ReviewJournal of oncology2015
Epithelial to Mesenchymal Transition in a Clinical Perspective.
Review in Journal of oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Is overexpression of TWIST, a transcriptional factor, a prognostic biomarker of head and neck carcinoma? Evidence from fifteen studies.Scientific reports · 2015Pooled it
- Prognostic prediction and immune correlation analysis of anoikis- and epithelial-mesenchymal transition-related genes in lung adenocarcinoma.Translational cancer research · 2026Article
- MicroRNA cluster 7/17/155 as a potential driver for high-grade breast tumors transformation through EGFR-associated EMT.Frontiers in cell and developmental biology · 2026Article
- Review
- Role of EMT in drug resistance of breast cancer: molecular mechanisms and therapeutic strategies.Frontiers in oncology · 2025Review
- Novel benzoylurea derivative decreases TRPM7 channel function and inhibits cancer cells migration.Channels (Austin, Tex.) · 2024Article
- Contribution of Autophagy to Epithelial Mesenchymal Transition Induction during Cancer Progression.Cancers · 2024Review
- Modeling epithelial-mesenchymal transition in patient-derived breast cancer organoids.Frontiers in oncology · 2024Article
- GATA6-AS1 suppresses epithelial-mesenchymal transition of pancreatic cancer under hypoxia through regulating SNAI1 mRNA stability.Journal of translational medicine · 2023Article
- Ferroptosis and EMT: key targets for combating cancer progression and therapy resistance.Cellular and molecular life sciences : CMLS · 2023Review
- An Overview of Epithelial-to-Mesenchymal Transition and Mesenchymal-to-Epithelial Transition in Canine Tumors: How Far Have We Come?Veterinary sciences · 2022Review
- The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis.Journal of hematology & oncology · 2022Review
- SHC4 promotes tumor proliferation and metastasis by activating STAT3 signaling in hepatocellular carcinoma.Cancer cell international · 2022Article
- RNA binding protein RBMS3 is a common EMT effector that modulates triple-negative breast cancer progression via stabilizing PRRX1 mRNA.Oncogene · 2021Article
- Article
- LINC00461 facilitates HNSCC development and reduces chemosensitivity by impairing miR-195-mediated inhibition of HOXA10.Molecular therapy oncolytics · 2021Article
- Polyphenols Modulating Effects of PD-L1/PD-1 Checkpoint and EMT-Mediated PD-L1 Overexpression in Breast Cancer.Nutrients · 2021Review
- MMP-7, -8, -9, E-cadherin, and beta-catenin expression in 34 ameloblastoma cases.Clinical and experimental dental research · 2021Article
- Melatonin and hyperbaric oxygen therapies suppress colorectal carcinogenesis through pleiotropic effects and multifaceted mechanisms.International journal of biological sciences · 2021Article
- MicroRNAs target the Wnt/β‑catenin signaling pathway to regulate epithelial‑mesenchymal transition in cancer (Review).Oncology reports · 2020Review
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor growth and metastatic dissemination rely on cellular plasticity. Among the different phenotypes acquired by cancer cells, epithelial to mesenchymal transition (EMT) has been extensively illustrated. Indeed, this transition allows an epithelial polarized cell to acquire a more mesenchymal phenotype with increased mobility and invasiveness. The role of EMT is quite clear during developmental stage. In the neoplastic context in many tumors EMT has been associated with a more aggressive tumor phenotype including local invasion and distant metastasis. EMT allows the cell to invade surrounding tissues and survive in the general circulation and through a stem cell phenotype grown in the host organ. The molecular pathways underlying EMT have also been clearly defined and their description is beyond the scope of this review. Here we will summarize and analyze the attempts made to block EMT in the therapeutic context. Indeed, till today, most of the studies are made in animal models. Few clinical trials are ongoing with no obvious benefits of EMT inhibitors yet. We point out the limitations of EMT targeting such tumor heterogeneity or the dynamics of EMT during disease progression.
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.