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Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags,...
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Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags, to Rodent Models

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neuro-oncology".

Deadline for manuscript submissions: closed (26 June 2022) | Viewed by 23765

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special Issue Editor

Dr. Hailiang Tang

E-Mail Website
Guest Editor
Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai 200433, China
Interests: traumatic brain injury; brain tumors; stem cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Despite the past two decades of research progress, glioma still remains the most challenging of all primary central nervous system (CNS) tumors. The complexity of its pathogenesis makes the disease hard to deal with, especially glioblastoma multiforme (GBM, WHO grade IV), the most aggressive brain tumor entity.

GBMs contain a population of glioma stem cells (GSCs) with self-renewal ability, which are partly responsible for tumor resistance and recurrence after standard therapy. Researchers recently also found that neural stem cells (NSCs) in the subventricular zone are a potential cell of origin, containing the driver mutations of GBM. In this Special Issue, we encourage manuscripts discussing common features between GSCs and NSCs, and that provide possible future therapeutic strategies.

Numerous genomic findings in glioma deeply impact both basic research and clinical outcomes. For example, the genetic alterations IDH1/2, NF1, ERBB2, and NFKBIA provide opportunities for the discovery of new drugs. Although current glioma treatment is still mainly based on traditional pathology, genomic tags now have an increasing role in clinical diagnosis, and assist in making treatment plans. In this Special Issue, we also welcome manuscripts discussing genomic findings in glioma.

Mouse models have also been widely used to investigate the cell of origin of glioma. Researchers have already reported the first genomic study of a mouse model of high-grade astrocytoma by manipulating tumor suppressors, including PTEN, P53, and Rb. It was shown that there was a close similarity in gene copy number and alteration between mouse glioma and human sample. This Special Issue welcomes manuscripts discussing glioma models in rodents and their value for future preclinical studies.

Thus, we are organizing a Special Issue in the journal Brain Sciences, with the aim to collect studies that focus on the pathogenesis of glioma, such as its cell origin, the role of GSCs, genomic alterations, animal models, etc. Original articles, clinical trials, and reviews related to this topic, but not case reports, are welcome for submission to this Special Issue.

Dr. Hailiang Tang
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. Brain Sciences 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 2200 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

  • glioma
  • stem cells
  • genomic
  • pathogenesis

Published Papers (11 papers)

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Editorial

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3 pages, 404 KiB  
Editorial
Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags, to Rodent Models
by Hailiang Tang, Xi Li and Rong Xie
Brain Sci. 2023, 13(1), 30; https://doi.org/10.3390/brainsci13010030 - 23 Dec 2022
Viewed by 903
Abstract
Glioma remains the toughest brain tumor among all primary central nervous system (CNS) tumors [...] Full article
(This article belongs to the Special Issue Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags, to Rodent Models)
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Research

