ArticleBMC cancer2019
Stochastic modelling of tyrosine kinase inhibitor rotation therapy in chronic myeloid leukaemia.
Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- Beyond IC50-A computational dynamic model of drug resistance in enzyme inhibition treatment.PLoS computational biology · 2024Article
- Methyl-Thiol-Bridged Oxadiazole and Triazole Heterocycles as Inhibitors of NF-κB in Chronic Myelogenous Leukemia Cells.Biomedicines · 2023Article
- Rotating between ponatinib and imatinib temporarily increases the efficacy of imatinib as shown in a chronic myeloid leukaemia model.Scientific reports · 2022Article
- Combating drug resistance in acute myeloid leukaemia by drug rotations: the effects of quizartinib and pexidartinib.Cancer cell international · 2021Article
- Multiregion Sequence Analysis to Predict Intratumor Heterogeneity and Clonal Evolution.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Inferring time-dependent population growth rates in cell cultures undergoing adaptation.BMC bioinformatics · 2020Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundResistance towards targeted cancer treatments caused by single nucleotide variations is a major issue in many malignancies. Currently, there are a number of available drugs for chronic myeloid leukaemia (CML), which are overcome by different sets of mutations. The main aim of this study was to explore if it can be possible to exploit this and create a treatment protocol that outperforms each drug on its own.
methodsWe present a computer program to test different treatment protocols against CML, based on available resistance mutation growth data. The evolution of a relatively stable pool of cancer stem cells is modelled as a stochastic process, with the growth of cells expressing a tumourigenic protein (here, Abl1) and any emerging mutants determined principally by the drugs used in the therapy.
resultsThere can be some benefit to Bosutinib-Ponatinib rotation therapy even if the mutation status is unknown, whereas Imatinib-Nilotinib rotation is unlikely to improve the outcomes. Furthermore, an interplay between growth inhibition and selection effects generates a non-linear relationship between drug doses and the risk of developing resistance.
conclusionsDrug rotation therapy might be able to delay the onset of resistance in CML patients without costly ongoing observation of mutation status. Moreover, the simulations give credence to the suggestion that lower drug concentrations may achieve better results following major molecular response in CML.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.