ArticleNature communications2022
Pro-inflammatory cytokines mediate the epithelial-to-mesenchymal-like transition of pediatric posterior fossa ependymoma.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
26 citing papers in PubMed, 27 citations in OpenAlex.
- A patient-derived organoid platform for predominantly posterior fossa adult ependymoma: histopathologic preservation, culture-associated transcriptomic remodeling, and in vivo tumorigenicity.Journal of neuro-oncology · 2026Article
- Chiral Titanium Dioxide Nanoparticles Induce Breast Cancer Lung Metastasis.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- A highly abundant circular RNA from the RMST locus plays a role in posterior fossa ependymoma pathogenesis.Brain pathology (Zurich, Switzerland) · 2026Article
- A longitudinal single-cell and spatial multiomic atlas of pediatric high-grade glioma.Cell reports. Medicine · 2026Article
- Ependymoma group-specific blood-brain barrier differences uncovered by a multi-omics approach.Scientific reports · 2026Article
- A programmable nanoreactor for photothermal immunotherapy via NIR-II triggered enzyme-catalyzed immunogenic tumor microenvironment remodeling.Asian journal of pharmaceutical sciences · 2026Article
- Molecular and Immune Mechanisms Governing Cancer Metastasis, Including Dormancy, Microenvironmental Niches, and Tumor-Specific Programs.International journal of molecular sciences · 2026Review
- Multimodal-based analysis of single-cell ATAC-seq data enables highly accurate delineation of clinically relevant tumor cell subpopulations.Genome medicine · 2026Article
- Konjac petroleum ether extract inhibits triple-negative breast cancer cell migration and invasion by attenuatingFrontiers in pharmacology · 2026Article
- Regulatory element modules as universal features for single-cell chromatin analysis.bioRxiv : the preprint server for biology · 2025Article
- Histopathological Assessment of Cellular Heterogeneity in Pediatric Ependymomas.Diagnostics (Basel, Switzerland) · 2025Article
- Multimodal analysis of pediatric pilocytic astrocytomas reveals tumor location-associated cellular and transcriptional heterogeneity.Neuro-oncology · 2025Article
- [Role of the TGFZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- EZHIP boosts neuronal-like synaptic gene programs and depresses polyamine metabolism.Acta neuropathologica communications · 2025Article
- Profiling extracellular vesicles from cerebrospinal fluid for classification of intradural spinal tumors.Scientific reports · 2025Article
- Loss of LDOC1 by chromatin compaction in mesenchymal tumor cells is required for PFA1 ependymoma growth.Neuro-oncology · 2025Article
- The Role of Chronic Inflammation in Pediatric Cancer.Cancers · 2025Review
- EpiCHAOS: a metric to quantify epigenomic heterogeneity in single-cell data.Genome biology · 2024Article
- Clustering-independent estimation of cell abundances in bulk tissues using single-cell RNA-seq data.Cell reports methods · 2024Article
- Clustering-independent estimation of cell abundances in bulk tissues using single-cell RNA-seq data.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Pediatric ependymoma is a devastating brain cancer marked by its relapsing pattern and lack of effective chemotherapies. This shortage of treatments is due to limited knowledge about ependymoma tumorigenic mechanisms. By means of single-nucleus chromatin accessibility and gene expression profiling of posterior fossa primary tumors and distal metastases, we reveal key transcription factors and enhancers associated with the differentiation of ependymoma tumor cells into tumor-derived cell lineages and their transition into a mesenchymal-like state. We identify NFκB, AP-1, and MYC as mediators of this transition, and show that the gene expression profiles of tumor cells and infiltrating microglia are consistent with abundant pro-inflammatory signaling between these populations. In line with these results, both TGF-β1 and TNF-α induce the expression of mesenchymal genes on a patient-derived cell model, and TGF-β1 leads to an invasive phenotype. Altogether, these data suggest that tumor gliosis induced by inflammatory cytokines and oxidative stress underlies the mesenchymal phenotype of posterior fossa ependymoma.
Indexed as
Identifiers
What OpenQuestion holds
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.