A review of prognostic molecular biomarkers for glioblastoma and their clinical significance for diagnosis and treatment DOI Creative Commons
Андрій Нетлюх, Т. А. Малышева, A.V. Zanevych

et al.

Ukrainian Interventional Neuroradiology and Surgery, Journal Year: 2024, Volume and Issue: 49(3), P. 59 - 71

Published: Oct. 17, 2024

Glioblastoma (GBM) is a WHO grade IV malignant brain tumor with poor prognosis, and it the most common primary in adults. The estimated overall survival rate for patients GBM less than 1.5 years, 5-year of about 5 %. Current treatment standards include maximal (Gross total) resection, which rarely achieved due to diffuse-invasive nature these tumors, radiotherapy concomitant chemotherapy, such as temozolomide. New technologies, including genetic research advanced statistical methods, enhance therapeutic approaches create new opportunities. Certain genes are crucial understanding tumorigenesis each subtype associated specific epigenetic changes. Our goal was conduct an up-to-date review molecular markers, namely isocitrate dehydrogenase 1 2 (IDH1/2), O-6-methylguanine-DNA methyltransferase (MGMT), p53 protein, epidermal growth factor receptor (EGFR), platelet-derived (PDGFR), 1p/19q codeletion, telomerase reverse transcriptase (TERT), circulating cells, microRNAs. Established biomarkers widely used clinical neuro-oncology practice play critical role improving diagnostics, determining predicting responses. roles MGMT IDH1/2 well-established. Many studies indicate better outcomes from surgical radiation treatments mutations genes. We also highlighted potential biomarkers, especially easily accessible blood require thorough future evaluation their prognostic and/or predictive utility settings. However, on other EGFR, PDGFR, alpha-thalassemia mental retardation X-linked syndrome protein (ATRX), TERT, loss heterozygosity chromosome 10, complexes, microRNAs, remains promising. Overall, identifying enables selection effective improves prognosis gliomas.

Language: Английский

The role of acetylation and deacetylation in cancer metabolism DOI Creative Commons
Cuicui Wang, Xiaoxin Ma

Clinical and Translational Medicine, Journal Year: 2025, Volume and Issue: 15(1)

Published: Jan. 1, 2025

Language: Английский

Citations

1
The Role of the Gut Microbiota in Modulating Signaling Pathways and Oxidative Stress in Glioma Therapies DOI Open Access
Aleksandra Krawczyk,

Gabriela Elzbieta Sladowska,

Barbara Strzałka‐Mrozik

et al.

Cancers, Journal Year: 2025, Volume and Issue: 17(5), P. 719 - 719

Published: Feb. 20, 2025

Tumors of the central nervous system (CNS), especially gliomas, pose a significant clinical challenge due to their aggressive nature and limited therapeutic options. Emerging research highlights critical role gut microbiota in regulating CNS health disease. The composition is essential for maintaining homeostasis, as it modulates immune responses, oxidative status, neuroinflammation. microbiota–gut–brain axis, bidirectional communication network, plays pivotal cancer disease treatment, exerting its influence through neural, endocrine, immunological, metabolic pathways. Recent studies suggest that influences solidification tumor microenvironment dysbiosis may promote glioma development by modulating systemic inflammation stress, which contributes tumorigenesis progression. This review interrogates impact on glioma, focusing pathways such NF-κB, MAPK, PI3K/Akt/mTOR, Kynurenine/AhR drive proliferation, evasion, therapy resistance. Furthermore, we explore emerging strategies, including probiotics microbiota-based interventions, show potential these enhancing immunotherapies checkpoint inhibitors. By multifaceted interactions between microbiota, tumors, this microbiota-targeted therapies manipulation complement enhance current treatments.

Language: Английский

Citations

1
Metabolic Reprogramming in Glioblastoma Multiforme: A Review of Pathways and Therapeutic Targets DOI Creative Commons

Ashley Irin Cortes Ballen,

Maryam Amosu,

Surya Ravinder

et al.

