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Mol Cell Oncol. 2017 Dec 18;5(1):e1403532. doi: 10.1080/23723556.2017.1403532. eCollection 2018.

Auto-Commentary on: "Targeting mitochondrial oxidative phosphorylation eradicates therapy-resistant chronic myeloid leukemia stem cells".

Molecular & cellular oncology

Lucie de Beauchamp, Pablo Baquero, Elodie M Kuntz, Eyal Gottlieb, G Vignir Helgason

Affiliations

  1. Wolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, College of Medical, Veterinary & Life Sciences, University of Glasgow, Glasgow UK.
  2. Cancer Research UK, Beatson Institute, Garscube Estate, Switchback Road, Glasgow, UK.
  3. Technion Integrated Cancer Center, Faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel.

PMID: 29404396 PMCID: PMC5791851 DOI: 10.1080/23723556.2017.1403532

Abstract

We have recently uncovered an abnormal increase in mitochondrial oxidative metabolism in therapy-resistant chronic myeloid leukaemia stem cells (LSCs). By simultaneously disrupting mitochondrial respiration and inhibiting BCR-ABL kinase activity using the antibiotic tigecycline and imatinib respectively, we effectively eradicated LSCs and prevented disease relapse in pre-clinical animal models.

Keywords: CML; Cancer stem cells; Imatinib; Leukaemia; Metabolism; OXPHOS; TCA cycle; Tigecycline; Tyrosine kinase inhibitor

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