Modelling inhibition of AKT phosphorylation in acute myeloid leukemia Available to Purchase

Constitutive activation of PI3K/AKT signaling pathway has been observed in Acute Myeloid Leukemia (AML) that caused by the mutation of Fms-like Tyrosine Kinase 3 in internal tandem duplication (FLT3-ITD). Constitutive activation of AKT resulted in the regulation of apoptosis by the growth of abnormal cells that uncontrollably (AML blast). In our previous work we had consider a mathematical model of PI3K/AKT signaling pathways in phosphorylation AKT. In this paper we carry out a modification of the model by including synthesis and degradation of proteins as well as the effect of small molecule inhibitor of PI3K/AKT pathways. Perifosine is one of a small molecule inhibitor which has been widely known in the treatment of AML as AKT inhibitor. Our simulation result suggested that the administration of Perifosine may reduce the activity of AKT Phosphorylation. This result also support of the hypothesis that PI3K/AKT pathways is a potential target theraphy in AML.