ReviewNature reviews. Cancer2021
Linking EMT programmes to normal and neoplastic epithelial stem cells.
Review in Nature reviews. Cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 344 papers, 1 of them a synthesis that pooled it.
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
344 citing papers in PubMed, 1 synthesis or guideline pooled it, 527 citations in OpenAlex.
- BioBERT-powered synergy: advanced bibliometric and molecular insights into prostate cancer bone metastasis.Frontiers in immunology · 2025Pooled it
- Trial
- Review
- Zeb1 Is a Determinant of EMT in Human MDA-MB-231 Breast Cancer Cells and M13-MDA231 Tumor Hybrids.International journal of molecular sciences · 2026Article
- MUC1 as a Survival Effector of Radiotherapy-Induced Epithelial Hybrid States in Basal-Like Breast Cancer.International journal of cancer · 2026Article
- Isthmin-2 is a first-trimester predictor of preeclampsia and fetal growth restriction.Nature medicine · 2026Article
- SMARCA4, STK11, and KEAP1 co-inactivation associates with poor prognosis and upregulation of the TGF-β pathway in lung adenocarcinoma.Translational oncology · 2026Article
- Article
- ICAM1high Neutrophils Sculpt Tumor Evolution and Metastasis Through Symbiotic Adhesion and Reverse Migration.Cancer research · 2026Article
- SNAI1 ablation alters integrin-mediated adhesion and endocytic fate.Cell death & disease · 2026Article
- MPND Loss Epigenetically Activates TGFβ/SMAD3 Signaling to Drive Tumor Progression and Metastasis in Non-Small Cell Lung Cancer.Cancer research · 2026Article
- Cancer stem cells are hyper-responsive sensors of the tumour microenvironment and regulate metastasis dynamics through YAP/TAZ.Nature cell biology · 2026Article
- A multi-omics integration of bulk and single-cell transcriptomics identifies and validates a 16-gene epithelial-mesenchymal transition prognostic signature in tongue squamous cell carcinoma.Translational cancer research · 2026Article
- HPV16 E7-Associated SERPINB3 Suppression and MYC-Related Epithelial Plasticity in Head and Neck Squamous Cell Carcinoma.Cancers · 2026Article
- Review
- Multiple distinct metastatic cell states are induced by epithelial-mesenchymal plasticity.bioRxiv : the preprint server for biology · 2026Article
- Cadmium Exposure Facilitates Oral Squamous Cell Carcinoma Progression and Epithelial-mesenchymal Transition Through the Upregulation of ATP1B4.Biological trace element research · 2026Article
- Multilayered control of mRNA delivery to cell protrusions drives localized mini-cytoplasm establishment for stress-induced cell activation.Nature communications · 2026Article
- Pancreatic Cancer-Derived Small Extracellular Vesicles Remodel Hepatic Pre-Metastatic Niche via Hybrid Epithelial-Mesenchymal States.International journal of molecular sciences · 2026Article
- Migrasomes program tissue microenvironment: from physiology to oncology, future perspectives in clinical advances.Journal of the National Cancer Center · 2026Review
284 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Epithelial stem cells serve critical physiological functions in the generation, maintenance and repair of diverse tissues through their ability to self-renew and spawn more specialized, differentiated cell types. In an analogous fashion, cancer stem cells have been proposed to fuel the growth, progression and recurrence of many carcinomas. Activation of an epithelial-mesenchymal transition (EMT), a latent cell-biological programme involved in development and wound healing, has been linked to the formation of both normal and neoplastic stem cells, but the mechanistic basis underlying this connection remains unclear. In this Perspective, we outline the instances where aspects of an EMT have been implicated in normal and neoplastic epithelial stem cells and consider the involvement of this programme during tissue regeneration and repair. We also discuss emerging concepts and evidence related to the heterogeneous and plastic cell states generated by EMT programmes and how these bear on our understanding of cancer stem cell biology and cancer metastasis. A more comprehensive accounting of the still-elusive links between EMT programmes and the stem cell state will surely advance our understanding of both normal stem cell biology and cancer pathogenesis.
Indexed as
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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.