumors. Only 5% of GBM patients survive beyond five years upon diagnosis. Hence, a deeper understanding of the cellular non-coding transcriptome might help identify biomarkers and therapeutic agents for a better treatment of glioma. Here, we delve into the functional roles of microRNA (miRNA), long non-coding RNA (lncRNA), and circular RNA (circRNA) in glioma tumorigenesis, discuss the function of their extracellular counterparts, and highlight their potential as biomarkers and therapeutic agents in glioma. Full article
(This article belongs to the Special Issue Glioma Metabolism, Epigenetics, and Microenvironment)
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25 pages, 3670 KiB  
Review
Lipid Metabolism in Glioblastoma: From De Novo Synthesis to Storage
by Yongjun Kou, Feng Geng and Deliang Guo
Biomedicines 2022, 10(8), 1943; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10081943 - 11 Aug 2022
Cited by 16 | Viewed by 5002
Abstract
Glioblastoma (GBM) is the most lethal primary brain tumor. With limited therapeutic options, novel therapies are desperately needed. Recent studies have shown that GBM acquires large amounts of lipids for rapid growth through activation of sterol regulatory element-binding protein 1 (SREBP-1), a master [...] Read more.
Glioblastoma (GBM) is the most lethal primary brain tumor. With limited therapeutic options, novel therapies are desperately needed. Recent studies have shown that GBM acquires large amounts of lipids for rapid growth through activation of sterol regulatory element-binding protein 1 (SREBP-1), a master transcription factor that regulates fatty acid and cholesterol synthesis, and cholesterol uptake. Interestingly, GBM cells divert substantial quantities of lipids into lipid droplets (LDs), a specific storage organelle for neutral lipids, to prevent lipotoxicity by increasing the expression of diacylglycerol acyltransferase 1 (DGAT1) and sterol-O-acyltransferase 1 (SOAT1), which convert excess fatty acids and cholesterol to triacylglycerol and cholesteryl esters, respectively. In this review, we will summarize recent progress on our understanding of lipid metabolism regulation in GBM to promote tumor growth and discuss novel strategies to specifically induce lipotoxicity to tumor cells through disrupting lipid storage, a promising new avenue for treating GBM. Full article
(This article belongs to the Special Issue Glioma Metabolism, Epigenetics, and Microenvironment)
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20 pages, 1346 KiB  
Review
The Intricate Epigenetic and Transcriptional Alterations in Pediatric High-Grade Gliomas: Targeting the Crosstalk as the Oncogenic Achilles’ Heel
by Paul Huchedé, Pierre Leblond and Marie Castets
Biomedicines 2022, 10(6), 1311; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10061311 - 03 Jun 2022
Cited by 1 | Viewed by 2977
Abstract
Pediatric high-grade gliomas (pHGGs) are a deadly and heterogenous subgroup of gliomas for which the development of innovative treatments is urgent. Advances in high-throughput molecular techniques have shed light on key epigenetic components of these diseases, such as K27M and G34R/V mutations on [...] Read more.
Pediatric high-grade gliomas (pHGGs) are a deadly and heterogenous subgroup of gliomas for which the development of innovative treatments is urgent. Advances in high-throughput molecular techniques have shed light on key epigenetic components of these diseases, such as K27M and G34R/V mutations on histone 3. However, modification of DNA compaction is not sufficient by itself to drive those tumors. Here, we review molecular specificities of pHGGs subcategories in the context of epigenomic rewiring caused by H3 mutations and the subsequent oncogenic interplay with transcriptional signaling pathways co-opted from developmental programs that ultimately leads to gliomagenesis. Understanding how transcriptional and epigenetic alterations synergize in each cellular context in these tumors could allow the identification of new Achilles’ heels, thereby highlighting new levers to improve their therapeutic management. Full article
(This article belongs to the Special Issue Glioma Metabolism, Epigenetics, and Microenvironment)
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16 pages, 902 KiB  
Review
The Roles and Regulation of m6A Modification in Glioblastoma Stem Cells and Tumorigenesis
by Peng Li, Hope T. Richard, Kezhou Zhu, Linlin Li and Suyun Huang
Biomedicines 2022, 10(5), 969; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10050969 - 22 Apr 2022
Cited by 3 | Viewed by 2190
Abstract
Glioblastoma is the most common and most lethal primary malignant brain tumor. N6-methyladenosine (m6A) is a widespread and abundant internal messenger RNA (mRNA) modification found in eukaryotes. Accumulated evidence demonstrates that m6A modification is aberrantly activated in [...] Read more.
Glioblastoma is the most common and most lethal primary malignant brain tumor. N6-methyladenosine (m6A) is a widespread and abundant internal messenger RNA (mRNA) modification found in eukaryotes. Accumulated evidence demonstrates that m6A modification is aberrantly activated in human cancers and is critical for tumorigenesis and metastasis. m6A modification is also strongly involved in key signaling pathways and is associated with prognosis in glioblastoma. Here, we briefly outline the functions of m6A and its regulatory proteins, including m6A writers, erasers, and readers of the fate of RNA. We also summarize the latest breakthroughs in this field, describe the underlying molecular mechanisms that contribute to the tumorigenesis and progression, and highlight the inhibitors targeting the factors in m6A modification in glioblastoma. Further studies focusing on the specific pathways of m6A modification could help identify biomarkers and therapeutic targets that might prevent and treat glioblastoma. Full article
(This article belongs to the Special Issue Glioma Metabolism, Epigenetics, and Microenvironment)
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