Structural and functional alterations of FLT3 in acute myeloid leukemia.
Structural and functional alterations of FLT3 in acute myeloid leukemia.
复制标题
DOI：
10.1158/1078-0432.ccr-08-1123
复制
发表时间：
2009-07-01
期刊：
影响因子：
--
通讯作者：
Appelbaum FR
中科院分区：
文献类型：
--
作者：
Meshinchi S;Appelbaum FR
Hematopoiesis is highly regulated through cytokine-induced stimulation of multiple signal transduction pathways in order to mediate appropriate differentiation and proliferation of specific progenitor populations. Ligand-induced stimulation of the FMS-like tyrosine kinase 3 (FLT3) leads to activation of multiple downstream effector pathways resulting in differentiation and proliferation of specific progenitor cell populations. Genomic alterations of the FLT3 gene leads to autonomous receptor activation, dysregulation of FLT3 signal transduction pathways, contributes to myeloid pathogenesis, and have been linked to response to therapy and clinical outcome. Exploring the mechanisms by which these FLT3 alterations lead to dysregulated proliferation would provide a better understanding of the molecular pathogenesis of AML and may provide insights into potential therapeutic interventions.
