Spred1 Deficit Promotes Treatment Resistance and Transformation of Chronic Phase CML

Spred1 knockout, regardless if occurred in HSCs or in endothelial cells, increased miR-126 in Lin−Sca-1+c-Kit+, a population enriched in leukemic stem cells (LSCs), resulting in expansion of LSCs, likely through hyperactivation of the MAPK/ERK pathway that augmented Bcl-2 expression and stability.