论文标题
通过离散时间离散的Markov链模型BCR-ABL1相互作用的慢性髓样白血病中的新型治疗靶标
Novel therapeutic targets in chronic myeloid leukaemia through a discrete time discrete Markov chain model of BCR-ABL1 interactions
论文作者
论文摘要
Chronic Myeloid Leukaemia (CML) is a blood-derived proliferative disorder, which is highly associated to a translocation of chromosomes 9 and 22 or the creation of Philadelphia chromosome Ph(+) cases, inducing the synthesis of a chimeric fusion protein, namely BCR-ABL1 (Breakpoint Cluster Region-Abelson 1 chimeric protein), which is known for driving the pathophysiology of但是，该疾病的变体也被认为是CML pH（ - ），但这些疾病仍然是总CML患者的一小部分。因此，提出了整个CML病理生理学是否需要BCR-ABL1融合蛋白的问题。通过随机描述，离散时间离散的马尔可夫链描述了BCR-ABL1的各种蛋白质 - 蛋白质相互作用，以更好地理解这些途径的信号传导途径和时间依赖性的演变，并提供预期的治疗蛋白靶标，以提高治疗的特异性和患者的预期。
Chronic Myeloid Leukaemia (CML) is a blood-derived proliferative disorder, which is highly associated to a translocation of chromosomes 9 and 22 or the creation of Philadelphia chromosome Ph(+) cases, inducing the synthesis of a chimeric fusion protein, namely BCR-ABL1 (Breakpoint Cluster Region-Abelson 1 chimeric protein), which is known for driving the pathophysiology of the disease, however variants of CML are also recognized as CML Ph(-), these nonetheless account for a small percentage of the overall CML patients; posing thus the question whether BCR-ABL1 fusion protein is required for the whole of the pathophysiology of CML. Hereof, through a stochastic description, a discrete time discrete Markov chain depicts the various protein-protein interactions of BCR-ABL1 to better understand signalling pathways and time-dependent evolution of these pathways, as well as to provide prospective therapeutic protein targets to improve both the specificity of the treatment and the life-expectancy of the patients.