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15 pages, 4586 KiB  
Article
Irreversible Electroporation Mediates Glioma Apoptosis via Upregulation of AP-1 and Bim: Transcriptome Evidence
by Shuangquan Yu, Lingchao Chen, Kun Song, Ting Shu, Zheng Fang, Lujia Ding, Jilong Liu, Lei Jiang, Guanqing Zhang, Bing Zhang and Zhiyong Qin
Brain Sci. 2022, 12(11), 1465; https://doi.org/10.3390/brainsci12111465 - 29 Oct 2022
Viewed by 1587
Abstract
The heat-sink effect and thermal damage of conventional thermal ablative technologies can be minimized by irreversible electroporation (IRE), which results in clear ablative boundaries and conservation of blood vessels, facilitating maximal safe surgical resection for glioblastoma. Although much comparative data about the death [...] Read more.
The heat-sink effect and thermal damage of conventional thermal ablative technologies can be minimized by irreversible electroporation (IRE), which results in clear ablative boundaries and conservation of blood vessels, facilitating maximal safe surgical resection for glioblastoma. Although much comparative data about the death forms in IRE have been published, the comprehensive genetic regulatory mechanism for apoptosis, among other forms of regulatory cell death (RCD), remains elusive. We investigated the electric field intensity threshold for apoptosis/necrosis (YO-PRO-1/PI co-staining) of the U251 human malignant glioma cell line with stepwise increased uniform field intensity. Time course samples (0–6 h) of apoptosis induction and sham treatment were collected for transcriptome sequencing. Sequencing showed that transcription factor AP-1 and its target gene Bim (Bcl2l11), related to the signaling pathway, played a major role in the apoptosis of glioma after IRE. The sequencing results were confirmed by qPCR and Western blot. We also found that the transcription changes also implicated three other forms of RCD: autophagy, necroptosis, and immunogenic cell death (ICD), in addition to apoptosis. These together imply that IRE possibly mediates apoptosis by the AP-1-Bim pathway, causes mixed RCD simultaneously, and has the potential to aid in the generation of a systemic antitumor immune response. Full article
(This article belongs to the Special Issue Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags, to Rodent Models)
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16 pages, 3467 KiB  
Article
Multiparametric Longitudinal Profiling of RCAS-tva-Induced PDGFB-Driven Experimental Glioma
by Hannes Becker, Salvador Castaneda-Vega, Kristin Patzwaldt, Justyna M. Przystal, Bianca Walter, Filippo C. Michelotti, Denis Canjuga, Marcos Tatagiba, Bernd Pichler, Susanne C. Beck, Eric C. Holland, Christian la Fougère and Ghazaleh Tabatabai
Brain Sci. 2022, 12(11), 1426; https://doi.org/10.3390/brainsci12111426 - 24 Oct 2022
Cited by 1 | Viewed by 2384
Abstract
Glioblastomas are incurable primary brain tumors harboring a heterogeneous landscape of genetic and metabolic alterations. Longitudinal imaging by MRI and [18F]FET-PET measurements enable us to visualize the features of evolving tumors in a dynamic manner. Yet, close-meshed longitudinal imaging time points [...] Read more.
Glioblastomas are incurable primary brain tumors harboring a heterogeneous landscape of genetic and metabolic alterations. Longitudinal imaging by MRI and [18F]FET-PET measurements enable us to visualize the features of evolving tumors in a dynamic manner. Yet, close-meshed longitudinal imaging time points for characterizing temporal and spatial metabolic alterations during tumor evolution in patients is not feasible because patients usually present with already established tumors. The replication-competent avian sarcoma-leukosis virus (RCAS)/tumor virus receptor-A (tva) system is a powerful preclinical glioma model offering a high grade of spatial and temporal control of somatic gene delivery in vivo. Consequently, here, we aimed at using MRI and [18F]FET-PET to identify typical neuroimaging characteristics of the platelet-derived growth factor B (PDGFB)-driven glioma model using the RCAS-tva system. Our study showed that this preclinical glioma model displays MRI and [18F]FET-PET features that highly resemble the corresponding established human disease, emphasizing the high translational relevance of this experimental model. Furthermore, our investigations unravel exponential growth dynamics and a model-specific tumor microenvironment, as assessed by histology and immunochemistry. Taken together, our study provides further insights into this preclinical model and advocates for the imaging-stratified design of preclinical therapeutic interventions. Full article
