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New Strategies in Diagnosis and Treatments for Brain Tumors

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

Deadline for manuscript submissions: closed (20 June 2022) | Viewed by 32151

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Special Issue Editor

Prof. Dr. Sven Rainer Kantelhardt

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Guest Editor

Department of Neurosurgery, University Medical Center, Johannes-Gutenberg-University Mainz, 55124 Mainz, Germany
Interests: glioma; brain tumor; neurosurgery; intraoperative imaging; intraoperative robotics and navigation; personal medicine (for brain tumors)

Special Issue Information

Dear Colleagues,

Brain tumors still rank among the most threatening diseases worldwide. The life expectancy of neuro-oncology patients has been rather stagnating in recent years. The field of scientific neuro-oncology is however developing rapidly. New treatment strategies, including non-invasive diagnostics using digital analysis-tools and artificial intelligence, enhanced surgical resection techniques and intraoperative imaging, as well as approaches focusing on tumor heterogeneity and molecular characteristics for the specific selection of radio- and chemo-therapies, are about to enter the clinical practice. These approaches carry the potential of turning the scales towards a more individual, personalized treatment and finally improve the prognosis of patients suffering from brain tumors. This Special Issue is dedicated to novel concepts and emerging technologies. It will provide an overview of the state of the art and current trends in diagnostics and therapeutic approaches of brain tumors.

Prof. Dr. Sven Rainer Kantelhardt
Guest Editor

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Keywords

glioma
brain tumor
molecular guided therapy
personal medicine
radiomics
digital analysis
artificial intelligence
intraoperative imaging
surgical resection

Published Papers (14 papers)

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Editorial

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5 pages, 201 KiB

Open AccessEditorial

New Strategies in Diagnosis and Treatments for Brain Tumors

by Sven Kantelhardt

Cancers 2023, 15(11), 2879; https://doi.org/10.3390/cancers15112879 - 23 May 2023

Viewed by 1072

Abstract

In general, cancer is one of the most frequent causes of death [...] Full article

(This article belongs to the Special Issue New Strategies in Diagnosis and Treatments for Brain Tumors)

Research

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12 pages, 4429 KiB

Open AccessArticle

Orthotopic Glioblastoma Models for Evaluation of the Clinical Target Volume Concept

by Rebecca Bütof, Pia Hönscheid, Rozina Aktar, Christian Sperling, Falk Tillner, Treewut Rassamegevanon, Antje Dietrich, Matthias Meinhardt, Daniela Aust, Mechthild Krause and Esther G. C. Troost

Cancers 2022, 14(19), 4559; https://doi.org/10.3390/cancers14194559 - 20 Sep 2022

Cited by 3 | Viewed by 1416

Abstract

In times of high-precision radiotherapy, the accurate and precise definition of the primary tumor localization and its microscopic spread is of enormous importance. In glioblastoma, the microscopic tumor extension is uncertain and, therefore, population-based margins for Clinical Target Volume (CTV) definition are clinically used, which could either be too small—leading to increased risk of loco-regional recurrences—or too large, thus, enhancing the probability of normal tissue toxicity. Therefore, the aim of this project is to investigate an individualized definition of the CTV in preclinical glioblastoma models based on specific biological tumor characteristics. The microscopic tumor extensions of two different orthotopic brain tumor models (U87MG_mCherry; G7_mCherry) were evaluated before and during fractionated radiotherapy and correlated with corresponding histological data. Representative tumor slices were analyzed using Matrix-Assisted Laser Desorption/Ionization (MALDI) and stained for putative stem-like cell markers as well as invasion markers. The edges of the tumor are clearly shown by the MALDI segmentation via unsupervised clustering of mass spectra and are consistent with the histologically defined border in H&E staining in both models. MALDI component analysis identified specific peaks as potential markers for normal brain tissue (e.g., 1339 m/z), whereas other peaks demarcated the tumors very well (e.g., 1562 m/z for U87MG_mCherry) irrespective of treatment. MMP14 staining revealed only a few positive cells, mainly in the tumor border, which could reflect the invasive front in both models. The results of this study indicate that MALDI information correlates with microscopic tumor spread in glioblastoma models. Therefore, an individualized CTV definition based on biological tumor characteristics seems possible, whereby the visualization of tumor volume and protein heterogeneity can be potentially used to define radiotherapy-sensitive and resistant areas. Full article

