Abstract
In this issue of Blood, Tamburini and colleagues have studied the regulation of protein translation control in primary AML cells and describe a mTORC1-independent mechanism of regulation of the translation initiation complex that can be targeted with 4EGI-1, a small molecule inhibitor of translation, leading to death of the cells.1 This and other recent studies add to a growing body of evidence that AML cells have a critical dependence on active protein translation, which may provide an Achilles' heel for the tumor cells that can be targeted therapeutically.
Reversing chemoresistance by small molecule inhibition of the translation initiation complex eIF4F