(This article belongs to the Special Issue Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags, to Rodent Models)
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16 pages, 3825 KiB  
Article
A Novel Necroptosis-Related Prognostic Signature of Glioblastoma Based on Transcriptomics Analysis and Single Cell Sequencing Analysis
by Yiwen Wu, Yi Huang, Chenhui Zhou, Haifeng Wang, Zhepei Wang, Jiawei Wu, Sheng Nie, Xinpeng Deng, Jie Sun and Xiang Gao
Brain Sci. 2022, 12(8), 988; https://doi.org/10.3390/brainsci12080988 - 26 Jul 2022
Cited by 1 | Viewed by 2595
Abstract
Background: Glioblastoma (GBM) is the most common and deadly brain tumor. The clinical significance of necroptosis (NCPS) genes in GBM is unclear. The goal of this study is to reveal the potential prognostic NCPS genes associated with GBM, elucidate their functions, and establish [...] Read more.
Background: Glioblastoma (GBM) is the most common and deadly brain tumor. The clinical significance of necroptosis (NCPS) genes in GBM is unclear. The goal of this study is to reveal the potential prognostic NCPS genes associated with GBM, elucidate their functions, and establish an effective prognostic model for GBM patients. Methods: Firstly, the NCPS genes in GBM were identified by single-cell analysis of the GSE182109 dataset in the GEO database and weighted co-expression network analysis (WGCNA) of The Cancer Genome Atlas (TCGA) data. Three machine learning algorithms (Lasso, SVM-RFE, Boruta) combined with COX regression were used to build prognostic models. The subsequent analysis included survival, immune microenvironments, and mutations. Finally, the clinical significance of NCPS in GBM was explored by constructing nomograms. Results: We constructed a GBM prognostic model composed of NCPS-related genes, including CTSD, AP1S1, YWHAG, and IER3, which were validated to have good performance. According to the above prognostic model, GBM patients in the TCGA and CGGA groups could be divided into two groups according to NCPS, with significant differences in survival analysis between the two groups and a markedly worse prognostic status in the high NCPS group (p < 0.001). In addition, the high NCPS group had higher levels of immune checkpoint-related gene expression, suggesting that they may be more likely to benefit from immunotherapy. Conclusions: Four genes (CTSD, AP1S1, YWHAG, and IER3) were screened through three machine learning algorithms to construct a prognostic model for GBM. These key and novel diagnostic markers may become new targets for diagnosing and treating patients with GBM. Full article
(This article belongs to the Special Issue Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags, to Rodent Models)
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13 pages, 1544 KiB  
Article
PS-NPs Induced Neurotoxic Effects in SHSY-5Y Cells via Autophagy Activation and Mitochondrial Dysfunction
by Qisheng Tang, Tianwen Li, Kezhu Chen, Xiangyang Deng, Quan Zhang, Hailiang Tang, Zhifeng Shi, Tongming Zhu and Jianhong Zhu
Brain Sci. 2022, 12(7), 952; https://doi.org/10.3390/brainsci12070952 - 20 Jul 2022
Cited by 17 | Viewed by 2611
Abstract
Polystyrene nanoparticles (PS-NPs) are organic pollutants that are widely detected in the environment and organisms, posing potential threats to both ecosystems and human health. PS-NPs have been proven to penetrate the blood–brain barrier and increase the incidence of neurodegenerative diseases. However, information relating [...] Read more.
