Relapse of acute myeloid leukemia (AML) is driven by populations of leukemic stem or progenitor cells (LSCs), which are resistant to chemotherapy. Here, Höckendorf et al. found the TNF superfamily member lymphotoxin alpha (Lta) as a repressor of AML. Its genetic deletion promoted AML progression in mouse AML models. Treatment with exogenous, recombinant LTα₃ induced cell death of AML progenitors and resulted in remission in mouse AML models, whereas the administration of recombinant LTα₃ did not result in cytotoxicity to healthy hematopoiesis seen in conventional therapeutic approaches. This work suggests that the stimulation of endogenous tumor-suppressive mechanisms may allow the clearing of malignant cells while preserving healthy hematopoiesis. —Amy E. Baek

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