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A stochastic model of myeloid cell lineages in hematopoiesis and pathway mutations in acute myeloid leukemia

A model for hematopoiesis is presented that explicitly includes the erythrocyte, granulocyte, and thrombocyte lineages and their common precursors. A small number of stem cells proliferate and differentiate through different compartments to produce the vast number of blood cells needed every day. Gr...

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Detalles Bibliográficos
Autores principales: Jäkel, Frank, Worm, Oliver, Lange, Sascha, Mertelsmann, Roland
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6166954/
https://www.ncbi.nlm.nih.gov/pubmed/30273383
http://dx.doi.org/10.1371/journal.pone.0204393
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author Jäkel, Frank
Worm, Oliver
Lange, Sascha
Mertelsmann, Roland
author_facet Jäkel, Frank
Worm, Oliver
Lange, Sascha
Mertelsmann, Roland
author_sort Jäkel, Frank
collection PubMed
description A model for hematopoiesis is presented that explicitly includes the erythrocyte, granulocyte, and thrombocyte lineages and their common precursors. A small number of stem cells proliferate and differentiate through different compartments to produce the vast number of blood cells needed every day. Growth factors regulate the proliferation of cells dependent on the current demand. We provide a steady state analysis of the model and rough parameter estimates. Furthermore, we extend the model to include mutations that alter the replicative capacity of cells and introduce differentiation blocks. With these mutations the model develops signs of acute myeloid leukemia.
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spelling pubmed-61669542018-10-19 A stochastic model of myeloid cell lineages in hematopoiesis and pathway mutations in acute myeloid leukemia Jäkel, Frank Worm, Oliver Lange, Sascha Mertelsmann, Roland PLoS One Research Article A model for hematopoiesis is presented that explicitly includes the erythrocyte, granulocyte, and thrombocyte lineages and their common precursors. A small number of stem cells proliferate and differentiate through different compartments to produce the vast number of blood cells needed every day. Growth factors regulate the proliferation of cells dependent on the current demand. We provide a steady state analysis of the model and rough parameter estimates. Furthermore, we extend the model to include mutations that alter the replicative capacity of cells and introduce differentiation blocks. With these mutations the model develops signs of acute myeloid leukemia. Public Library of Science 2018-10-01 /pmc/articles/PMC6166954/ /pubmed/30273383 http://dx.doi.org/10.1371/journal.pone.0204393 Text en © 2018 Jäkel et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Jäkel, Frank
Worm, Oliver
Lange, Sascha
Mertelsmann, Roland
A stochastic model of myeloid cell lineages in hematopoiesis and pathway mutations in acute myeloid leukemia
title A stochastic model of myeloid cell lineages in hematopoiesis and pathway mutations in acute myeloid leukemia
title_full A stochastic model of myeloid cell lineages in hematopoiesis and pathway mutations in acute myeloid leukemia
title_fullStr A stochastic model of myeloid cell lineages in hematopoiesis and pathway mutations in acute myeloid leukemia
title_full_unstemmed A stochastic model of myeloid cell lineages in hematopoiesis and pathway mutations in acute myeloid leukemia
title_short A stochastic model of myeloid cell lineages in hematopoiesis and pathway mutations in acute myeloid leukemia
title_sort stochastic model of myeloid cell lineages in hematopoiesis and pathway mutations in acute myeloid leukemia
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6166954/
https://www.ncbi.nlm.nih.gov/pubmed/30273383
http://dx.doi.org/10.1371/journal.pone.0204393
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