ReviewMedical oncology (Northwood, London, England)2017
Epithelial-to-mesenchymal transition in tumor progression.
Review in Medical oncology (Northwood, London, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 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
85 citing papers in PubMed.
- Review
- Review
- Article
- ProAgio, a Novel Integrin αvβ3 Targeted Cytotoxin, Suppresses Tumor Growth and Reprograms the PDAC Microenvironment.bioRxiv : the preprint server for biology · 2026Article
- The role of MELK in cancer: mechanisms and therapeutic options.Frontiers in oncology · 2026Review
- Article
- Bile metabolite palmitic acid augments the migration of gallbladder cancer cells through the ROS/NF-кB signaling pathway.Scientific reports · 2025Article
- A potential therapeutic molecule target: lncRNA AK023507 inhibits the metastasis of breast cancer by regulating the WNT/DOCK4/β-catenin axis.Breast cancer research and treatment · 2025Article
- Circulating Progranulin: A Promising Novel Diagnostic and Prognostic Biomarker in Canine Oncology.Animals : an open access journal from MDPI · 2025Article
- Detection and isolation of viable cancer cells mediated by spytag and spycatcher using conditionally replicative adenovirus and magnetic microbeads.Scientific reports · 2025Article
- Surface-Enhanced Raman Spectroscopy for Biomedical Applications: Recent Advances and Future Challenges.ACS applied materials & interfaces · 2025Review
- Review
- The Combined Impact of Curcumin: Piperine and Sorafenib on microRNAs and Different Pathways in Breast Cancer Cells.Indian journal of clinical biochemistry : IJCB · 2025Article
- The prognostic and therapeutic potential of vimentin in colorectal cancer.Molecular biology reports · 2024Review
- Different contractility modes control cell escape from multicellular spheroids and tumor explants.APL bioengineering · 2024Article
- Cell fusion between tumor cells and macrophages promotes the metastasis of OSCC patient through the activation of the chemokine signaling pathway.Cancer medicine · 2024Article
- Epithelial-Mesenchymal Transition Induced by a Metal Mixture in Liver Cells With Antioxidant Barrier Decreased.Oxidative medicine and cellular longevity · 2024Article
- Non-coding RNAs and exosomal non-coding RNAs in lung cancer: insights into their functions.Frontiers in cell and developmental biology · 2024Review
- Mechanotransduction pathways in regulating epithelial-mesenchymal plasticity.Current opinion in cell biology · 2023Review
- HOXA13 promotes the proliferation, migration, and invasion of nasopharyngeal carcinoma HNE1 cells by upregulating the expression of Snail and MMP-2.Scientific reports · 2023Article
25 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial-to-mesenchymal transition (EMT) is a biological process in which a non-motile epithelial cell changes to a mesenchymal state with invasive capacities. However, the EMT program is involved in both physiological and pathological processes. Cancer-associated EMT is known to contribute to increase invasiveness and metastasis, resistance to therapies, and generation of cell populations with stem cell-like characteristics and therefore is deeply involved in tumor progression. This process is finely orchestrated by multiple signaling pathways and regulatory transcriptional networks. The hallmark of EMT is the loss of epithelial surface markers, mainly E-cadherin, and the acquisition of mesenchymal phenotype. These events can be mediated by EMT transcription factors which can cooperate with several enzymes to repress the E-cadherin expression and regulate EMT at the epigenetic and post-translational level. A growing body of evidence indicates that cancer cells can reside in various phenotypic states along the EMT spectrum, where cells can jointly retain epithelial traits with mesenchymal ones. This type of phenotypic plasticity endows cancer cells with tumor-initiating potential. The identification of the signaling pathways and modulators that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes and possible therapeutic interventions.
Indexed as
Identifiers
28560682What 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.