Polystyrene nanoparticles (PS-NPs) are organic pollutants that are widely detected in the environment and organisms, posing potential threats to both ecosystems and human health. PS-NPs have been proven to penetrate the blood–brain barrier and increase the incidence of neurodegenerative diseases. However, information relating to the pathogenic molecular mechanism is still unclear. This study investigated the neurotoxicity and regulatory mechanisms of PS-NPs in human neuroblastoma SHSY-5Y cells. The results show that PS-NPs caused obvious mitochondrial damages, as evidenced by inhibited cell proliferation, increased lactate dehydrogenase release, stimulated oxidative stress responses, elevated Ca2+ level and apoptosis, and reduced mitochondrial membrane potential and adenosine triphosphate levels. The increased release of cytochrome c and the overexpression of apoptosis-related proteins apoptotic protease activating factor-1 (Apaf-1), cysteinyl aspartate specific proteinase-3 (caspase-3), and caspase-9 indicate the activation of the mitochondrial apoptosis pathway. In addition, the upregulation of autophagy markers light chain 3-II (LC3-II), Beclin-1, and autophagy-related protein (Atg) 5/12/16L suggests that PS-NPs could promote autophagy in SHSY-5Y cells. The RNA interference of Beclin-1 confirms the regulatory role of autophagy in PS-NP-induced neurotoxicity. The administration of antioxidant N-acetylcysteine (NAC) significantly attenuated the cytotoxicity and autophagy activation induced by PS-NP exposure. Generally, PS-NPs could induce neurotoxicity in SHSY-5Y cells via autophagy activation and mitochondria dysfunction, which was modulated by mitochondrial oxidative stress. Mitochondrial damages caused by oxidative stress could potentially be involved in the pathological mechanisms for PS-NP-induced neurodegenerative diseases. Full article
(This article belongs to the Special Issue Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags, to Rodent Models)
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13 pages, 4920 KiB  
Article
PTPRN Serves as a Prognostic Biomarker and Correlated with Immune Infiltrates in Low Grade Glioma
by Peng Li, Fanfan Chen, Chen Yao, Kezhou Zhu, Bei Zhang and Zelong Zheng
Brain Sci. 2022, 12(6), 763; https://doi.org/10.3390/brainsci12060763 - 10 Jun 2022
Cited by 2 | Viewed by 2168
Abstract
Background: Glioma is one of the most common malignant tumors of the central nervous system. Immune infiltration of tumor microenvironment was associated with overall survival in low grade glioma (LGG). However, effects of Tyrosine phosphatase receptor type N (PTPRN) on the progress of [...] Read more.
Background: Glioma is one of the most common malignant tumors of the central nervous system. Immune infiltration of tumor microenvironment was associated with overall survival in low grade glioma (LGG). However, effects of Tyrosine phosphatase receptor type N (PTPRN) on the progress of LGG and its correlation with tumor infiltration are unclear. Methods: Here, datasets of LGG were from The Cancer Genome Atlas (TCGA) and normal samples were from GTEx dataset. Gepia website and Human Protein Atlas (HPA) Database were used to analyze the mRNA and protein expression of PTPRN. We evaluated the influence of PTPRN on survival of LGG patients. MethSurv was used to explore the expression and prognostic patterns of single CpG methylation of PTPRN gene in LGG. The correlations between the clinical information and PTPRN expression were analyzed using logistic regression and Multivariate Cox regression. We also explored the correlation between PTPRN expression and cancer immune infiltration by TIMER. Gene set enrichment analysis (GSEA) was formed using TCGA RNA-seq datasets. Results: PTPRN mRNA and protein expression decreased in LGG compared to normal brain tissue in TCGA and HPA database. Kaplan-Meier analysis showed that the high expression level of PTPRN correlated with a good overall survival (OS) of patients with LGG. The Multivariate Cox analysis demonstrated that PTPRN expression and other clinical-pathological factors (age, WHO grade, IDH status, and primary therapy outcome) significantly correlated with OS of LGG patients. The DNA methylation pattern of PTPRN with significant prognostic value were confirmed, including cg00672332, cg06971096, cg01382864, cg03970036, cg10140638, cg16166796, cg03545227, and cg25569248. Interestingly, PTPRN expression level significantly negatively correlated with infiltrating level of B cell, CD4+ T cells, Macrophages, Neutrophils, and DCs in LGG. Finally, GSEA showed that signaling pathways, mainly associated with tumor microenvironment and immune cells, were significantly enriched in PTPRN high expression. Conclusion: PTPRN is a potential biomarker and correlates with tumor immune infiltration in LGG. Full article
