Metabolic characterization of imatinib-resistant BCR-ABL T315I chronic myeloid leukemia cells indicates down-regulation of glycolytic pathway and low ROS production

References

• Daley GQ, Van Etten RA, Baltimore D. Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome. Science. 1990;247:824–830.
   PubMed Web of Science ®Google Scholar
• Kominsky DJ, Klawitter J, Brown JL, et al. Abnormalities in glucose uptake and metabolism in imatinib-resistant human BCR-ABL-positive cells. Clin Cancer Res. 2009;15:3442–3450.
   PubMed Web of Science ®Google Scholar
• Barnes K, McIntosh E, Whetton AD, et al. Chronic myeloid leukaemia: an investigation into the role of Bcr-Abl-induced abnormalities in glucose transport regulation. Oncogene. 2005;24:3257–3267.
   PubMed Web of Science ®Google Scholar
• DeBerardinis RJ, Lum JJ, Hatzivassiliou G, et al. The biology of cancer: metabolic reprogramming fuels cell growth and proliferation. Cell Metab. 2008;7:11–20.
   PubMed Web of Science ®Google Scholar
• Hughes TP, Kaeda J, Branford S, et al. Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia. N Engl J Med. 2003;349:1423–1432.
   PubMed Web of Science ®Google Scholar
• Kluza J, Jendoubi M, Ballot C, et al. Exploiting mitochondrial dysfunction for effective elimination of imatinib-resistant leukemic cells. PLoS One. 2011;6:e21924.
   PubMed Web of Science ®Google Scholar
• Gorre ME, Mohammed M, Ellwood K, et al. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science. 2001;293:876–880.
   PubMed Web of Science ®Google Scholar
• Pemovska T, Johnson E, Kontro M, et al. Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation. Nature. 2015;519:102–105.
   PubMed Web of Science ®Google Scholar
• Weisberg E, Manley PW, Breitenstein W, et al. Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. Cancer Cell. 2005;7:129–141.
   PubMed Web of Science ®Google Scholar
• Scappini B, Gatto S, Onida F, et al. Changes associated with the development of resistance to imatinib (STI571) in two leukemia cell lines expressing p210 Bcr/Abl protein. Cancer. 2004;100:1459–1471.
   PubMed Web of Science ®Google Scholar
• Ricci C, Scappini B, Divoky V, et al. Mutation in the ATP-binding pocket of the ABL kinase domain in an STI571-resistant BCR/ABL-positive cell line. Cancer Res. 2002;62:5995–5998.
   PubMed Web of Science ®Google Scholar
• Beran M, Pisa P, O'Brien S, et al. Biological properties and growth in SCID mice of a new myelogenous leukemia cell line (KBM-5) derived from chronic myelogenous leukemia cells in the blastic phase. Cancer Res. 1993;53:3603–3610.
   PubMed Web of Science ®Google Scholar
• Shah NP, Nicoll JM, Nagar B, et al. Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. Cancer Cell. 2002;2:117–125.
   PubMed Web of Science ®Google Scholar
• Griswold IJ, MacPartlin M, Bumm T, et al. Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib. Mol Cell Biol. 2006;26:6082–6093.
   PubMed Web of Science ®Google Scholar
• Moreno-Sanchez R, Rodriguez-Enriquez S, Marin-Hernandez A, et al. Energy metabolism in tumor cells. FEBS J. 2007;274:1393–1418.
   PubMed Web of Science ®Google Scholar
• Pelicano H, Martin DS, Xu RH, et al. Glycolysis inhibition for anticancer treatment. Oncogene. 2006;25:4633–4646.
   PubMed Web of Science ®Google Scholar
• Hsu PP, Sabatini DM. Cancer cell metabolism: Warburg and beyond. Cell. 2008;134:703–707.
   PubMed Web of Science ®Google Scholar
• Sauer H, Wartenberg M, Hescheler J. Reactive oxygen species as intracellular messengers during cell growth and differentiation. Cell Physiol Biochem. 2001;11:173–186.
   PubMed Web of Science ®Google Scholar
• Jeon SM, Chandel NS, Hay N. AMPK regulates NADPH homeostasis to promote tumour cell survival during energy stress. Nature. 2012;485:661–665.
   PubMed Web of Science ®Google Scholar
• Redaelli S, Piazza R, Rostagno R, et al. Activity of bosutinib, dasatinib, and nilotinib against 18 imatinib-resistant BCR/ABL mutants. J Clin Oncol. 2009;27:469–471.
   PubMed Web of Science ®Google Scholar
• Mahon FX, Deininger MW, Schultheis B, et al. Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor STI571: diverse mechanisms of resistance. Blood. 2000;96:1070–1079.
   PubMed Web of Science ®Google Scholar
• Klawitter J, Kominsky DJ, Brown JL, et al. Metabolic characteristics of imatinib resistance in chronic myeloid leukaemia cells. Br J Pharmacol. 2009;158:588–600.
   PubMed Web of Science ®Google Scholar
• Azam M, Seeliger MA, Gray NS, et al. Activation of tyrosine kinases by mutation of the gatekeeper threonine. Nat Struct Mol Biol. 2008;15:1109–1118.
   PubMed Web of Science ®Google Scholar
• Cole A, Wang Z, Coyaud E, et al. Inhibition of the mitochondrial protease ClpP as a therapeutic strategy for human acute myeloid leukemia. Cancer Cell. 2015;27:864–876.
   PubMed Web of Science ®Google Scholar
• Capdeville R, Buchdunger E, Zimmermann J, et al. Glivec (STI571, imatinib), a rationally developed, targeted anticancer drug. Nat Rev Drug Discov. 2002;1:493–502.
   PubMed Web of Science ®Google Scholar
• Magnusson MK, Meade KE, Nakamura R, et al. Activity of STI571 in chronic myelomonocytic leukemia with a platelet-derived growth factor beta receptor fusion oncogene. Blood. 2002;100:1088–1091.
   PubMed Web of Science ®Google Scholar
• Burchert A, Wang Y, Cai D, et al. Compensatory PI3-kinase/Akt/mTor activation regulates imatinib resistance development. Leukemia. 2005;19:1774–1782.
   PubMed Web of Science ®Google Scholar
• Wang Y, Cai D, Brendel C, et al. Adaptive secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF) mediates imatinib and nilotinib resistance in BCR/ABL + progenitors via JAK-2/STAT-5 pathway activation. Blood. 2007;109:2147–2155.
   PubMed Web of Science ®Google Scholar
• Riganti C, Gazzano E, Polimeni M, et al. The pentose phosphate pathway: an antioxidant defense and a crossroad in tumor cell fate. Free Radic Biol Med. 2012;53:421–436.
   PubMed Web of Science ®Google Scholar