ReviewCellular and molecular life sciences : CMLS2018
Signaling pathways and mesenchymal transition in pediatric high-grade glioma.
Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 61 citations in OpenAlex.
- Engineered Microvascular Model of the Blood-Brain-Tumor Barrier Reveals Endothelial Remodeling in Diffuse Midline Glioma.Advanced healthcare materials · 2026Article
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- Extracellular Vesicles from Plasma of Patients with Glioblastoma Promote Invasion of Glioblastoma Cells Even After Tumor Resection.Biomedicines · 2024Article
- Diffuse midline glioma invasion and metastasis rely on cell-autonomous signaling.Neuro-oncology · 2024Article
- Ferroptosis and EMT: key targets for combating cancer progression and therapy resistance.Cellular and molecular life sciences : CMLS · 2023Review
- The Critical Role of RNA mCellular and molecular neurobiology · 2023Review
- Radiotherapy and radio-sensitization in H3CNS neuroscience & therapeutics · 2023Review
- Cyclin-dependent kinase subunit2 (CKS2) promotes malignant phenotypes and epithelial-mesenchymal transition-like process in glioma by activating TGFβ/SMAD signaling.Cancer medicine · 2023Article
- Single-Cell Analysis of Unidirectional Migration of Glioblastoma Cells Using a Fiber-Based Scaffold.ACS applied bio materials · 2023Article
- AURKA and PLK1 inhibition selectively and synergistically block cell cycle progression in diffuse midline glioma.iScience · 2022Article
- Diffuse Intrinsic Pontine Glioma: Molecular Landscape, Evolving Treatment Strategies and Emerging Clinical Trials.Journal of personalized medicine · 2022Review
- TMCO1 expression promotes cell proliferation and induces epithelial-mesenchymal transformation in human gliomas.Medical oncology (Northwood, London, England) · 2022Article
- Deploying Kinase Inhibitors to Study Pediatric Gliomas.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Global research trends and hotspots on glioma stem cells.Frontiers in oncology · 2022Article
- Review
- Development and pre-clinical testing of a novel hypoxia-activated KDAC inhibitor.Cell chemical biology · 2021Article
- Blocking hsa_circ_0006168 suppresses cell proliferation and motility of human glioblastoma cells by regulating hsa_circ_0006168/miR-628-5p/IGF1R ceRNA axis.Cell cycle (Georgetown, Tex.) · 2021Article
- A pilot radiogenomic study of DIPG reveals distinct subgroups with unique clinical trajectories and therapeutic targets.Acta neuropathologica communications · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pediatric high-grade gliomas (pHGG), including diffuse intrinsic pontine gliomas (DIPG), are the most lethal types of cancer in children. In recent years, it has become evident that these tumors are driven by epigenetic events, mainly mutations involving genes encoding Histone 3, setting them apart from their adult counterparts. These tumors are exceptionally resistant to chemotherapy and respond only temporarily to radiotherapy. Moreover, their delicate location and diffuse growth pattern make complete surgical resection impossible. In many other forms of cancer, chemo- and radioresistance, in combination with a diffuse, invasive phenotype, are associated with a transcriptional program termed the epithelial-to-mesenchymal transition (EMT). Activation of this program allows cancer cells to survive individually, invade surrounding tissues and metastasize. It also enables them to survive exposure to cytotoxic therapy, including chemotherapeutic drugs and radiation. We here suggest that EMT plays an important, yet poorly understood role in the biology and therapy resistance of pHGG and DIPG. This review summarizes the current knowledge on the major signal transduction pathways and transcription factors involved in the epithelial-to-mesenchymal transition in cancer in general and in pediatric HGG and DIPG in particular. Despite the fact that the mesenchymal transition has not yet been specifically studied in pHGG and DIPG, activation of pathways and high levels of transcription factors involved in EMT have been described. We conclude that the mesenchymal transition is likely to be an important element of the biology of pHGG and DIPG and warrants further investigation for the development of novel therapeutics.
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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.