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Articles

Enhanced cytotoxicity of bisantrene when combined with venetoclax, panobinostat, decitabine and olaparib in acute myeloid leukemia cells

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Pages 1634-1644 | Received 15 Oct 2021, Accepted 03 Feb 2022, Published online: 20 Feb 2022

References

  • Papazoglou P, Peng L, Sachinidis A. Epigenetic mechanisms involved in the cardiovascular toxicity of anticancer drugs. Front Cardiovasc Med. 2021;8:658900.
  • Spadea A, Petti MC, Aloespiriti MA, et al. Bisantrene in relapsed and refractory acute myelogenous leukemia. Leuk Lymphoma. 1993;9(3):217–220.
  • Marinello J, Delcuratolo M, Capranico G. Anthracyclines as topoisomerase II poisons: from early studies to new perspectives. IJMS. 2018;19(11):pii:3480.
  • Su R, Dong L, Li Y, et al. Targeting FTO suppresses cancer stem cell maintenance and immune evasion. Cancer Cell. 2020;38(1):79–96.
  • Tosi P, Visani G, Colombini R, et al. Phase II study of bisantrene in relapsed/refractory acute non lymphoid leukemias (ANLL). Haematologica. 1989;74(6):555–558.
  • Mills GM, Dahlberg S, Cowan J, et al. Phase II evaluation of bisantrene in acute leukemia. A southwest oncology group study. Am J Clin Oncol. 1989;12(6):507–510.
  • Canaani J, Danylesko I, Shemtov N, et al. A phase II study of bisantrene in patients with relapsed/refractory acute myeloid leukemia. Eur J Haematol. 2021;106(2):260–266.
  • Valdez BC, Murray D, Li Y, et al. Synergism of the anthracene-derivative anti-cancer agent bisantrene with nucleoside analogs and a BCL-2 inhibitor in acute myeloid leukemia cells. J Clin Exp Oncol. 2021;10:4.
  • Naqvi K, Konopleva M, Ravandi F. Targeted therapies in acute myeloid leukemia: a focus on FLT-3 inhibitors and ABT199. Expert Rev Hematol. 2017;10(10):863–874.
  • Mihalyova J, Jelinek T, Growkova K, et al. Venetoclax: a new wave in hematooncology. Exp Hematol. 2018;61:10–25.
  • Laubach JP, Moreau P, San-Miguel JF, et al. Panobinostat for the treatment of multiple myeloma. Clin Cancer Res. 2015;21(21):4767–4773.
  • Maiso P, Colado E, Ocio EM, et al. The synergy of panobinostat plus doxorubicinin acute myeloid leukemia suggests a role for HDAC inhibitors in the control of DNA repair. Leukemia. 2009;23(12):2265–2274.
  • Wieduwilt MJ, Pawlowska N, Thomas S, et al. Histone deacetylase inhibition with panobinostat combined with intensive induction chemotherapy in older patients with acute myeloid leukemia: phase I study results. Clin Cancer Res. 2019;25(16):4917–4923.
  • Jüttermann R, Li E, Jaenisch R. Toxicity of 5-aza-2'-deoxycytidine to mammalian cells is mediated primarily by covalent trapping of DNA methyltransferase rather than DNA demethylation. Proc Natl Acad Sci U S A. 1994; 91(25):11797–11801.
  • Li K, Hu C, Mei C, et al. Sequential combination of decitabine and idarubicin synergistically enhances anti-leukemia effect followed by demethylating WNT pathway inhibitor promoters and downregulating WNT pathway nuclear target. J Transl Med. 2014;12:167.
  • Ye XN, Zhou XP, Wei JY, et al. Epigenetic priming with decitabine followed by low-dose idarubicin/cytarabine has an increased anti-leukemic effect compared to traditional chemotherapy in high-risk myeloid neoplasms. Leuk Lymphoma. 2016;57(6):1311–1318.
  • Wei H, Yu X. Functions of PARylation in DNA damage repair pathways. Genomics Proteomics Bioinformatics. 2016;14(3):131–139.
  • Murai J, Huang SY, Das BB, et al. Trapping of PARP1 and PARP2 by clinical PARP inhibitors. Cancer Res. 2012;72(21):5588–5599.
