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首页> 外文期刊>Mathematical Biosciences: An International Journal >An analysis of strategic treatment interruptions during imatinib treatment of chronic myelogenous leukemia with imatinib-resistant mutations
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An analysis of strategic treatment interruptions during imatinib treatment of chronic myelogenous leukemia with imatinib-resistant mutations

机译：伊马替尼耐药耐药突变的慢性粒细胞白血病伊马替尼治疗期间战略治疗中断的分析

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摘要

Chronic myelogenous leukemia (CML) is a cancer of the white blood cells that results from increased and uncontrolled growth of myeloid cells in the bone marrow and the accumulation of these cells in the blood. The most common form of treatment for CML is imatinib, a tyrosine kinase inhibitor. Although imatinib is an effective treatment for CML and most patients treated with imatinib do attain some form of remission, imatinib does not completely eradicate all leukemia cells, and if treatment is stopped, all patients eventually relapse (Cortes, 2005). In Kim (2008), the authors developed a mathematical model for the dynamics of CML under imatinib treatment that incorporates the anti-leukemia immune response, and in Paquin (2011), the authors used this mathematical model to study strategic treatment interruptions as a potential therapeutic strategy for CML patients. Although the authors presented the results of several numerical simulations in Paquin (2011), the studies in that work did not include the possibility of imatinib-resistant mutations or an initial population of imatinib-resistant leukemia cells. As resistance is a significant consideration in any drug treatment, it is important to study the efficacy of the strategic treatment interruption plan in the presence of imatinib resistance. In this work, we modify the delay differential equations model of Kim (2008), Paquin (2011) to include the possibility of imatinib resistance, and we analyze strategic treatment interruptions as a potential therapeutic tool in the case of patients with imatinib-resistance leukemia cells. (C) 2015 Elsevier Inc. All rights reserved.
机译：慢性粒细胞性白血病（CML）是白细胞的癌症，其源于骨髓中髓样细胞生长的增加和不受控制的生长以及这些细胞在血液中的积累。 CML的最常见治疗形式是酪氨酸激酶抑制剂伊马替尼。尽管伊马替尼是治疗CML的有效方法，大多数接受伊马替尼治疗的患者的确能达到某种形式的缓解，但伊马替尼不能完全根除所有白血病细胞，如果停止治疗，所有患者最终都会复发（Cortes，2005年）。在Kim（2008）中，作者开发了包含抗白血病免疫反应的依马替尼治疗下CML动力学的数学模型，在Paquin（2011）中，作者使用此数学模型研究了潜在的战略性治疗中断CML患者的治疗策略。尽管作者在Paquin（2011）中提供了一些数值模拟的结果，但该研究并未包括伊马替尼耐药性突变或伊马替尼耐药性白血病细胞初始种群的可能性。由于耐药性是任何药物治疗中的重要考虑因素，因此，在存在伊马替尼耐药性的情况下，研究策略性治疗中断计划的有效性非常重要。在这项工作中，我们修改了Kim（2008），Paquin（2011）的延迟微分方程模型，以包括伊马替尼耐药的可能性，并且我们分析了策略性治疗中断作为伊马替尼耐药性白血病患者的潜在治疗工具细胞。 （C）2015 Elsevier Inc.保留所有权利。

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