(This article belongs to the Special Issue New Strategies in Diagnosis and Treatments for Brain Tumors)

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21 pages, 5897 KiB

Open AccessArticle

Overexpression of NNMT in Glioma Aggravates Tumor Cell Progression: An Emerging Therapeutic Target

by Wei Sun, Yongxiang Zou, Zheng Cai, Jinxiang Huang, Xinjie Hong, Qiang Liang and Weilin Jin

Cancers 2022, 14(14), 3538; https://doi.org/10.3390/cancers14143538 - 21 Jul 2022

Cited by 7 | Viewed by 2425

Abstract

Purpose: Increasing evidence has revealed that nicotinamide N-methyltransferase (NNMT) is a key factor influencing the prognosis of tumors. The present study aimed to investigate the role of NNMT in glioma and to elucidate the associated functional mechanisms. Methods: Clinical samples were analyzed by immunohistochemical staining and Western blotting to evaluate NNMT expression in glioma and normal brain tissues. The correlation between NNMT expression and glioma was analyzed using the Cancer Genome Atlas (TCGA) database. Additionally, NNMT was knocked down in two types of glioma cells, U87 and U251, to evaluate the invasive ability of these cells. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to validate NNMT knockdown in the cells. Furthermore, ELISA was used to determine the balance between nicotinamide adenine dinucleotide and nicotinamide adenine dinucleotide hydrogen (NAD/NADH ratio), which verified the altered methylation patterns in the cells. The glioma xenograft mouse models were used to verify the regulatory role of NNMT, GAP43, and SIRT1. Results: Analysis based on our clinical glioma samples and TCGA database revealed that overexpression of NNMT was associated with poor prognosis of patients. Knockdown of NNMT reduced the invasive ability of glioma cells, and downregulation of its downstream protein GAP43 occurred due to altered cellular methylation caused by NNMT overexpression. Gene Set Enrichment Analysis confirmed that NNMT modulated the NAD-related signaling pathway and showed a negative association between NNMT and SIRT1. Moreover, the regulatory roles of NNMT, GAP43, and SIRT1 were confirmed in glioma xenograft mouse models. Conclusion: Overexpression of NNMT causes abnormal DNA methylation through regulation of the NAD/NADH ratio, which in turn leads to the downregulation of GAP43 and SIRT1, eventually altering the biological behavior of tumor cells. Full article

(This article belongs to the Special Issue New Strategies in Diagnosis and Treatments for Brain Tumors)

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16 pages, 2406 KiB

Open AccessArticle

Detection of IDH1 Mutations in Plasma Using BEAMing Technology in Patients with Gliomas

by Santiago Cabezas-Camarero, Vanesa García-Barberán, Rebeca Pérez-Alfayate, Isabel Casado-Fariñas, Hillary Sloane, Frederick S. Jones and Pedro Pérez-Segura

Cancers 2022, 14(12), 2891; https://doi.org/10.3390/cancers14122891 - 11 Jun 2022