Cells, Journal Year: 2024, Volume and Issue: 13(18), P. 1574 - 1574

Published: Sept. 19, 2024

Glioblastoma (GBM) is an aggressive and highly malignant primary brain tumor characterized by rapid growth a poor prognosis for patients. Despite advancements in treatment, the median survival time GBM patients remains low. One of crucial challenges understanding treating GBMs involves its remarkable cellular heterogeneity adaptability. Central to proliferation cells their ability undergo metabolic reprogramming. Metabolic reprogramming process that allows cancer alter metabolism meet increased demands survive often oxygen- nutrient-deficient microenvironment. These changes include Warburg effect, alterations several key pathways including glutamine metabolism, fatty acid synthesis, tricarboxylic (TCA) cycle, uptake utilization glutamine, more. complexity adaptability deeper offers hope developing more effective therapeutic interventions against GBMs.

Language: Английский

Citations

6
Targeting metabolic reprogramming in glioblastoma as a new strategy to overcome therapy resistance DOI Creative Commons
Simona D’Aprile, Simona Denaro,

Anna Gervasi

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2025, Volume and Issue: 13

Published: Feb. 26, 2025

Glioblastoma (GBM) is one of the deadliest tumors due to its high aggressiveness and resistance standard therapies, resulting in a dismal prognosis. This lethal tumor carries out metabolic reprogramming order modulate specific pathways, providing metabolites that promote GBM cells proliferation limit efficacy treatments. Indeed, remodels glucose metabolism undergoes Warburg effect, fuelling glycolysis even when oxygen available. Moreover, recent evidence revealed rewiring nucleotide, lipid iron metabolism, not only an increased growth, but also radio- chemo-resistance. Thus, while on hand advantage for GBM, other it may represent exploitable target hamper progression. Lately, number studies focused drugs targeting uncover their effects therapy resistance, demonstrating some these are effective, combination with conventional treatments, sensitizing radiotherapy chemotherapy. However, heterogeneity could lead plethora alterations among subtypes, hence treatment might be effective proneural mesenchymal ones, which more aggressive resistant approaches. review explores key mechanisms involvement highlighting how acts as double-edged sword taking into account pathways seem offer promising options GBM.

Language: Английский

Citations

0
RBMS1 promotes the proliferation of glioma cells via regulation of the c-Myc–SSH1 axis DOI Creative Commons
Shen Gu, Weining Wu, Chao Wu

et al.

Biochemical and Biophysical Research Communications, Journal Year: 2025, Volume and Issue: unknown, P. 151586 - 151586

Published: March 1, 2025

Language: Английский

Citations

0
Improving HEK293-based AAV-production using GSMMs, and a multi-omics approach DOI Creative Commons
Leopold Zehetner, Diana Széliová, Barbara Kraus

et al.

Metabolic Engineering, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

Citations

0
Metabolic reprogramming in glioblastoma: a rare case of recurrence to scalp metastasis DOI Creative Commons
Amir Barzegar Behrooz,

Hamid Latifi-Navid,

Narges Zolfaghari

et al.

BJC Reports, Journal Year: 2025, Volume and Issue: 3(1)

Published: April 24, 2025

Glioblastoma (GB), an aggressive brain malignancy with a poor prognosis of 1.5-2 years, rarely exhibits extracranial metastasis (ECM). However, metabolic reprogramming has emerged as key driver GB progression and invasiveness. This study presents rare case recurrent scalp metastasis, exploring how shifts enable cells to evade treatment adapt hostile environments, offering insights for developing innovative therapies. Tandem mass spectrometry (MS/MS) was employed analyze amino acid profiles in both the metastatic stages GB. Systems biology approaches were used uncover genetic alterations associated from recurrence metastasis. Our analysis revealed distinct utilization patterns patient molecular phenotype wild-type IDH-1&2, TERT mutation, non-mutated BRAF EGFR, non-methylated MGMT. During significant differences observed between blood cerebrospinal fluid (CSF) samples. Additionally, protein-protein interaction (PPI) identified genomic drivers potentially responsible transition Beyond established risk factors such craniotomy, biopsies, ventricular shunting, radiation therapy, our findings suggest that plays crucial role Targeting these could provide new avenues managing preventing GB, making this important focus future research.

