ArticleFrontiers in oncology2013
Stochastic Hypothesis of Transition from Inborn Neutropenia to AML: Interactions of Cell Population Dynamics and Population Genetics.
Article in Frontiers in oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Predicting Time to Relapse in Acute Myeloid Leukemia through Stochastic Modeling of Minimal Residual Disease Based on Clonality Data.Computational and systems oncology · 2021Article
- Application of the Moran Model in Estimating Selection Coefficient of Mutated CSF3R Clones in the Evolution of Severe Congenital Neutropenia to Myeloid Neoplasia.Frontiers in physiology · 2020Article
- Mutation, drift and selection in single-driver hematologic malignancy: Example of secondary myelodysplastic syndrome following treatment of inherited neutropenia.PLoS computational biology · 2019Article
- Tumor evolution: Linear, branching, neutral or punctuated?Biochimica et biophysica acta. Reviews on cancer · 2017Review
- Phenotypic equilibrium as probabilistic convergence in multi-phenotype cell population dynamics.PloS one · 2017Article
- Emergence of heterogeneity in acute leukemias.Biology direct · 2016Article
- Old and new faces of neutropenia in children.Haematologica · 2016Article
- Normal vs. Malignant hematopoiesis: the complexity of acute leukemia through systems biology.Frontiers in genetics · 2015Article
- Simulating cancer: computational models in oncology.Frontiers in oncology · 2013Article
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Authors and funding
2 authors.
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Abstract
We present a stochastic model of driver mutations in the transition from severe congenital neutropenia to myelodysplastic syndrome to acute myeloid leukemia (AML). The model has the form of a multitype branching process. We derive equations for the distributions of the times to consecutive driver mutations and set up simulations involving a range of hypotheses regarding acceleration of the mutation rates in successive mutant clones. Our model reproduces the clinical distribution of times at diagnosis of secondary AML. Surprisingly, within the framework of our assumptions, stochasticity of the mutation process is incapable of explaining the spread of times at diagnosis of AML in this case; it is necessary to additionally assume a wide spread of proliferative parameters among disease cases. This finding is unexpected but generally consistent with the wide heterogeneity of characteristics of human cancers.
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