Cited by 7 | Viewed by 1941

Abstract

Molecular testing using blood-based liquid biopsy approaches has not been widely investigated in patients with glioma. A prospective single-center study enrolled patients with gliomas ranging from grade II to IV. Peripheral blood (PB) was drawn at different timepoints for circulating tumour DNA (ctDNA) monitoring. Next-generation sequencing (NGS) was used for the study of isocitrate dehydrogenase 1 (IDH1) mutations in the primary tumor. Beads, Emulsion, Amplification and Magnetics (BEAMing) was used for the study of IDH1 mutations in plasma and correlated with the NGS results in the tumor. Between February 2017 and July 2018, ten patients were enrolled, six with IDH1-mutant and four with IDH1 wild-type gliomas. Among the six IDH-mutant gliomas, three had the same IDH1 mutation detected in plasma (50%), and the IDH1-positive ctDNA result was obtained in patients either at diagnosis (no treatment) or during progressive disease. While the false-negative rate reached 86% (18/21), 15 out of the 18 (83%) plasma-negative results were from PB collected from the six IDH-mutant patients at times at which there was no accompanying evidence of tumor progression, as assessed by MRI. There were no false-positive cases in plasma collected from patients with IDH1 wild-type tumors. BEAMing detected IDH1 mutations in the plasma of patients with gliomas, with a modest clinical sensitivity (true positivity rate) but with 100% clinical specificity, with complete agreement between the mutant loci detected in tumor and plasma. Larger prospective studies should be conducted to expand on these findings, and further explore the clearance of mutations in PB from IDH1-positive patients in response to therapy. Full article

(This article belongs to the Special Issue New Strategies in Diagnosis and Treatments for Brain Tumors)

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18 pages, 3963 KiB

Open AccessArticle

Prognostic Neurotransmitter Receptors Genes Are Associated with Immune Response, Inflammation and Cancer Hallmarks in Brain Tumors

by Yuri Belotti, Serenella Tolomeo, Rongjun Yu, Wan-Teck Lim and Chwee Teck Lim

Cancers 2022, 14(10), 2544; https://doi.org/10.3390/cancers14102544 - 21 May 2022

Cited by 11 | Viewed by 3022

Abstract

Glioblastoma multiforme (GBM) is one of the most aggressive forms of cancer. Neurotransmitters (NTs) have recently been linked with the uncontrolled proliferation of cancer cells, but the role of NTs in the progression of human gliomas is still largely unexplored. Here, we investigate the genes encoding for neurotransmitter receptors (NTRs) by analyzing public transcriptomic data from GBM and LGG (low-grade glioma) samples. Our results showed that 50 out of the 98 tested NTR genes were dysregulated in brain cancer tissue. Next, we identified and validated NTR-associated prognostic gene signatures for both LGG and GBM. A subset of 10 NTR genes (DRD1, HTR1E, HTR3B, GABRA1, GABRA4, GABRB2, GABRG2, GRIN1, GRM7, and ADRA1B) predicted a positive prognosis in LGG and a negative prognosis in GBM. These genes were progressively downregulated across glioma grades and exhibited a strong negative correlation with genes associated with immune response, inflammasomes, and established cancer hallmarks genes in lower grade gliomas, suggesting a putative role in inhibiting cancer progression. This study might have implications for the development of novel therapeutics and preventive strategies that target regulatory networks associated with the link between the autonomic nervous system, cancer cells, and the tumor microenvironment. Full article

(This article belongs to the Special Issue New Strategies in Diagnosis and Treatments for Brain Tumors)

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13 pages, 1511 KiB

Open AccessArticle

Valganciclovir as Add-on to Second-Line Therapy in Patients with Recurrent Glioblastoma

by Mattia Russel Pantalone, Afsar Rahbar, Cecilia Söderberg-Naucler and Giuseppe Stragliotto

Cancers 2022, 14(8), 1958; https://doi.org/10.3390/cancers14081958 - 13 Apr 2022

Cited by 12 | Viewed by 2355

Abstract

Glioblastoma invariably recurs despite aggressive and multimodal first-line treatment and no standardized second-line therapy exists. We previously reported that treatment with the antiviral drug valganciclovir as an add-on to standard therapy significantly prolonged overall survival in 102 patients with newly diagnosed glioblastoma compared to contemporary controls. Here we present the results of retrospective survival analyses including patients with glioblastoma that initiated valganciclovir therapy after recurrence. Twenty-nine patients with recurrent glioblastoma received valganciclovir as an add-on to second-line therapy at Karolinska University Hospital. Contemporary controls were 109 patients with glioblastoma who received similar second-line therapy at our institution. We retrospectively analyzed survival data of these patients. Patients with recurrent glioblastoma who received valganciclovir had longer median overall survival after recurrence than controls (12.1 vs. 7.4 months, respectively, p = 0.0028). The drug was well tolerated. Both patients who underwent re-operation and patients that were not re-operated after recurrence benefitted significantly from valganciclovir therapy. Valganciclovir prolonged survival after recurrence both in patients with an unmethylated and methylated MGMT promoter gene. Valganciclovir was safe to use and prolonged median survival after recurrence for patients with recurrent glioblastoma, re-operated or not after recurrence, and with methylated or unmethylated MGMT promoter gene. Full article

