ArticlePLoS computational biology2011
Modeling evolutionary dynamics of epigenetic mutations in hierarchically organized tumors.
Article in PLoS computational biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- Advances in Colorectal Cancer Cell Biology and Clonal Evolution.International journal of molecular sciences · 2026Review
- Inferring Tumor Proliferative Organization from Phylogenetic Tree Measures in a Computational Model.Systematic biology · 2020Article
- Spatially constrained tumour growth affects the patterns of clonal selection and neutral drift in cancer genomic data.PLoS computational biology · 2019Article
- Characterization of Ablation Thresholds for 3D-Cultured Patient-Derived Glioma Stem Cells in Response to High-Frequency Irreversible Electroporation.Research (Washington, D.C.) · 2019Article
- Multicompartment cell-based modeling of confined migration: regulation by cell intrinsic and extrinsic factors.Molecular biology of the cell · 2018Article
- Heritable tumor cell division rate heterogeneity induces clonal dominance.PLoS computational biology · 2018Article
- Catch my drift? Making sense of genomic intra-tumour heterogeneity.Biochimica et biophysica acta. Reviews on cancer · 2017Review
- Addiction to the IGF2-ID1-IGF2 circuit for maintenance of the breast cancer stem-like cells.Oncogene · 2017Article
- In silico modeling for tumor growth visualization.BMC systems biology · 2016Article
- Feedback Regulation in a Cancer Stem Cell Model can Cause an Allee Effect.Bulletin of mathematical biology · 2016Article
- Bidirectional interconversion of stem and non-stem cancer cell populations: A reassessment of theoretical models for tumor heterogeneity.Molecular & cellular oncology · 2016Review
- Agent-Based Modeling of Cancer Stem Cell Driven Solid Tumor Growth.Methods in molecular biology (Clifton, N.J.) · 2016Article
- Simulation-based Bayesian Analysis of Complex Data.Summer Computer Simulation Conference : (SCSC 2015) : 2015 Summer Simulation Multi-Conference (SummerSim'15) : Chicago, Illinois, USA, 26-29 July 2015. Summer Computer Simulation Conference (2015 : Chicago, Illinois) · 2015Article
- Cancer Molecular Evolution.Journal of molecular evolution · 2015Article
- Heterogeneity of chemokine cell-surface receptor expression in triple-negative breast cancer.American journal of cancer research · 2015Article
- An agent-based model of cancer stem cell initiated avascular tumour growth and metastasis: the effect of seeding frequency and location.Journal of the Royal Society, Interface · 2014Article
- From computational modelling of the intrinsic apoptosis pathway to a systems-based analysis of chemotherapy resistance: achievements, perspectives and challenges in systems medicine.Cell death & disease · 2014Review
- Population dynamics of cancer cells with cell state conversions.Quantitative biology (Beijing, China) · 2013Article
- Exploiting ecological principles to better understand cancer progression and treatment.Interface focus · 2013Review
- Evolution of intratumoral phenotypic heterogeneity: the role of trait inheritance.Interface focus · 2013Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cancer stem cell (CSC) concept is a highly debated topic in cancer research. While experimental evidence in favor of the cancer stem cell theory is apparently abundant, the results are often criticized as being difficult to interpret. An important reason for this is that most experimental data that support this model rely on transplantation studies. In this study we use a novel cellular Potts model to elucidate the dynamics of established malignancies that are driven by a small subset of CSCs. Our results demonstrate that epigenetic mutations that occur during mitosis display highly altered dynamics in CSC-driven malignancies compared to a classical, non-hierarchical model of growth. In particular, the heterogeneity observed in CSC-driven tumors is considerably higher. We speculate that this feature could be used in combination with epigenetic (methylation) sequencing studies of human malignancies to prove or refute the CSC hypothesis in established tumors without the need for transplantation. Moreover our tumor growth simulations indicate that CSC-driven tumors display evolutionary features that can be considered beneficial during tumor progression. Besides an increased heterogeneity they also exhibit properties that allow the escape of clones from local fitness peaks. This leads to more aggressive phenotypes in the long run and makes the neoplasm more adaptable to stringent selective forces such as cancer treatment. Indeed when therapy is applied the clone landscape of the regrown tumor is more aggressive with respect to the primary tumor, whereas the classical model demonstrated similar patterns before and after therapy. Understanding these often counter-intuitive fundamental properties of (non-)hierarchically organized malignancies is a crucial step in validating the CSC concept as well as providing insight into the therapeutical consequences of this model.
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