A hypothetical-mathematical model of acute myeloid leukemia pathogenesis

Abstract

Acute myeloid leukaemia is defined by the expansion of a mutated haematopoietic stem cell clone, with the inhibition of surrounding normal clones. Haematopoiesis can be seen as an evolutionary tree, starting with one cell that undergoes several divisions during the expansion phase, afterwards losing functional cells during the aging-related contraction phase. During divisions, offspring cells acquire ‘variations’, which can be either normal or abnormal. If an abnormal variation is present in more than 25% of the final cells, a monoclonal, leukemic pattern occurs. Such a pattern develops if: (A1) The abnormal variation occurs early, during the first or second divisions; (A2) The variation confers exceptional proliferative capacity; (B) A sizable proportion of the normal clones are destroyed and a previously non-significant abnormal clone gains relative dominance over a depleted environment; (C) The abnormal variation confers relative ‘immortality’, rendering it significant during the contraction phase. Combinations of these pathways further enhance the leukemic risk of the system. A simple mathematical model is used in order to characterize normal and leukemic states and to explain the above cellular processes generating monoclonal leukemic patterns.

Authors

Andrei Cucuianu

Radu Precup
Department of Mathematics, Babes-Bolyai University, Cluj-Napoca, Romania

Keywords

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Paper coordinates

A. Cucuianu, R. Precup, A hypothetical-mathematical model of acute myeloid leukemia pathogenesis, Comput. Math. Methods Med. 11 (2010), 49-65, https://doi.org/10.1080/17486700902973751

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About this paper

Journal

Computational and Mathematical  Methods in Medicine

Publisher Name

Hindawi Publishing Corporation

Print ISSN
1748-670X
Online ISSN

1748-6718

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