  • Molenaar RJ, Radivoyevitch T, Nagata Y, et al. IDH1/2 mutations sensitize acute myeloid leukemia to PARP inhibition and this is reversed by IDH1/2-mutant inhibitors. Clin Cancer Res. 2018;24(7):1705–1715.
  • Tavares TS, Hofman J, Lekešová A, et al. Olaparib synergizes the anticancer activity of daunorubicin via interaction with AKR1C3. Cancers (Basel). 2020;12(11):3127.
  • Valdez BC, Li Y, Murray D, et al. The synergistic cytotoxicity of clofarabine, fludarabine and busulfan in AML cells involves ATM pathway activation and chromatin remodeling. Biochem Pharmacol. 2011;81(2):222–232.
  • Valdez BC, Li Y, Murray D, et al. Comparison of the cytotoxicity of cladribine and clofarabine when combined with fludarabine and busulfan in AML cells: enhancement of cytotoxicity with epigenetic modulators. Exp Hematol. 2015;43(6):448–461.
  • Santi DV, Norment A, Garrett CE. Covalent bond formation between a DNA-cytosine methyltransferase and DNA containing 5-azacytosine. Proc Natl Acad Sci U S A. 1984;81(22):6993–6997.
  • Wyllie AH. Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation. Nature. 1980;284(5756):555–556.
  • Aoki H, Kang PM, Hampe J, et al. Direct activation of mitochondrial apoptosis machinery by c-Jun N-terminal kinase in adult cardiac myocytes. J Biol Chem. 2002;277(12):10244–10250.
  • Ichijo H. From receptors to stress-activated MAP kinases. Oncogene. 1999;18(45):6087–6093.
  • Cantley LC. The phosphoinositide 3-kinase pathway. Science. 2002;296(5573):1655–1657.
  • Morita M, Gravel SP, Hulea L, et al. mTOR coordinates protein synthesis, mitochondrial activity and proliferation. Cell Cycle. 2015;14(4):473–480.
  • Sparagana SP, Roach ES. Tuberous sclerosis complex. Curr Opin Neurol. 2000;13(2):115–119.
  • Manning BD, Tee AR, Logsdon MN, et al. Identification of the tuberous sclerosis complex-2 tumor suppressor gene product tuberin as a target of the phosphoinositide 3-kinase/akt pathway. Mol Cell. 2002;10(1):151–162.
  • Kawano Y, Kypta R. Secreted antagonists of the WNT signalling pathway. J Cell Sci. 2003;116(Pt 13):2627–2634.
  • Xie C, Drenberg C, Edwards H, et al. Panobinostat enhances cytarabine and daunorubicin sensitivities in AML cells through suppressing the expression of BRCA1, CHK1, and Rad51. PLoS ONE. 2013;8(11):e79106.
  • Al-Hamamah MA, Alotaibi MR, Ahmad SF, et al. Genetic and epigenetic alterations induced by the small-molecule panobinostat: a mechanistic study at the chromosome and gene levels. DNA Repair (Amst). 2019;78:70–80.
  • Souers AJ, Leverson JD, Boghaert ER, et al. ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets. Nat Med. 2013;19(2):202–208.
  • Hollenbach PW, Nguyen AN, Brady H, et al. A comparison of azacitidine and decitabine activities in acute myeloid leukemia cell lines. PLoS One. 2010;5(2):e9001.
  • Garcia TB, Snedeker JC, Baturin D, et al. A small-molecule inhibitor of WEE1, AZD1775, synergizes with olaparib by impairing homologous recombination and enhancing DNA damage and apoptosis in acute leukemia. Mol Cancer Ther. 2017;16(10):2058–2068.
  • Hayakawa J, Depatie C, Ohmichi M, et al. The activation of c-Jun NH2-terminal kinase (JNK) by DNA-damaging agents serves to promote drug resistance via activating transcription factor 2 (ATF2)-dependent enhanced DNA repair. J Biol Chem. 2003;278(23):20582–20592.
  • Steinhusen U, Badock V, Bauer A, et al. Apoptosis-induced cleavage of beta-catenin by caspase-3 results in proteolytic fragments with reduced transactivation potential. J Biol Chem. 2000;275(21):16345–16353.