Increased cellular glutathione and protection by bone marrow stromal cells account for the resistance of non-acute promylocytic leukemia acute myeloid leukemia cells to arsenic trioxidein vivo
In this issue of Blood, Marlein et al1 identify a tumor-specific NOX2-dependent transfer of mitochondria from bone marrow stromal cells (BMSCs) to acute myeloid leukemia (AML) cells via AML-derived tunneling nanotubes (see figure), supporting inhibition of NOX2 as a novel therapeutic strategy in AML.