2017
DOI: 10.1371/journal.pone.0179700
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Dynamical models of mutated chronic myelogenous leukemia cells for a post-imatinib treatment scenario: Response to dasatinib or nilotinib therapy

Abstract: Targeted inhibition of the oncogenic BCR-ABL1 fusion protein using the ABL1 tyrosine kinase inhibitor imatinib has become standard therapy for chronic myelogenous leukemia (CML), with most patients reaching total and durable remission. However, a significant fraction of patients develop resistance, commonly due to mutated ABL1 kinase domains. This motivated development of second-generation drugs with broadened or altered protein kinase selectivity profiles, including dasatinib and nilotinib. Imatinib-resistant… Show more

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Cited by 7 publications
(10 citation statements)
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“…Due to the homogeneity of the disease and the availability of high quality time course data, CML has attracted mathematical modeling approaches with different foci [Catlin et al, 2005, Michor et al, 2005, Roeder et al, 2006, Dingli et al, 2010, Stein et al, 2011, Komarova and Wodarz, 2009, Woywod et al, 2017. Several models also studied the role of the immune system in CML and made particular assumptions about the underlying mechanisms [Kim et al, 2008, Wodarz, 2010.…”
Section: Discussionmentioning
confidence: 99%
“…Due to the homogeneity of the disease and the availability of high quality time course data, CML has attracted mathematical modeling approaches with different foci [Catlin et al, 2005, Michor et al, 2005, Roeder et al, 2006, Dingli et al, 2010, Stein et al, 2011, Komarova and Wodarz, 2009, Woywod et al, 2017. Several models also studied the role of the immune system in CML and made particular assumptions about the underlying mechanisms [Kim et al, 2008, Wodarz, 2010.…”
Section: Discussionmentioning
confidence: 99%
“…In cases of failure of imatinib, second-line treatment is based on second-generation TKIs such as dasatinib and nilotinib [ 15 , 16 ], authorized in November 2006 and November 2007, respectively [ 17 , 18 ]. These new drugs were initially approved for second-line treatment through phase II studies [ 19 ], then, based on the results of phase III studies, for first-line treatment as an alternative to imatinib [ 20 22 ].…”
Section: Introductionmentioning
confidence: 99%
“…More physiologically accurate, nonlinear models that account for cell-cell signaling and lineage branching is expected to improve clinical relevance. Mathematical models that incorporate feedback signaling have been developed in normal ( Engel et al, 2004; Marciniak-Czochra et al, 2009; Mahadik et al, 2019 ) ( Mon Père et al, 2021 ) and diseased ( Wodarz, 2008; Sachs et al, 2011; Krinner et al, 2013; Stiehl et al, 2014; Stiehl et al, 2015; Crowell et al, 2016; Woywod et al, 2017; Jiao et al, 2018; Stiehl et al, 2018; Zenati et al, 2018; Park et al, 2019; Sharp et al, 2020 ) hematopoiesis. Because of the vast number of possible ways in which feedback models of normal hematopoiesis and leukemia can be configured, mathematical models tend to greatly simplify the lineage architectures and the feedback interactions among the cell types.…”
Section: Introductionmentioning
confidence: 99%
“…Later work extended this approach to investigate clonal selection and therapy resistance ( Stiehl et al, 2014 ), the role of cytokines on leukemia progression ( Stiehl et al, 2018 ), combination treatment strategies ( Banck and Görlich, 2019 ) and niche competition ( Stiehl et al, 2020 ). Clonal competition was also considered in an ODE feedback model of CML ( Woywod et al, 2017 ) and a stochastic model with feedback ( Dinh et al, 2021 ). Simpler unbranched lineage models of normal and leukemic cells in which only the normal cells respond to feedback but normal and leukemic cells compete for space in the bone marrow have been used to investigate regimes of co-existence of normal and leukemic cells ( Crowell et al, 2016; Jiao et al, 2018 ) and to design combination therapies using optimal control algorithms ( Sharp et al, 2020 ).…”
Section: Introductionmentioning
confidence: 99%