We describe here a simple model for the interaction between leukemic cells and the autologous immune response in chronic phase chronic myelogenous leukemia (CML). This model is a simplified version of the model we proposed in Clapp et al. (Cancer Res 75:4053-4062, 2015).
View Article and Find Full Text PDFMany chronic myelogenous leukemia (CML) patients in chronic phase who respond well to imatinib therapy show fluctuations in their leukemic loads in the long-term. We developed a mathematical model of CML that incorporates the intervention of an autologous immune response. Our results suggest that the patient's immune system plays a crucial role in imatinib therapy in maintaining disease control over time.
View Article and Find Full Text PDFSensory input to the lamprey central pattern generator (CPG) for locomotion is known to have a significant role in modulating lamprey swimming. Lamprey CPGs are known to have the ability to entrain to a bending stimulus, that is, in the presence of a rhythmic signal, the CPG will change its frequency to match the stimulus frequency. Bending experiments in which the lamprey spinal cord has been removed and mechanically bent back and forth at a single point have been used to determine the range of frequencies that can entrain the CPG rhythm.
View Article and Find Full Text PDFDrug Discov Today Dis Models
November 2014
Recently, there has been significant activity in the mathematical community, aimed at developing quantitative tools for studying leukemia and lymphoma. Mathematical models have been applied to evaluate existing therapies and to suggest novel therapies. This article reviews the recent contributions of mathematical modeling to leukemia and lymphoma research.
View Article and Find Full Text PDFImatinib and other tyrosine kinase inhibitors (TKI) have improved treatment of chronic myelogenous leukemia (CML); however, most patients are not cured. Deeper mechanistic understanding may improve TKI combination therapies to better control the residual leukemic cell population. In analyzing our patients' data, we found that many patients who otherwise responded well to imatinib therapy still showed variations in their BCR-ABL transcripts.
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