ReviewMolecular oncology2017
The EMT spectrum and therapeutic opportunities.
Review in Molecular oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed.
- Current therapeutic interventions to target cancer stem cells for metastasis.International journal of clinical oncology · 2026Review
- Targeting Tumour Heterogeneity through sequential timing of anti-hallmark combination therapies -a hypothesis for implementation.Frontiers in immunology · 2026Review
- ER Stress Is Associated with a "Mesenchymal Drift" in an Anaplastic Thyroid Carcinoma Cell Line.Cancers · 2025Article
- The regulatory network of epithelial-mesenchymal transition-associated non-coding RNAs in thyroid cancer: molecular mechanisms, clinical implications, and therapeutic strategies.Frontiers in oncology · 2025Review
- Modeling ncRNA-Mediated Circuits in Cell Fate Decision: From Systems Biology to Synthetic Biology.Methods in molecular biology (Clifton, N.J.) · 2025Review
- CCL2 promotes EGFR-TKIs resistance in non-small cell lung cancer via the AKT-EMT pathway.Acta biochimica et biophysica Sinica · 2024Article
- Targeting EMT using low-dose Teniposide by downregulating ZEB2-driven activation of RNA polymerase I in breast cancer.Cell death & disease · 2024Article
- Cellular geometry and epithelial-mesenchymal plasticity intersect with PIEZO1 in breast cancer cells.Communications biology · 2024Article
- Exploring the relationship between anastasis and mitochondrial ROS-mediated ferroptosis in metastatic chemoresistant cancers: a call for investigation.Frontiers in immunology · 2024Review
- Influence of CCancers · 2023Article
- Review
- Article
- SLUG and SNAIL as Potential Immunohistochemical Biomarkers for Renal Cancer Staging and Survival.International journal of molecular sciences · 2023Article
- Antimetastatic Activity of Apoptolidin A by Upregulation of N-Myc Downstream-Regulated Gene 1 Expression in Human Colorectal Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Tumor cell plasticity in targeted therapy-induced resistance: mechanisms and new strategies.Signal transduction and targeted therapy · 2023Review
- Article
- Article
- Natural Compound Shikonin Induces Apoptosis and Attenuates Epithelial to Mesenchymal Transition in Radiation-Resistant Human Colon Cancer Cells.Biomolecules & therapeutics · 2022Article
- EMT-Related Gene Signature Predicts the Prognosis in Uveal Melanoma Patients.Journal of oncology · 2022Article
- SLUG-related partial epithelial-to-mesenchymal transition is a transcriptomic prognosticator of head and neck cancer survival.Molecular oncology · 2022Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carcinomas are phenotypically arrayed along an epithelial-mesenchymal transition (EMT) spectrum, a developmental program currently exploited to understand the acquisition of drug resistance through a re-routing of growth factor signaling. This review collates the current approaches employed in developing therapeutics against cancer-associated EMT, and provides an assessment of their respective strengths and drawbacks. We reflect on the close relationship between EMT and chemoresistance against current targeted therapeutics, with a special focus on the epigenetic mechanisms that link these processes. This prompts the hypothesis that carcinoma-associated EMT shares a common epigenetic pathway to cellular plasticity as somatic cell reprogramming during tissue repair and regeneration. Indeed, their striking resemblance suggests that EMT in carcinoma is a pathological adaptation of an intrinsic program of cellular plasticity that is crucial to tissue homeostasis. We thus propose a revised approach that targets the epigenetic mechanisms underlying pathogenic EMT to arrest cellular plasticity regardless of upstream cancer-driving mutations.
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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.