Language: Английский

Citations

0
Targeting oxidative stress-mediated regulated cell death as a vulnerability in cancer DOI Creative Commons

Danyao Chen,

Ziyu Guo, Lei Yao

et al.

Redox Biology, Journal Year: 2025, Volume and Issue: unknown, P. 103686 - 103686

Published: May 1, 2025

Reactive oxygen species (ROS), regulators of cellular behaviors ranging from signaling to cell death, have complex production and control mechanisms maintain a dynamic redox balance under physiological conditions. Redox imbalance is frequently observed in tumor cells, where ROS within tolerable limits promote oncogenic transformation, while excessive induce range regulated death (RCD). As such, targeting ROS-mediated as vulnerability cancer. However, the precise regulatory networks governing cancer their therapeutic applications remain inadequately characterized. In this Review, we first provide comprehensive overview underlying highlighting balance. Next, discuss paradoxical nature system can growth or suppress it, depending on context. We also systematically explored role pathways revealed cross-linking cells. Following this, focus intricate regulation RCD its current therapy. further summarize potential ROS-induced RCD-based therapies, particularly those mediated by drugs specific mechanisms. Finally, address measurement oxidative damage research, discussing existing challenges future prospects hope review will offer promise for clinical application stress-mediated

Language: Английский

Citations

0
Unlocking the Gateway: The Spatio-Temporal Dynamics of the p53 Family Driven by the Nuclear Pores and Its Implication for the Therapeutic Approach in Cancer DOI Open Access
Dini Kurnia Ikliptikawati,

Kei Makiyama,

Masaharu Hazawa

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(13), P. 7465 - 7465

Published: July 7, 2024

The p53 family remains a captivating focus of an extensive number current studies. Accumulating evidence indicates that abnormalities rank among the most prevalent in cancer. Given numerous existing studies, which mostly on mutations, expression profiles, and functional perturbations exhibited by members across diverse malignancies, this review will concentrate more less explored facets regarding activation stabilization nuclear pore complex (NPC) cancer, drawing several integrates broad spectrum signals is subject to regulatory mechanisms enact necessary cellular response. It widely acknowledged each stage regulation, from synthesis degradation, significantly influences its functionality executing specific tasks. Over recent decades, large body data has established closely linked with protein stabilization, involve intricate interactions various components. These often transcend canonical pathways. This new knowledge expanded regulation genes themselves epigenomics proteomics, whereby interaction partners increase complexity compared earlier paradigms. Specifically, studies have recently shown involvement NPC such interactions, underscoring further regulation. Furthermore, we also discuss therapeutic strategies based developments field combination targeted therapies.

Language: Английский

Citations

2
ZIPK collaborates with STAT5A in p53-mediated ROS accumulation in hyperglycemia-induced vascular injury DOI Creative Commons

Qichao Wu,

Tingting Xie,

Chang Fu

et al.

Acta Biochimica et Biophysica Sinica, Journal Year: 2024, Volume and Issue: unknown

Published: July 1, 2024

In this study we investigate the role of Zipper-interacting protein kinase (ZIPK) in high glucose-induced vascular injury, focusing on its interaction with STAT5A and effects p53 inducible nitric oxide synthase (NOS2) expression. Human umbilical vein endothelial cells (HUVECs) are cultured under normal (5 mM) (25 glucose conditions. Protein gene expression levels assessed by western blot analysis qPCR respectively, while ROS measured via flow cytometry. ZIPK is manipulated using overexpression plasmids, siRNAs, shRNAs. The inhibitor TC-DAPK6 evaluated a diabetic rat model. Our results show that significantly upregulates ZIPK, STAT5A, p53, NOS2 expressions HUVECs, thus increasing oxidative stress. Silencing STAT5A reduces reactive oxygen species (ROS) accumulation. essential for accumulation, silencing ZIPK reverses these effects. Overexpression combined attenuates alterations expression, thereby preventing cell damage. Coimmunoprecipitation reveals direct between nucleus high-glucose condition. In rats, treatment decreases expressions. findings suggest plays critical injury STAT5A-mediated pathways, proposing potential therapeutic target complications.

Language: Английский

Citations

2