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Recent experimental evidence suggests that acute myeloid leukemias mayoriginate from multiple clones of malignant cells. Nevertheless it is not knownhow the observed clones may differ with respect to cell properties such asproliferation and self-renewal. There are scarcely any data on how these cellproperties change due to chemotherapy and relapse. We propose a newmathematical model to investigate the impact of cell properties on multi-clonalcomposition of leukemias. Model results imply that enhanced self-renewal may bea key mechanism in the clonal selection process. Simulations suggest that fastproliferating and highly self-renewing cells dominate at primary diagnosiswhile relapse following therapy-induced remission is triggered mostly by highlyself-renewing but slowly proliferating cells. Comparison of simulation resultsto patient data demonstrates that the proposed model is consistent withclinically observed dynamics based on a clonal selection process.

Clonal selection and therapy resistance in acute leukemias: Mathematical modelling explains different proliferation patterns at diagnosis and relapse