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Impact of Genetic Targets on Cancer Therapy in Acute Myelogenous Leukemia

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Impact of Genetic Targets on Cancer Therapy

Part of the book series: Advances in Experimental Medicine and Biology ((volume 779))

Abstract

Acute myelogenous leukemia (AML) is characterized by uncontrolled proliferation of the cells of myeloid origin. It can present at all ages, but is more common in adults. It is one of the most common leukemias in adults and continues to pose significant challenge in diagnosis and long-term management.

AML is a disease at the forefront of genetic and genomic approaches to medicine. It is a disease that has witnessed rapid advances in terms of diagnosis, classification, prognosis and ultimately individualized therapy. Newly diagnosed AML patients are now routinely stratified according to cytogenetics and molecular markers which guides long-term prognosis and treatment. On the other hand, with few exceptions, the initial treatment (also known as induction treatment) of AML has been ‘one-size-fits-all’. It remains a great challenge for patients and physicians to consolidate and translate these advances into eventual success in clinic [1, 2].

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References

  1. Fernandez HF. New trends in the standard of care for initial therapy of acute myeloid leukemia. Hematol Am Soc Hematol Educ Prog. 2010;1:56–61.

    Article  Google Scholar 

  2. Löwenberg B, et al. Cytarabine dose for acute myeloid leukemia. N Engl J Med. 2011;364(11):1027–36.

    Article  PubMed  Google Scholar 

  3. Niu C, et al. Studies on treatment of acute promyelocytic leukemia with arsenic trioxide: remission induction, follow-up, and molecular monitoring in 11 newly diagnosed and 47 relapsed acute promyelocytic leukemia patients. Blood. 1999;94(10):3315–24.

    PubMed  CAS  Google Scholar 

  4. Park JH, et al. Early death rate in acute promyelocytic leukemia remains high despite all-trans retinoic acid. Blood. 2011;118(5):1248–54.

    Article  PubMed  CAS  Google Scholar 

  5. Park JH, Tallman MS. Managing acute promyelocytic leukemia without conventional chemotherapy: is it possible? Expert Rev Hematol. 2011;4(4):427–36.

    Article  PubMed  Google Scholar 

  6. Licht JD. Acute promyelocytic leukemia—weapons of mass differentiation. N Engl J Med. 2009;360(9):928–30.

    Article  PubMed  CAS  Google Scholar 

  7. Burnett AK, Knapper S. Targeting treatment in AML. Hematol Am Soc Hematol Educ Program. 2007;1:429–34.

    Article  Google Scholar 

  8. Patel JP, et al. Prognostic relevance of integrated genetic profiling in acute myeloid leukemia. N Engl J Med. 2012;366(12):1079–89.

    Article  PubMed  CAS  Google Scholar 

  9. Mayer RJ, et al. Intensive postremission chemotherapy in adults with acute myeloid leukemia. Cancer and Leukemia Group B. N Engl J Med. 1994;331(14):896–903.

    Article  PubMed  CAS  Google Scholar 

  10. Koreth J, et al. Allogeneic stem cell transplantation for acute myeloid leukemia in first complete remission. JAMA: J Am Med Assoc. 2009;301(22):2349–61.

    Article  CAS  Google Scholar 

  11. Petrie K, Zelent A. Marked for death. Nat Cell Biol. 2008;10(5):507–9.

    Article  PubMed  CAS  Google Scholar 

  12. Sanz MA, et al. Management of acute promyelocytic leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet. Blood. 2009;113(9):1875–91.

    Article  PubMed  CAS  Google Scholar 

  13. Nasr R, et al. Eradication of acute promyelocytic leukemia-initiating cells through PML-RARA degradation. Nat Med. 2008;14(12):1333–42.

    Article  PubMed  CAS  Google Scholar 

  14. Park JH, Tallman MS. Treatment of acute promyelocytic leukemia without cytotoxic chemotherapy. Oncology (Williston Park). 2011;25(8):733–41.

    Google Scholar 

  15. Mathews V, et al. Single-agent arsenic trioxide in the treatment of newly diagnosed acute promyelocytic leukemia: durable remissions with minimal toxicity. Blood. 2006;107(7):2627–32.

    Article  PubMed  CAS  Google Scholar 

  16. Foran JM. New prognostic markers in acute myeloid leukemia: perspective from the clinic. ASH Educ Prog Book. 2010;2010(1):47–55.

    Google Scholar 

  17. Döhner H, et al. Diagnosis and management of acute myeloid leukemia in adults: recommendations from an international expert panel, on behalf of the European LeukemiaNet. Blood. 2010;115(3):453–74.

