ArticleNPJ systems biology and applications2025
An integrative phenotype-structured partial differential equation model for the population dynamics of epithelial-mesenchymal transition.
Article in NPJ systems biology and applications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed.
- A multilevel hierarchical framework for quantification of experimental heterogeneity in population snapshot data.PLoS computational biology · 2026Article
- A Phenotype-Structured PDE Framework for Investigating the Role of Hypoxic Memory on Tumor Invasion under Cyclic Hypoxia.Bulletin of mathematical biology · 2026Article
- A multiscale model reveals how ERK/p38-regulated dormancy shapes tumor-immune dynamics and immunoediting outcomes.Frontiers in immunology · 2026Article
- A phenotype-structured PDE framework for investigating the role of hypoxic memory on tumor invasion under cyclic hypoxia.bioRxiv : the preprint server for biology · 2025Article
- Phenotype structuring in collective cell migration: a tutorial of mathematical models and methods.Journal of mathematical biology · 2025Review
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Abstract
Phenotypic heterogeneity along the epithelial-mesenchymal (E-M) axis contributes to cancer metastasis and drug resistance. Recent experimental efforts have collated detailed time-course data on the emergence and dynamics of E-M heterogeneity in a cell population. However, it remains unclear how different intra- and inter-cellular processes shape the dynamics of E-M heterogeneity. Here, using Cell Population Balance model, we capture the dynamics of cell density along E-M phenotypic axis resulting from interplay between-(a) intracellular regulatory interaction among biomolecules, (b) cell division and death and (c) stochastic cell-state transition. We find that while the existence of E-M heterogeneity depends on intracellular regulation, heterogeneity gets enhanced with stochastic cell-state transitions and diminished by growth rate differences. Further, resource competition among E-M cells can lead to both bi-phasic growth of the total population and/or bi-stability in the phenotypic composition. Overall, our model highlights complex interplay between cellular processes shaping dynamic patterns of E-M heterogeneity.
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