ReviewJournal of clinical medicine2016
EMT in Breast Carcinoma-A Review.
Review in Journal of clinical medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 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
140 citing papers in PubMed, 234 citations in OpenAlex.
- Response to neoadjuvant chemotherapy in early breast cancers is associated with epithelial-mesenchymal transition and tumor-infiltrating lymphocytes.Molecular oncology · 2025Trial
- Evaluation of Itraconazole as a repurposed small molecule inhibitor of EMT in breast cancer: a molecular docking and dynamics study.Journal of molecular modeling · 2026Article
- Damnacanthal Suppresses Breast Cancer Cells by Inducing Apoptosis and Cell Cycle Arrest via NF-ĸB Signaling.Pharmacology research & perspectives · 2026Article
- Gelatin-methacryloyl hydrogel stiffness influences epithelial-mesenchymal transition in MCF7 but not MDA-MB-231 breast cancer cells in 3D culture.Biology open · 2026Article
- The Role of the Cell Surface Heparan Sulfate Proteoglycan Syndecan-3 in Breast Cancer Pathophysiology.Cells · 2025Article
- Atractylodes lancea Crude Extract Suppresses Triple-Negative Breast Cancer Metastasis via NF-kB signaling Pathway Inhibition.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- CRISPR/dCas9-TET1-mediated epigenetic editing reactivates miR-200c in breast cancer cells.Scientific reports · 2025Article
- Inhibitory Impact of the Amino Benzoic Derivative DAB-2-28 on the Process of Epithelial-Mesenchymal Transition in Human Breast Cancer Cells.Molecules (Basel, Switzerland) · 2025Article
- Exploring the antineoplastic potential of α-mangostin in breast cancer.Natural products and bioprospecting · 2025Review
- Text Mining Strategy Identifies Gene Networks Under Control of miR-21 in Breast Cancer Development.Cancer medicine · 2025Article
- Characterization of Disseminated Tumor Cells (DTCs) in Patients with Triple-Negative Breast Cancer (TNBC).Cells · 2025Article
- Leucine-rich repeat-containing 56 promotes breast cancer progression via modulation of the RhoA/ROCKs signaling axis.Molecular biomedicine · 2025Article
- Exploring the role of EMT in ovarian cancer progression using a multiscale mathematical model.NPJ systems biology and applications · 2025Article
- Caveolin-1: an ambiguous entity in breast cancer.Molecular cancer · 2025Review
- Histone acetylation modulators in breast cancer.Breast cancer research : BCR · 2025Review
- PKN2 Is a Dependency of the Mesenchymal-like Cancer Cell State.Cancer discovery · 2025Article
- Angiotensin 1-7 and the Non-Peptide MAS-R Agonist AVE0991 Inhibit Breast Cancer Cell Migration and Invasion.Biomedicines · 2025Article
- E-cadherin staining in the diagnosis of lobular versus ductal neoplasms of the breast: the emperor has no clothes.Histopathology · 2025Review
- Non-coding RNAs as key regulators of epithelial-mesenchymal transition in breast cancer.Frontiers in cell and developmental biology · 2025Review
- Molecular roles of microRNA-21 and exosomal miR-21 in gastrointestinal cancers: diagnostic, therapeutic, and drug resistance insights.Frontiers in molecular biosciences · 2025Review
80 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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial to mesenchymal transition (EMT) is a cellular program that is involved in embryonic development; wound healing, but also in tumorigenesis. Breast carcinoma (BC) is the most common cancer in women worldwide, and the majority of deaths (90%) are caused by invasion and metastasis. The EMT plays an important role in invasion and subsequent metastasis. Several distinct biological events integrate a cascade that leads not only to a change from an epithelial to mesenchymal phenotype, but allows for detachment, migration, invasion and ultimately, colonization of a second site. Understanding the biological intricacies of the EMT may provide important insights that lead to the development of therapeutic targets in pre-invasive and invasive breast cancer, and could be used as biomarkers identifying tumor subsets with greater chances of recurrence, metastasis and therapeutic resistance leading to death.
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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.