(This article belongs to the Special Issue New Strategies in Diagnosis and Treatments for Brain Tumors)

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16 pages, 9312 KiB

Open AccessArticle

NOX2-Induced High Glycolytic Activity Contributes to the Gain of COL5A1-Mediated Mesenchymal Phenotype in GBM

by Youngjoon Park, Minwoo Park, Junhyung Kim, Juwon Ahn, Jeongmin Sim, Ji-In Bang, Jinhyung Heo, Hyejeong Choi, Kyunggi Cho, Mihye Lee, Jong-Seok Moon and Jaejoon Lim

Cancers 2022, 14(3), 516; https://doi.org/10.3390/cancers14030516 - 20 Jan 2022

Cited by 7 | Viewed by 2124

Abstract

The alteration of the cellular metabolism is a hallmark of glioma. The high glycolytic phenotype is a critical factor in the pathogenesis of high-grade glioma, including glioblastoma multiforme (GBM). GBM has been stratified into three subtypes as the proneural, mesenchymal, and classical subtypes. High glycolytic activity was found in mesenchymal GBM relative to proneural GBM. NADPH oxidase 2 (NOX2) has been linked to cellular metabolism and epithelial-mesenchymal transition (EMT) in tumors. The role of NOX2 in the regulation of the high glycolytic phenotype and the gain of the mesenchymal subtype in glioma remain unclear. Here, our results show that the levels of NOX2 were elevated in patients with GBM. NOX2 induces hexokinase 2 (HK2)-dependent high glycolytic activity in U87MG glioma cells. High levels of NOX2 are correlated with high levels of HK2 and glucose uptake in patients with GBM relative to benign glioma. Moreover, NOX2 increases the expression of mesenchymal-subtype-related genes, including COL5A1 and FN1 in U87MG glioma cells. High levels of NOX2 are correlated with high levels of COL5A1 and the accumulation of extracellular matrix (ECM) in patients with GBM relative to benign glioma. Furthermore, high levels of HK2 are correlated with high levels of COL5A1 in patients with GBM relative to benign glioma. Our results suggest that NOX2-induced high glycolytic activity contributes to the gain of the COL5A1-mediated mesenchymal phenotype in GBM. Full article

(This article belongs to the Special Issue New Strategies in Diagnosis and Treatments for Brain Tumors)

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19 pages, 3784 KiB

Open AccessArticle

GSK-3 Inhibition Is Cytotoxic in Glioma Stem Cells through Centrosome Destabilization and Enhances the Effect of Radiotherapy in Orthotopic Models

by Anke Brüning-Richardson, Gary C. Shaw, Daniel Tams, Tim Brend, Hitesh Sanganee, Simon T. Barry, Gregory Hamm, Richard J. A. Goodwin, John G. Swales, Henry King, Lynette Steele, Ruth Morton, Anastasia Widyadari, Thomas A. Ward, Filomena Esteves, Marjorie Boissinot, Georgia Mavria, Alastair Droop, Sean E. Lawler and Susan C. Short

Cancers 2021, 13(23), 5939; https://doi.org/10.3390/cancers13235939 - 25 Nov 2021

