References
- Apperley JF. Chronic myeloid leukaemia. Lancet. 2015;385(9976):1447–1459.
- de Lavallade H. Chronic myeloid leukaemia. Medicine. 2013;41(5):275–277.
- Nowell P, Hungerford D. A minute chromosome in human chronic granulocytic leukemia. Science. 1960;132:1497.
- Apperley JF. Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia. Lancet Oncol. 2007;8(11):1018–1029.
- Druker BJ, Tamura S, Buchdunger E, et al. Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells. Nat Med. 1996;2(5):561–566.
- Buchdunger E, Zimmermann J, Mett H, et al. Inhibition of the Abl protein-tyrosine kinase in vitro and in vivo by a 2-phenylaminopyrimidine derivative. Cancer Res. 1996;56(1):100–104.
- Jabbour E, Kantarjian H. Chronic myeloid leukemia: 2018 update on diagnosis, therapy and monitoring. Am J Hematol. 2018;93(3):442–459.
- Rossari F, Minutolo F, Orciuolo E. Past, present, and future of Bcr-Abl inhibitors: from chemical development to clinical efficacy. J Hematol Oncol. 2018;11(1):84.
- Zhang J, Adrian FJ, Jahnke W, et al. Targeting Bcr-Abl by combining allosteric with ATP-binding-site inhibitors. Nature. 2010;463(7280):501–506.
- Eide CA, Zabriskie MS, Savage Stevens SL, et al. Combining the allosteric inhibitor asciminib with ponatinib suppresses emergence of and restores efficacy against highly resistant BCR-ABL1 mutants. Cancer Cell. 2019;36(4):431–443 e5.
- de Lavallade H, Apperley JF, Khorashad JS, et al. Imatinib for newly diagnosed patients with chronic myeloid leukemia: incidence of sustained responses in an intention-to-treat analysis. J Clin Oncol. 2008;26(20):3358–3363.
- Lucas CM, Wang L, Austin GM, et al. A population study of imatinib in chronic myeloid leukaemia demonstrates lower efficacy than in clinical trials. Leukemia. 2008;22(10):1963–1966.
- Paltoglou S, Roberts BJ. HIF-1alpha and EPAS ubiquitination mediated by the VHL tumour suppressor involves flexibility in the ubiquitination mechanism, similar to other RING E3 ligases. Oncogene. 2007;26(4):604–609.
- Ema M, Hirota K, Mimura J, et al. Molecular mechanisms of transcription activation by HLF and HIF1alpha in response to hypoxia: their stabilization and redox signal-induced interaction with CBP/p300. Embo J. 1999;18(7):1905–1914.
- Masoud GN, Li W. HIF-1α pathway: role, regulation and intervention for cancer therapy. Acta Pharm Sin B. 2015;5(5):378–389.
- Ai Z, Lu Y, Qiu S, et al. Overcoming cisplatin resistance of ovarian cancer cells by targeting HIF-1-regulated cancer metabolism. Cancer Lett. 2016;373(1):36–44.
- Shukla SK, Purohit V, Mehla K, et al. MUC1 and HIF-1alpha signaling crosstalk induces anabolic glucose metabolism to impart gemcitabine resistance to pancreatic cancer. Cancer Cell. 2017;32(1):71–87 e7.
- Raninga PV, Di Trapani G, Vuckovic S, et al. TrxR1 inhibition overcomes both hypoxia-induced and acquired bortezomib resistance in multiple myeloma through NF-кβ inhibition. Cell Cycle. 2016;15(4):559–572.
- Soni S, Padwad YS. HIF-1 in cancer therapy: two decade long story of a transcription factor. Acta Oncol. 2017;56(4):503–515.
- Giuntoli S, Rovida E, Barbetti V, et al. Hypoxia suppresses BCR/Abl and selects imatinib-insensitive progenitors within clonal CML populations. Leukemia. 2006;20(7):1291–1293.
- Giuntoli S, Tanturli M, Di Gesualdo F, et al. Glucose availability in hypoxia regulates the selection of chronic myeloid leukemia progenitor subsets with different resistance to imatinib-mesylate. Haematologica. 2011;96(2):204–212.
- Ng KP, Manjeri A, Lee KL, et al. Physiologic hypoxia promotes maintenance of CML stem cells despite effective BCR-ABL1 inhibition. Blood. 2014;123(21):3316–3326.
- Tanturli M, Giuntoli S, Barbetti V, et al. Hypoxia selects bortezomib-resistant stem cells of chronic myeloid leukemia. PLoS One. 2011;6(2):e17008.
- Nimmanapalli R, Bali P, O'Bryan E, et al. Arsenic trioxide inhibits translation of mRNA of bcr-abl, resulting in attenuation of Bcr-Abl levels and apoptosis of human leukemia cells. Cancer Res. 2003; 63(22):7950–7958.
