ArticleQuantitative biology (Beijing, China)2013
Population dynamics of cancer cells with cell state conversions.
Article in Quantitative biology (Beijing, China), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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.
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Who cites it
8 citing papers in PubMed.
- Article
- A mathematical model for phenotypic heterogeneity in breast cancer with implications for therapeutic strategies.Journal of the Royal Society, Interface · 2022Article
- Alternative models of cancer stem cells: The stemness phenotype model, 10 years later.World journal of stem cells · 2021Review
- Electrical Impedance Spectroscopy for Monitoring Chemoresistance of Cancer Cells.Micromachines · 2020Review
- Modeling differentiation-state transitions linked to therapeutic escape in triple-negative breast cancer.PLoS computational biology · 2019Article
- Epithelial/mesenchymal plasticity: how have quantitative mathematical models helped improve our understanding?Molecular oncology · 2017Review
- Phenotypic equilibrium as probabilistic convergence in multi-phenotype cell population dynamics.PloS one · 2017Article
- Overshoot in biological systems modelled by Markov chains: a non-equilibrium dynamic phenomenon.IET systems biology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Cancer stem cell (CSC) theory suggests a cell-lineage structure in tumor cells in which CSCs are capable of giving rise to the other non-stem cancer cells (NSCCs) but not vice versa. However, an alternative scenario of bidirectional interconversions between CSCs and NSCCs was proposed very recently. Here we present a general population model of cancer cells by integrating conventional cell divisions with direct conversions between different cell states, namely, not only can CSCs differentiate into NSCCs by asymmetric cell division, NSCCs can also dedifferentiate into CSCs by cell state conversion. Our theoretical model is validated when applying the model to recent experimental data. It is also found that the transient increase in CSCs proportion initiated from the purified NSCCs subpopulation cannot be well predicted by the conventional CSC model where the conversion from NSCCs to CSCs is forbidden, implying that the cell state conversion is required especially for the transient dynamics. The theoretical analysis also gives the condition such that our general model can be equivalently reduced into a simple Markov chain with only cell state transitions keeping the same cell proportion dynamics.
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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.