Cited by 3 | Viewed by 2746 | Correction

Abstract

Background: Previous data on glycogen synthase kinase 3 (GSK-3) inhibition in cancer models support a cytotoxic effect with selectivity for tumor cells compared to normal tissue but the effect of these inhibitors in glioma has not been widely studied. Here, we investigate their potential as cytotoxics in glioma. Methods: We assessed the effect of pharmacologic GSK-3 inhibition on established (U87, U251) and patient-derived (GBM1, GBM4) glioblastoma (GBM) cell lines using cytotoxicity assays as well as undertaking a detailed investigation of the effect on cell cycle, mitosis, and centrosome biology. We also assessed drug uptake and efficacy of GSK-3 inhibition alone and in combination with radiation in xenograft models. Results: Using the selective GSK-3 inhibitor AZD2858, we demonstrated single agent cytotoxicity in two patient-derived glioma cell lines (GBM1, GBM4) and two established cell lines (U251 and U87) with IC₅₀ in the low micromolar range promoting centrosome disruption, failed mitosis, and S-phase arrest. Glioma xenografts exposed to AZD2858 also showed growth delay compared to untreated controls. Combined treatment with radiation increased the cytotoxic effect of clinical radiation doses in vitro and in orthotopic glioma xenografts. Conclusions: These data suggest that GSK-3 inhibition promotes cell death in glioma through disrupting centrosome function and promoting mitotic failure and that AZD2858 is an effective adjuvant to radiation at clinical doses. Full article

(This article belongs to the Special Issue New Strategies in Diagnosis and Treatments for Brain Tumors)

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13 pages, 1662 KiB

Open AccessArticle

Identification of an Immunogenic Medulloblastoma-Specific Fusion Involving EPC2 and GULP1

by Claudia Paret, Nadine Lehmann, Hannah Bender, Maximilian Sprang, Clemens J. Sommer, Denis Cana, Larissa Seidmann, Arthur Wingerter, Marie A. Neu, Khalifa El Malki, Francesca Alt, Lea Roth, Federico Marini, Malte Ottenhausen, Martin Glaser, Markus Knuf, Alexandra Russo and Joerg Faber

Cancers 2021, 13(22), 5838; https://doi.org/10.3390/cancers13225838 - 21 Nov 2021

Cited by 3 | Viewed by 2457

Abstract

Medulloblastoma is the most common malignant brain tumor in children. Immunotherapy is yet to demonstrate dramatic results in medulloblastoma, one reason being the low rate of mutations creating new antigens in this entity. In tumors with low mutational burden, gene fusions may represent a source of tumor-specific neoantigens. Here, we reviewed the landscape of fusions in medulloblastoma and analyzed their predicted immunogenicity. Furthermore, we described a new in-frame fusion protein identified by RNA-Seq. The fusion involved two genes on chromosome 2 coding for the enhancer of polycomb homolog 2 (EPC2) and GULP PTB domain containing engulfment adaptor 1 (GULP1) respectively. By qRT-PCR analysis, the fusion was detected in 3 out of 11 medulloblastoma samples, whereby 2 samples were from the same patients obtained at 2 different time points (initial diagnosis and relapse), but not in other pediatric brain tumor entities. Cloning of the full-length sequence indicated that the fusion protein contains the N-terminal enhancer of polycomb-like domain A (EPcA) of EPC2 and the coiled-coil domain of GULP1. In silico analyses predicted binding of the neoantigen-derived peptide to HLA-A*0201. A total of 50% of the fusions described in the literature were also predicted to produce an immunogenic peptide. The EPC2-GULP1 fusion peptide was able to induce a de novo T cell response characterized by interferon gamma release of CD8⁺ cytotoxic T cells in vitro. While the functional relevance of this fusion in medulloblastoma biology remains to be clarified, our data support an immunotherapeutic approach for pediatric medulloblastoma patients carrying the EPC2-GULP1 fusion and other immunogenic fusions. Full article

(This article belongs to the Special Issue New Strategies in Diagnosis and Treatments for Brain Tumors)

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21 pages, 4876 KiB

Open AccessArticle

Algorithmically Deduced FREM2 Molecular Pathway Is a Potent Grade and Survival Biomarker of Human Gliomas

by Marianna Zolotovskaia, Victor Tkachev, Maxim Sorokin, Andrew Garazha, Ella Kim, Sven Rainer Kantelhardt, Sven-Ernö Bikar, Alja Zottel, Neja Šamec, Denis Kuzmin, Bettina Sprang, Alexey Moisseev, Alf Giese, Victor Efimov, Ivana Jovčevska and Anton Buzdin

