The overshoot and phenotypic equilibrium in characterizing cancer dynamics of reversible phenotypic plasticity
From MaRDI portal
(Redirected from Publication:304808)
Abstract: The paradigm of phenotypic plasticity indicates reversible relations of different cancer cell phenotypes, which extends the cellular hierarchy proposed by the classical cancer stem cell (CSC) theory. Since it is still question able if the phenotypic plasticity is a crucial improvement to the hierarchical model or just a minor extension to it, it is worthwhile to explore the dynamic behavior characterizing the reversible phenotypic plasticity. In this study we compare the hierarchical model and the reversible model in predicting the cell-state dynamics observed in biological experiments. Our results show that the hierarchical model shows significant disadvantages over the reversible model in describing both long-term stability (phenotypic equilibrium) and short-term transient dynamics (overshoot) of cancer cells. In a very specific case in which the total growth of population due to each cell type is identical, the hierarchical model predicts neither phenotypic equilibrium nor overshoot, whereas thereversible model succeeds in predicting both of them. Even though the performance of the hierarchical model can be improved by relaxing the specific assumption, its prediction to the phenotypic equilibrium strongly depends on a precondition that may be unrealistic in biological experiments, and it also fails to capture the overshoot of CSCs. By comparison, it is more likely for the reversible model to correctly describe the stability of the phenotypic mixture and various types of overshoot behavior.
Recommendations
- The phenotypic equilibrium of cancer cells: from average-level stability to path-wise convergence
- Mathematical modelling of plasticity and phenotype switching in cancer cell populations
- A multi-phenotypic cancer model with cell plasticity
- A mathematical study of the impact of cell plasticity on tumour control probability
- Replicator dynamics of cancer stem cell: selection in the presence of differentiation and plasticity
- The effects of phenotypic plasticity on the fixation probability of mutant cancer stem cells
- Dynamics and bifurcations in a simple quasispecies model of tumorigenesis
- Evolution of cancer cell populations under cytotoxic therapy and treatment optimisation: insight from a phenotype-structured model
- A Bistable Field Model of Cancer Dynamics
- A Bayesian statistical analysis of stochastic phenotypic plasticity model of cancer cells
Cites work
- scientific article; zbMATH DE number 3292104 (Why is no real title available?)
- A multi-phenotypic cancer model with cell plasticity
- A multicompartment mathematical model of cancer stem cell-driven tumor growth dynamics
- Branching Processes
- Feedback regulation in multistage cell lineages
- Non-negative matrices and Markov chains. 2nd ed
- The noise and the KISS in the cancer stem cells niche
- The phenotypic equilibrium of cancer cells: from average-level stability to path-wise convergence
Cited in
(6)- On tumoural growth and treatment under cellular dedifferentiation
- Inference on autoregulation in gene expression with variance-to-mean ratio
- The phenotypic equilibrium of cancer cells: from average-level stability to path-wise convergence
- Replicator dynamics of cancer stem cell: selection in the presence of differentiation and plasticity
- Cell population growth kinetics in the presence of stochastic heterogeneity of cell phenotype
- A Bayesian statistical analysis of stochastic phenotypic plasticity model of cancer cells
This page was built for publication: The overshoot and phenotypic equilibrium in characterizing cancer dynamics of reversible phenotypic plasticity
Report a bug (only for logged in users!)Click here to report a bug for this page (MaRDI item Q304808)