(This article belongs to the Special Issue Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags, to Rodent Models)
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15 pages, 5736 KiB  
Article
TRP Family Genes Are Differently Expressed and Correlated with Immune Response in Glioma
by Chaoyou Fang, Houshi Xu, Yibo Liu, Chenkai Huang, Xiaoyu Wang, Zeyu Zhang, Yuanzhi Xu, Ling Yuan, Anke Zhang, Anwen Shao and Meiqing Lou
Brain Sci. 2022, 12(5), 662; https://doi.org/10.3390/brainsci12050662 - 19 May 2022
Cited by 2 | Viewed by 2014
Abstract
(1) Background: glioma is the most prevalent primary tumor of the human central nervous system and accompanies extremely poor prognosis in patients. The transient receptor potential (TRP) channels family consists of six different families, which are closely associated with cancer cell proliferation, differentiation, [...] Read more.
(1) Background: glioma is the most prevalent primary tumor of the human central nervous system and accompanies extremely poor prognosis in patients. The transient receptor potential (TRP) channels family consists of six different families, which are closely associated with cancer cell proliferation, differentiation, migration, and invasion. TRP family genes play an essential role in the development of tumors. Nevertheless, the function of these genes in gliomas is not fully understood. (2) Methods: we analyze the gene expression data of 28 TRP family genes in glioma patients through bioinformatic analysis. (3) Results: the study showed the aberrations of TRP family genes were correlated to prognosis in glioma. Then, we set enrichment analysis and selected 10 hub genes that may play an important role in glioma. Meanwhile, the expression of 10 hub genes was further established according to different grades, survival time, IDH mutation status, and 1p/19q codeletion status. We found that TRPC1, TRPC3, TRPC4, TRPC5, TRPC6, MCOLN1, MCOLN2, and MCOLN3 were significantly correlated to the prognosis in glioma patients. Furthermore, we illustrated that the expression of hub genes was associated with immune activation and immunoregulators (immunoinhibitors, immunostimulators, and MHC molecules) in glioma. (4) Conclusions: we proved that TRP family genes are promising immunotherapeutic targets and potential clinical biomarkers in patients with glioma. Full article
(This article belongs to the Special Issue Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags, to Rodent Models)
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16 pages, 6117 KiB  
Article
Immune Landscape in PTEN-Related Glioma Microenvironment: A Bioinformatic Analysis
by Alice Giotta Lucifero and Sabino Luzzi
Brain Sci. 2022, 12(4), 501; https://doi.org/10.3390/brainsci12040501 - 14 Apr 2022
Cited by 8 | Viewed by 2483
Abstract
Introduction: PTEN gene mutations are frequently found in the genetic landscape of high-grade gliomas since they influence cell proliferation, proangiogenetic pathways, and antitumoral immune response. The present bioinformatics analysis explores the PTEN gene expression profile in HGGs as a prognostic factor for survival, [...] Read more.
Introduction: PTEN gene mutations are frequently found in the genetic landscape of high-grade gliomas since they influence cell proliferation, proangiogenetic pathways, and antitumoral immune response. The present bioinformatics analysis explores the PTEN gene expression profile in HGGs as a prognostic factor for survival, especially focusing on the related immune microenvironment. The effects of PTEN mutation on the susceptibility to conventional chemotherapy were also investigated. Methods: Clinical and genetic data of GBMs and normal tissue samples were acquired from The Cancer Genome Atlas (TCGA)-GBM and Genotype-Tissue Expression (GTEx) online databases, respectively. The genetic differential expressions were analyzed in both groups via the one-way ANOVA test. Kaplan–Meier survival curves were applied to estimate the overall survival (OS) and disease-free survival (DFS). The Genomics of Drug Sensitivity in Cancer platform was chosen to assess the