Elodie M. Kuntz

TL;DR: It is demonstrated that primitive CML cells rely on upregulated oxidative metabolism for their survival, and combination treatment with imatinib and tigecycline, an antibiotic that inhibits mitochondrial protein translation, selectively eradicates CML LSCs both in vitro and in a xenotransplantation model of human CML.

TL;DR: It is presented that while HCQ is ineffective, Lys05-mediated autophagy inhibition reduces LSCs quiescence and drives myeloid cell expansion, providing a strong rationale for clinical use of second generation autophagic inhibitors as a novel treatment for CML patients with LSC persistence.

TL;DR: It is demonstrated that knockdown of ATG7 results in decreased glycolysis and increased flux of labeled carbons through the mitochondrial tricarboxylic acid cycle, which leads to increased oxidative phosphorylation and mitochondrial ROS accumulation.

TL;DR: By simultaneously disrupting mitochondrial respiration and inhibiting BCR-ABL kinase activity using the antibiotic tigecycline and imatinib respectively, LSCs are effectively eradicated and disease relapse is prevented in pre-clinical animal models.

TL;DR: The antibiotic tigecycline, an inhibitor of mitochondrial translation, reduced this aberrant oxidative metabolism and selectively induced death in primitive CML cells at a clinically achievable concentration.