- Brugarolas J, Lei K, Hurley RL, et al. Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1/TSC2 tumor suppressor complex. Genes Dev. 2004;18(23):2893–2904.
- DeYoung MP, Horak P, Sofer A, et al. Hypoxia regulates TSC1/2-mTOR signaling and tumor suppression through REDD1-mediated 14-3-3 shuttling. Genes Dev. 2008;22(2):239–251.
- Marhold M, Tomasich E, El-Gazzar A, et al. HIF1α regulates mTOR signaling and viability of prostate cancer stem cells. Mol Cancer Res. 2015;13(3):556–564.
- Kishi K. A new leukemia cell line with Philadelphia chromosome characterized as basophil precursors. Leuk Res. 1985;9(3):381–390.
- Lozzio BB, Lozzio CB, Bamberger EG, et al. A multipotential leukemia cell line (K-562) of human origin. Proc Soc Exp Biol Med. 1981;166(4):546–550.
- Clapper E, Wang S, Raninga PV, et al. Cross-talk between Bcr-abl and the thioredoxin system in chronic myeloid leukaemia: implications for CML treatment. Antioxidants (Basel). 2020;9(3):207.
- Sze JH, Raninga PV, Nakamura K, et al. Anticancer activity of a Gold(I) phosphine thioredoxin reductase inhibitor in multiple myeloma. Redox Biol. 2020;28:101310.
- Au PC, Helliwell C, Wang MB. Characterizing RNA-protein interaction using cross-linking and metabolite supplemented nuclear RNA-immunoprecipitation. Mol Biol Rep. 2014;41(5):2971–2977.
- Lawless SJ, Kedia-Mehta N, Walls JF, et al. Glucose represses dendritic cell-induced T cell responses. Nat Commun. 2017;8:15620.
- Chen C, Tang Q, Zhang Y, et al. Metabolic reprogramming by HIF-1 activation enhances survivability of human adipose-derived stem cells in ischaemic microenvironments. Cell Prolif. 2017;50(5):e12363.
- Shoshani T, Faerman A, Mett I, et al. Identification of a novel hypoxia-inducible factor 1-responsive gene, RTP801, involved in apoptosis. Mol Cell Biol. 2002;22(7):2283–2293.
- Hagner PR, Mazan-Mamczarz K, Dai B, et al. Ribosomal protein S6 is highly expressed in non-Hodgkin lymphoma and associates with mRNA containing a 5' terminal oligopyrimidine tract. Oncogene. 2011;30(13):1531–1541.
- Eliasson P, Jonsson JI. The hematopoietic stem cell niche: low in oxygen but a nice place to be. J Cell Physiol. 2010;222(1):17–22.
- Parmar K, Mauch P, Vergilio JA, et al. Distribution of hematopoietic stem cells in the bone marrow according to regional hypoxia. Proc Natl Acad Sci USA. 2007;104(13):5431–5436.
- Huang ZY, Zhang LH, Zhao C, et al. High HIF-1alpha expression predicts poor prognosis of patients with colon adenocarcinoma. Int J Clin Exp Pathol. 2018;11(12):5635–5646.
- Jogi A, Ehinger A, Hartman L, et al. Expression of HIF-1α is related to a poor prognosis and tamoxifen resistance in contralateral breast cancer. PLoS One. 2019;14(12):e0226150.
- Barliya T, Mandel M, Livnat T, et al. Degradation of HIF-1alpha under hypoxia combined with induction of Hsp90 polyubiquitination in cancer cells by hypericin: a unique cancer therapy. PLoS One. 2011;6(9):e22849.
- Fumagalli S, Thomas G. S6 phosphorylation and signal transduction. Translational Control of Gene Expression. Mathews MB. 2000.
- Knaup KX, Jozefowski K, Schmidt R, et al. Mutual regulation of hypoxia-inducible factor and mammalian target of rapamycin as a function of oxygen availability. Mol Cancer Res. 2009;7(1):88–98.
- Dengler VL, Galbraith M, Espinosa JM. Transcriptional regulation by hypoxia inducible factors. Crit Rev Biochem Mol Biol. 2014;49(1):1–15.
- Liu W, Shen SM, Zhao XY, et al. Targeted genes and interacting proteins of hypoxia inducible factor-1. Int J Biochem Mol Biol. 2012;3(2):165–178.
- Jabbour EJ, Cortes JE, Kantarjian HM. Resistance to tyrosine kinase inhibition therapy for chronic myelogenous leukemia: a clinical perspective and emerging treatment options. Clin Lymphoma Myeloma Leuk. 2013;13(5):515–529.