ReviewMolecular cancer research : MCR2020
Epithelial-Mesenchymal Transition Programs and Cancer Stem Cell Phenotypes: Mediators of Breast Cancer Therapy Resistance.
Review in Molecular cancer research : MCR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 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.
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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.
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Who cites it
99 citing papers in PubMed, 128 citations in OpenAlex.
- Unlocking the ferroptotic window: Lipidomic rewiring and metabolic addiction in EMT-driven breast cancer resistance.Cell death discovery · 2026Review
- Spatiotemporal organisation of residual disease in mouse and human BRCA1-deficient mammary tumours and breast cancer.Nature communications · 2026Article
- Hallmarks of epithelial-mesenchymal plasticity in cancer.Molecular cancer · 2026Review
- A clinical decision framework for redox-adapted, EMT-high cancers: From ferroptosis resistance to precision therapeutic stratification.Redox biology · 2026Review
- Treatment of Mesenchymal Stem Cell-Derived Extracellular Vesicles with Extract of CulturedCurrent issues in molecular biology · 2026Article
- Damnacanthal Suppresses Breast Cancer Cells by Inducing Apoptosis and Cell Cycle Arrest via NF-ĸB Signaling.Pharmacology research & perspectives · 2026Article
- IFFO1 inhibits breast cancer by coordinating mitochondrial fission and fatty acid synthesis via the LaminA/C-PGC1α axis.Oncogenesis · 2026Article
- Recognition of immunogenomic signature and prognostic value of the subtype of epithelial-mesenchymal transition in breast cancer.Biochemistry and biophysics reports · 2026Article
- Unraveling the role of 3-mercaptopyruvate sulfurtransferase-derived hydrogen sulfide in triple-negative breast cancer chemoresistance.Frontiers in pharmacology · 2026Article
- CD44 knockdown and TGF‑β inhibition modulate cell proliferation and invasion in claudin‑low breast cancer cells.Oncology reports · 2026Article
- From Worms to Tumors: Conserved Strategies of Cellular Arrest and Survival Governing Dormancy.Cancer research · 2025Review
- Breast Cancer Stem Cells and Immunogenicity Profile in High-Risk Early Triple-Negative Breast Cancer: A Pilot Study.International journal of molecular sciences · 2025Article
- Unleashing the potential of Genistein and its derivatives as effective therapeutic agents for breast cancer treatment.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
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- Anti‑proliferative effects ofOncology letters · 2025Article
- Despicable role of epithelial-mesenchymal transition in breast cancer metastasis: ExhibitingCancer pathogenesis and therapy · 2025Review
- Cancer 3D Models: Essential Tools for Understanding and Overcoming Drug Resistance.Oncology research · 2025Review
- Resistance to spindle inhibitors in glioblastoma depends on STAT3 and therapy induced senescence.iScience · 2024Article
- Modeling intratumor heterogeneity in breast cancer.Biofabrication · 2024Review
39 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 1 institution in 1 country.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) programs play essential functions in normal morphogenesis and organogenesis, including that occurring during mammary gland development and glandular regeneration. Historically, EMT programs were believed to reflect a loss of epithelial gene expression signatures and morphologies that give way to those associated with mesenchymal cells and their enhanced migratory and invasive behaviors. However, accumulating evidence now paints EMT programs as representing a spectrum of phenotypic behaviors that also serve to enhance cell survival, immune tolerance, and perhaps even metastatic dormancy. Equally important, the activation of EMT programs in transformed mammary epithelial cells not only enhances their acquisition of invasive and metastatic behaviors, but also expands their generation of chemoresistant breast cancer stem cells (BCSC). Importantly, the net effect of these events results in the appearance of recurrent metastatic lesions that remain refractory to the armamentarium of chemotherapies and targeted therapeutic agents deployed against advanced stage breast cancers. Here we review the molecular and cellular mechanisms that contribute to the pathophysiology of EMT programs in human breast cancers and how these events impact their "stemness" and acquisition of chemoresistant phenotypes.
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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.