ReviewGenes & diseases2026
The significance of epithelial-mesenchymal transition (EMT) in the initiation, plasticity, and treatment of glioblastoma.
Review in Genes & diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed.
- Whole-Transcriptome Profiling of Murine GL261 Glioma Reveals Signatures Consistent with Distinct Immune Reprogramming Induced by Oncolytic Virotherapy with VV-GMCSF-Lact and Anti-PD-1 Therapy.International journal of molecular sciences · 2026Article
- Anticancer Properties of Selected Wood-Inhabiting Fungi.Nutrients · 2026Review
- Exploring the Role of Long Non-Coding RNAs in Mediating Cisplatin Resistance in Glioma/Glioblastoma Cells.International journal of molecular sciences · 2026Review
- Therapeutic potential of targeting macrophage polarization in metastatic gastric cancer: a review on core mechanisms and clinical progress.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Pharmacological Ascorbate Restrains Epithelial-Mesenchymal Transition and Invasion in Glioblastoma Cells via Extracellular HInternational journal of molecular sciences · 2026Article
- Hyperglycaemia-Induced Metabolic Stress Promotes EMT-Driven Therapeutic Resistance in Cancer: Evidence of a Deleterious Feed-Forward Cycle.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Epithelial-mesenchymal transition and its role in drug resistance of cervical cancer.Molecular biology reports · 2026Review
- The Role of CRISPR and Its Therapeutic Applications in Glioblastoma.International journal of molecular sciences · 2026Review
- Reconstructing the glioblastoma microenvironment in heterotypic 3D spheroids: a multicellular model to study tumor-stromal crosstalk.Frontiers in bioengineering and biotechnology · 2026Article
- Review
- IL1B-Expressing Exhausted CD4Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial‒mesenchymal transition (EMT) is a dynamic cellular process in which epithelial cells lose their characteristics and acquire mesenchymal traits, leading to enhanced migratory, invasive, and stem-like properties. EMT is a fundamental mechanism in cancer progression, including in glioblastoma (GBM), an aggressive brain tumor known for its poor prognosis and resistance to treatment. In GBM, EMT has been implicated in tumor initiation, plasticity, metastasis, and treatment resistance, making it a key factor in the pathophysiology of the disease. The process of EMT can promote tumor cell migration and invasion, facilitating the spread of cancer cells within the brain. Additionally, EMT is believed to contribute to the maintenance of cancer stem cells, which are thought to be responsible for tumor recurrence and resistance to conventional therapies. Given these multifaceted roles, understanding the molecular pathways and regulatory networks that drive EMT in GBM is critical for identifying new therapeutic targets. This review summarized the roles of EMT in GBM initiation and progression, its impact on cancer cell behavior, and the challenges of targeting EMT in therapy, highlighting potential strategies to overcome resistance and improve treatment outcomes.
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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 Socratic graph.