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
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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