ArticleMethods in molecular biology (Clifton, N.J.)2021
Mathematical Modeling of Plasticity and Heterogeneity in EMT.
Article in Methods in molecular biology (Clifton, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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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Who cites it
9 citing papers in PubMed.
- Masters of adaptation: How cancer and immune cell plasticity mediates tumor progression.PLoS biology · 2025Review
- Modeling the dynamics of EMT reveals genes associated with pan-cancer intermediate states and plasticity.NPJ systems biology and applications · 2025Article
- Co-Expression Network Analysis Unveiled lncRNA-mRNA Links Correlated to Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor Resistance and/or Intermediate Epithelial-to-Mesenchymal Transition Phenotypes in a Human Non-Small Cell Lung Cancer Cellular Model System.International journal of molecular sciences · 2024Article
- Review
- Transcriptional and post-transcriptional control of epithelial-mesenchymal plasticity: why so many regulators?Cellular and molecular life sciences : CMLS · 2022Review
- Volumetric compression develops noise-driven single-cell heterogeneity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Epithelial-to-Mesenchymal Transition in Fibrosis: Concepts and Targeting Strategies.Frontiers in pharmacology · 2021Review
- Understanding the Complex Milieu of Epithelial-Mesenchymal Transition in Cancer Metastasis: New Insight Into the Roles of Transcription Factors.Frontiers in oncology · 2021Review
- Mechanisms Governing Metabolic Heterogeneity in Breast Cancer and Other Tumors.Frontiers in oncology · 2021Review
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
Abstract
The epithelial-mesenchymal transition (EMT) and the corresponding reverse process, mesenchymal-epithelial transition (MET), are dynamic and reversible cellular programs orchestrated by many changes at both biochemical and morphological levels. A recent surge in identifying the molecular mechanisms underlying EMT/MET has led to the development of various mathematical models that have contributed to our improved understanding of dynamics at single-cell and population levels: (a) multi-stability-how many phenotypes can cells attain during an EMT/MET?, (b) reversibility/irreversibility-what time and/or concentration of an EMT inducer marks the "tipping point" when cells induced to undergo EMT cannot revert?, (c) symmetry in EMT/MET-do cells take the same path when reverting as they took during the induction of EMT?, and (d) non-cell autonomous mechanisms-how does a cell undergoing EMT alter the tendency of its neighbors to undergo EMT? These dynamical traits may facilitate a heterogenous response within a cell population undergoing EMT/MET. Here, we present a few examples of designing different mathematical models that can contribute to decoding EMT/MET dynamics.
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Registered trials
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