Cancers 2021, 13(16), 4117; https://doi.org/10.3390/cancers13164117 - 16 Aug 2021

Cited by 9 | Viewed by 2602

Abstract

Gliomas are the most common malignant brain tumors with high mortality rates. Recently we showed that the FREM2 gene has a role in glioblastoma progression. Here we reconstructed the FREM2 molecular pathway using the human interactome model. We assessed the biomarker capacity of FREM2 expression and its pathway as the overall survival (OS) and progression-free survival (PFS) biomarkers. To this end, we used three literature and one experimental RNA sequencing datasets collectively covering 566 glioblastomas (GBM) and 1097 low-grade gliomas (LGG). The activation level of deduced FREM2 pathway showed strong biomarker characteristics and significantly outperformed the FREM2 expression level itself. For all relevant datasets, it could robustly discriminate GBM and LGG (p < 1.63 × 10⁻¹³, AUC > 0.74). High FREM2 pathway activation level was associated with poor OS in LGG (p < 0.001), and low PFS in LGG (p < 0.001) and GBM (p < 0.05). FREM2 pathway activation level was poor prognosis biomarker for OS (p < 0.05) and PFS (p < 0.05) in LGG with IDH mutation, for PFS in LGG with wild type IDH (p < 0.001) and mutant IDH with 1p/19q codeletion(p < 0.05), in GBM with unmethylated MGMT (p < 0.05), and in GBM with wild type IDH (p < 0.05). Thus, we conclude that the activation level of the FREM2 pathway is a potent new-generation diagnostic and prognostic biomarker for multiple molecular subtypes of GBM and LGG. Full article

(This article belongs to the Special Issue New Strategies in Diagnosis and Treatments for Brain Tumors)

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12 pages, 20366 KiB

Open AccessArticle

Magnetic Resonance Relaxometry for Tumor Cell Density Imaging for Glioma: An Exploratory Study via ¹¹C-Methionine PET and Its Validation via Stereotactic Tissue Sampling

by Manabu Kinoshita, Masato Uchikoshi, Souichiro Tateishi, Shohei Miyazaki, Mio Sakai, Tomohiko Ozaki, Katsunori Asai, Yuya Fujita, Takahiro Matsuhashi, Yonehiro Kanemura, Eku Shimosegawa, Jun Hatazawa, Shin-ichi Nakatsuka, Haruhiko Kishima and Katsuyuki Nakanishi

Cancers 2021, 13(16), 4067; https://doi.org/10.3390/cancers13164067 - 12 Aug 2021

Cited by 12 | Viewed by 2151

Abstract

One of the most crucial yet challenging issues for glioma patient care is visualizing non-contrast-enhancing tumor regions. In this study, to test the hypothesis that quantitative magnetic resonance relaxometry reflects glioma tumor load within tissue and that it can be an imaging surrogate for visualizing non-contrast-enhancing tumors, we investigated the correlation between T1- and T2-weighted relaxation times, apparent diffusion coefficient (ADC) on magnetic resonance imaging, and ¹¹C-methionine (MET) on positron emission tomography (PET). Moreover, we compared the T1- and T2-relaxation times and ADC with tumor cell density (TCD) findings obtained via stereotactic image-guided tissue sampling. Regions that presented a T1-relaxation time of >1850 ms but <3200 ms or a T2-relaxation time of >115 ms but <225 ms under 3 T indicated a high MET uptake. In addition, the stereotactic tissue sampling findings confirmed that the T1-relaxation time of 1850–3200 ms significantly indicated a higher TCD (p = 0.04). However, ADC was unable to show a significant correlation with MET uptake or with TCD. Finally, synthetically synthesized tumor load images from the T1- and T2-relaxation maps were able to visualize MET uptake presented on PET. Full article

(This article belongs to the Special Issue New Strategies in Diagnosis and Treatments for Brain Tumors)

