ArticleOncology letters2016
Epithelial-mesenchymal transition in glioblastoma progression.
Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
181 citing papers in PubMed, 282 citations in OpenAlex.
- G protein-coupled estrogen receptor (GPER) modulates epithelial-mesenchymal transition-like phenotype in human glioblastoma cells.Cell adhesion & migration · 2026Article
- The novel [RSC advances · 2026Article
- The potential role of miR-34a and miR-34c in the regulation of pediatric high-grade glioma 4 aggressiveness.Pediatric research · 2026Article
- Engineered Microvascular Model of the Blood-Brain-Tumor Barrier Reveals Endothelial Remodeling in Diffuse Midline Glioma.Advanced healthcare materials · 2026Article
- Integrated Transcriptomic Analysis Reveals Coordinated Gliovascular Remodeling Across Diffuse Glioma Grades.Cancers · 2026Article
- Pharmacological Ascorbate Restrains Epithelial-Mesenchymal Transition and Invasion in Glioblastoma Cells via Extracellular HInternational journal of molecular sciences · 2026Article
- Tumor Electric Field Therapy Inhibits Epithelial-Mesenchymal Transition, Invasion, and Migration of Glioblastoma by Targeting the c-FOS/CXCL14 Axis.CNS neuroscience & therapeutics · 2026Article
- Primary glioma cell culture: from monolayer to organoids.Protoplasma · 2026Review
- Redundancy in Growth Factor Receptor Signaling in Adult Astrocytoma Resistance to Small-Molecule Tyrosine Kinase Inhibitors.International journal of molecular sciences · 2026Review
- Expression of Epithelial-Mesenchymal Transition-Related Genes in Primary Brain Tumors.Iranian biomedical journal · 2026Article
- Histopathological Assessment of Cellular Heterogeneity in Pediatric Ependymomas.Diagnostics (Basel, Switzerland) · 2025Article
- Troxerutin Potentiated Temozolomide Induced Antitumor Effect in 2D and 3D Glioblastoma Models.Journal of cellular and molecular medicine · 2025Article
- Transposable element dynamics in glioblastoma stem cells: insights from locus-specific quantification.Mobile DNA · 2025Article
- NOD2 Promotes Glioblastoma Progression Through Effects on Epithelial-Mesenchymal Transition and Cancer Stemness.Biomedicines · 2025Article
- Review
- Effects ofMarine drugs · 2025Article
- Current Applications of Single-Cell RNA Sequencing in Glioblastoma: A Scoping Review.Brain sciences · 2025Review
- Pathways underlying selective neuronal vulnerability in Alzheimer's disease: Contrasting the vulnerable locus coeruleus to the resilient substantia nigra.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Integrated proteomics and N-glycoproteomic characterization of glioblastoma multiform revealed N-glycosylation heterogeneities as well as alterations in sialyation and fucosylation.Clinical proteomics · 2025Article
- EIF4A3-Induced Circ_0059914 Promoted Angiogenesis and EMT of Glioma via the miR-1249/VEGFA Pathway.Molecular neurobiology · 2025Article
121 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) is a reversible biological process that occurs in epithelial cells. EMT ultimately leads to the acquisition of a mesenchymal phenotype, characterized by increased cell motility and resistance to genotoxic agents. These processes mostly overlap with the acquirement of stem cell properties in differentiated tumor cells. With regard to gliomas, the clinical picture is heterogeneous, even within the same grades and histological categories of the disease. Furthermore, the areas of invasion and responses to radiochemotherapy are markedly different among cases, and occasionally even in the same patient. Such phenotypic diversity in glioma tissues may be caused by various microenvironmental factors, as well as intrinsic genetic alterations. The current review focuses on the EMT-inducing factors that are present in gliomas; these typically vary from those observed in epithelial cancers, as no basement membrane is present. Furthermore, the most important cell-cell contact factor, E-cadherin, is rarely expressed in gliomas. The microenvironment that induces EMT in gliomas is characterized by hypoxia and the enrichment of myeloid cells following stimulation by transforming growth factor-β. Anti-vascular endothelial growth factor therapy, including the use of bevacizumab, may be a suitable candidate to modulate the glioma microenvironment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.