response of PTEN-mutated GBMs to temozolomide (TMZ). p < 0.05 was fixed as statistically significant. On Tumor Immune Estimation Resource and Gene Expression Profiling Interactive Analysis databases, the linkage between immune cell recruitment and PTEN status was assessed through Spearman’s correlation analysis. Results: PTEN was found mutated in 22.2% of the 617 TCGA-GBMs patients, with a higher log2-transcriptome per million reads compared to the GTEx group (255 samples). Survival curves revealed a worse OS and DFS, albeit not significant, for the high-PTEN profile GBMs. Spearman’s analysis of immune cells demonstrated a strong positive correlation between the PTEN status and infiltration of Treg (ρ = 0.179) and M2 macrophages (ρ = 0.303). The half-maximal inhibitor concentration of TMZ was proven to be lower for PTEN-mutated GBMs compared with PTEN wild-types. Conclusions: PTEN gene mutations prevail in GBMs and are strongly related to poor prognosis and least survival. The infiltrating immune lymphocytes Treg and M2 macrophages populate the glioma microenvironment and control the mechanisms of tumor progression, immune escape, and sensitivity to standard chemotherapy. Broader studies are required to confirm these findings and turn them into new therapeutic perspectives. Full article
(This article belongs to the Special Issue Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags, to Rodent Models)
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8 pages, 694 KiB  
Article
Safety and Efficacy of Hypofractionated Stereotactic Radiotherapy with Anlotinib Targeted Therapy for Glioblastoma at the First Recurrence: A Preliminary Report
by Yun Guan, Jing Li, Xiu Gong, Huaguang Zhu, Chao Li, Guanghai Mei, Xiaoxia Liu, Li Pan, Jiazhong Dai, Yang Wang, Enmin Wang, Ying Liu and Xin Wang
Brain Sci. 2022, 12(4), 471; https://doi.org/10.3390/brainsci12040471 - 02 Apr 2022
Cited by 4 | Viewed by 1827
Abstract
(1) Background: Hypofractionated stereotactic radiotherapy (HSRT) and anti-vascular endothelial growth factor (VEGF) antibodies have been reported to have a promising survival benefit in recent studies. Anlotinib is a new oral VEGF receptor inhibitor. This report describes our experience using HSRT and anlotinib for [...] Read more.
(1) Background: Hypofractionated stereotactic radiotherapy (HSRT) and anti-vascular endothelial growth factor (VEGF) antibodies have been reported to have a promising survival benefit in recent studies. Anlotinib is a new oral VEGF receptor inhibitor. This report describes our experience using HSRT and anlotinib for recurrent glioblastoma (rGBM). (2) Methods: Between December 2019 and June 2020, rGBM patients were retrospectively analysed. Anlotinib was prescribed at 12 mg daily during HSRT. Adjuvant anlotinib was administered d1-14 every 3 weeks. The primary endpoint was the objective response rate (ORR). Secondary endpoints included overall survival (OS), progression-free survival (PFS) after salvage treatment, and toxicity. (3) Results: Five patients were enrolled. The prescribed dose was 25.0 Gy in 5 fractions. The median number of cycles of anlotinib was 21 (14–33). The ORR was 100%. Three (60%) patients had the best outcome of a partial response (PR), and 2 (40%) achieved a complete response (CR). One patient died of tumour progression at the last follow-up. Two patients had grade 2 hand-foot syndrome. (4) Conclusions: Salvage HSRT combined with anlotinib showed a favourable outcome and acceptable toxicity for rGBM. A prospective phase II study (NCT04197492) is ongoing to further investigate the regimen. Full article
(This article belongs to the Special Issue Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags, to Rodent Models)
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17 pages, 3466 KiB  
Article
Comparison of Immune Checkpoint Molecules PD-1 and PD-L1 in Paired Primary and Recurrent Glioma: Increasing Trend When Recurrence
by Wei Yu, Anwen Shao, Xiaoqiu Ren, Zexin Chen, Jinghong Xu and Qichun Wei
Brain Sci. 2022, 12(2), 266; https://doi.org/10.3390/brainsci12020266 - 14 Feb 2022
Cited by 1 | Viewed by 2037
Abstract