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18 pages, 4268 KiB

Open AccessArticle

Large-Scale Transcriptomics-Driven Approach Revealed Overexpression of CRNDE as a Poor Survival Prognosis Biomarker in Glioblastoma

by Maxim Sorokin, Mikhail Raevskiy, Alja Zottel, Neja Šamec, Marija Skoblar Vidmar, Alenka Matjašič, Andrej Zupan, Jernej Mlakar, Maria Suntsova, Denis V. Kuzmin, Anton Buzdin and Ivana Jovčevska

Cancers 2021, 13(14), 3419; https://doi.org/10.3390/cancers13143419 - 8 Jul 2021

Cited by 15 | Viewed by 2414

Abstract

Glioblastoma is the most common and malignant brain malignancy worldwide, with a 10-year survival of only 0.7%. Aggressive multimodal treatment is not enough to increase life expectancy and provide good quality of life for glioblastoma patients. In addition, despite decades of research, there are no established biomarkers for early disease diagnosis and monitoring of patient response to treatment. High throughput sequencing technologies allow for the identification of unique molecules from large clinically annotated datasets. Thus, the aim of our study was to identify significant molecular changes between short- and long-term glioblastoma survivors by transcriptome RNA sequencing profiling, followed by differential pathway-activation-level analysis. We used data from the publicly available repositories The Cancer Genome Atlas (TCGA; number of annotated cases = 135) and Chinese Glioma Genome Atlas (CGGA; number of annotated cases = 218), and experimental clinically annotated glioblastoma tissue samples from the Institute of Pathology, Faculty of Medicine in Ljubljana corresponding to 2–58 months overall survival (n = 16). We found one differential gene for long noncoding RNA CRNDE whose overexpression showed correlation to poor patient OS. Moreover, we identified overlapping sets of congruently regulated differential genes involved in cell growth, division, and migration, structure and dynamics of extracellular matrix, DNA methylation, and regulation through noncoding RNAs. Gene ontology analysis can provide additional information about the function of protein- and nonprotein-coding genes of interest and the processes in which they are involved. In the future, this can shape the design of more targeted therapeutic approaches. Full article

(This article belongs to the Special Issue New Strategies in Diagnosis and Treatments for Brain Tumors)

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Review

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23 pages, 934 KiB

Open AccessReview

Tumor Progression and Treatment-Related Changes: Radiological Diagnosis Challenges for the Evaluation of Post Treated Glioma

by Danlei Qin, Guoqiang Yang, Hui Jing, Yan Tan, Bin Zhao and Hui Zhang

Cancers 2022, 14(15), 3771; https://doi.org/10.3390/cancers14153771 - 3 Aug 2022

Cited by 12 | Viewed by 2593

Abstract

As the most common neuro-epithelial tumors of the central nervous system in adults, gliomas are highly malignant and easy to recurrence, with a dismal prognosis. Imaging studies are indispensable for tracking tumor progression (TP) or treatment-related changes (TRCs). During follow-up, distinguishing TRCs from TP in treated patients with gliomas remains challenging as both share similar clinical symptoms and morphological imaging characteristics (with new and/or increasing enhancing mass lesions) and fulfill criteria for progression. Thus, the early identification of TP and TRCs is of great significance for determining the prognosis and treatment. Histopathological biopsy is currently the gold standard for TP and TRC diagnosis. However, the invasive nature of this technique limits its clinical application. Advanced imaging methods (e.g., diffusion magnetic resonance imaging (MRI), perfusion MRI, magnetic resonance spectroscopy (MRS), positron emission tomography (PET), amide proton transfer (APT) and artificial intelligence (AI)) provide a non-invasive and feasible technical means for identifying of TP and TRCs at an early stage, which have recently become research hotspots. This paper reviews the current research on using the abovementioned advanced imaging methods to identify TP and TRCs of gliomas. First, the review focuses on the pathological changes of the two entities to establish a theoretical basis for imaging identification. Then, it elaborates on the application of different imaging techniques and AI in identifying the two entities. Finally, the current challenges and future prospects of these techniques and methods are discussed. Full article

(This article belongs to the Special Issue New Strategies in Diagnosis and Treatments for Brain Tumors)

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