Purpose: This study aims to investigate PD-1/PD-L1 expression patterns in paired primary and recurrent gliomas. Methods: From January 2008 to December 2014, 42 patients who underwent surgical resections of primary and recurrent gliomas were retrospectively included. PD-1/PD-L1 protein expression in tumors was [...] Read more.
Purpose: This study aims to investigate PD-1/PD-L1 expression patterns in paired primary and recurrent gliomas. Methods: From January 2008 to December 2014, 42 patients who underwent surgical resections of primary and recurrent gliomas were retrospectively included. PD-1/PD-L1 protein expression in tumors was evaluated through immunohistochemistry. Results: In primary gliomas, PD-1 and PD-L1 expression was evident in 9 (22.0%) and 14 (33.3%) patients. In the paired recurrent glioma, PD-1 and PD-L1 expression was evident in 25 (61.0%) and 31 (74.0%) lesions. Both PD-1 and PD-L1 showed significantly enhanced expression after recurrence (p < 0.005; p < 0.005). For PD-L1 expression in recurrent gliomas, the adjuvant therapy group showed significantly increased expression compared to primary gliomas (p < 0.005). For PD-1- primary gliomas, if the matched recurrent gliomas showed PD-1+, the PFS became worse than the remaining recurrent gliomas PD-1- (12.7 vs. 25.9 months, p = 0.032). Interestingly, for PD-L1- primary gliomas, if the matched recurrent gliomas showed PD-L1+, the OS became better than the remaining recurrent gliomas PD-L1- (33.8 vs. 17.5 months, p < 0.001). Conclusions: In the study, we found the expression of PD-1/PD-L1 increased significantly in recurrent gliomas and the elevated level of PD-L1 was tightly associated with adjuvant treatment, suggesting the potential therapeutic and predictive value of PD-1 and PD-L1 in the treatment of recurrent gliomas. Full article
(This article belongs to the Special Issue Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags, to Rodent Models)
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13 pages, 2142 KiB  
Article
Identification of an IL-4-Related Gene Risk Signature for Malignancy, Prognosis and Immune Phenotype Prediction in Glioma
by Ying Qi, Xinyu Yang, Chunxia Ji, Chao Tang and Liqian Xie
Brain Sci. 2022, 12(2), 181; https://doi.org/10.3390/brainsci12020181 - 29 Jan 2022
Cited by 3 | Viewed by 2009
Abstract
Background: Emerging molecular and genetic biomarkers have been introduced to classify gliomas in the past decades. Here, we introduced a risk signature based on the cellular response to the IL-4 gene set through Least Absolute Shrinkage and Selection Operator (LASSO) regression analysis. Methods: [...] Read more.
Background: Emerging molecular and genetic biomarkers have been introduced to classify gliomas in the past decades. Here, we introduced a risk signature based on the cellular response to the IL-4 gene set through Least Absolute Shrinkage and Selection Operator (LASSO) regression analysis. Methods: In this study, we provide a bioinformatic profiling of our risk signature for the malignancy, prognosis and immune phenotype of glioma. A cohort of 325 patients with whole genome RNA-seq expression data from the Chinese Glioma Genome Atlas (CGGA) dataset was used as the training set, while another cohort of 667 patients from The Cancer Genome Atlas (TCGA) dataset was used as the validating set. The LASSO model identified a 10-gene signature which was considered as the optimal model. Results: The signature was confirmed to be a good predictor of clinical and molecular features involved in the malignancy of gliomas. We also identified that our risk signature could serve as an independently prognostic biomarker in patients with gliomas (p < 0.0001). Correlation analysis showed that our risk signature was strongly correlated with the Tregs, M0 macrophages and NK cells infiltrated in the microenvironment of glioma, which might be a supplement to the existing incomplete innate immune mechanism of glioma phenotypes. Conclusions: Our IL-4-related gene signature was associated with more aggressive and immunosuppressive phenotypes of gliomas. The risk score could predict prognosis independently in glioma, which might provide a new insight for understanding the IL-4 involved mechanism of gliomas. Full article
(This article belongs to the Special Issue Pathogenesis Study of Glioma: From Glioma Stem Cells, Genomic Tags, to Rodent Models)
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