    Article  PubMed  Google Scholar 

  18. Erba HP. Prognostic factors in elderly patients with AML and the implications for treatment. Hematol Am Soc Hematol Educ Program. 2007;1:420–8.

    Article  Google Scholar 

  19. Schlenk RF, et al. Mutations and treatment outcome in cytogenetically normal acute myeloid leukemia. N Engl J Med. 2008;358(18):1909–18.

    Article  PubMed  CAS  Google Scholar 

  20. Shen Y, et al. Gene mutation patterns and their prognostic impact in a cohort of 1185 patients with acute myeloid leukemia. Blood. 2011;118(20):5593–603.

    Article  PubMed  CAS  Google Scholar 

  21. Takahashi S. Downstream molecular pathways of FLT3 in the pathogenesis of acute myeloid leukemia: biology and therapeutic implications. J Hematol Oncol. 2011;4(1):13.

    Article  PubMed  CAS  Google Scholar 

  22. Sallmyr A, et al. Internal tandem duplication of FLT3 (FLT3/ITD) induces increased ROS production, DNA damage, and misrepair: implications for poor prognosis in AML. Blood. 2008;111(6):3173–82.

    Article  PubMed  CAS  Google Scholar 

  23. Pemmaraju N, et al. FLT3 inhibitors in the treatment of acute myeloid leukemia. Cancer. 2011;117(15):3293–304.

    Article  PubMed  CAS  Google Scholar 

  24. Soucy TA, et al. An inhibitor of NEDD8-activating enzyme as a new approach to treat cancer. Nature. 2009;458(7239):732–6.

    Article  PubMed  CAS  Google Scholar 

  25. Small D. FLT3 mutations: biology and treatment. ASH Educ Prog Book. 2006;1:178–84.

    Google Scholar 

  26. Fathi AT, Chabner BA. FLT3 inhibition as therapy in acute myeloid leukemia: a record of trials and tribulations. Oncologist. 2011;16(8):1162–74.

    Article  PubMed  CAS  Google Scholar 

  27. Ley TJ, et al. DNMT3A mutations in acute myeloid leukemia. N Engl J Med. 2010;363(25):2424–33.

    Article  PubMed  CAS  Google Scholar 

  28. Marie J, Lundberg AS, Ajami A. Effect of the presence of P-glycoprotein (MDR1) on the ability of AML patients to achieve complete remission: results of a meta-analysis of the literature in Journal of Clinical Oncology. ASCO Annual Meeting Proceedings (Post-Meeting Edition), 2010.

    Google Scholar 

  29. Marcucci G, et al. IDH1 and IDH2 gene mutations identify novel molecular subsets within de novo cytogenetically normal acute myeloid leukemia: a cancer and leukemia group b study. J Clin Oncol. 2010;28(14):2348–55.

    Article  PubMed  CAS  Google Scholar 

  30. Lu C, et al. IDH mutation impairs histone demethylation and results in a block to cell differentiation. Nature. 2012;483:474–8. Advance online publication.

    Article  PubMed  CAS  Google Scholar 

  31. Metzeler KH, et al. TET2 mutations improve the new European leukemianet risk classification of acute myeloid leukemia: a cancer and leukemia group b study. J Clin Oncol. 2011;29(10):1373–81.

    Article  PubMed  Google Scholar 

  32. Dombret H, Preudhomme C, Boissel N. Core binding factor acute myeloid leukemia (CBF-AML): is high-dose Ara-C (HDAC) consolidation as effective as you think? Curr Opin Hematol. 2009;16(2):92–7. doi:10.1097/MOH.0b013e3283257b18.

    Article  PubMed  CAS  Google Scholar 

  33. Klein R, Marcucci G. Familial acute myeloid leukemia (AML) with mutated CEBPA. In Pagon R, Bird T, Dolan CR editors. GeneReviews [Internet].Seattle: University of Washington; 2010.

    Google Scholar 

  34. Spoo AC, et al. CXCR4 is a prognostic marker in acute myelogenous leukemia. Blood. 2007;109(2):786–91.

    Article  PubMed  CAS  Google Scholar 

  35. Nervi B, et al. Chemosensitization of acute myeloid leukemia (AML) following mobilization by the CXCR4 antagonist AMD3100. Blood. 2009;113(24):6206–14.

    Article  PubMed  CAS  Google Scholar 

  36. Meltzer PS. Cancer genomics: small RNAs with big impacts. Nature. 2005;435(7043):745–6.

    Article  PubMed  CAS  Google Scholar 

  37. Marcucci G, et al. MicroRNA expression in cytogenetically normal acute myeloid leukemia. N Engl J Med. 2008;358(18):1919–28.

    Article  PubMed  CAS  Google Scholar 

  38. Mardis ER, et al. Recurring mutations found by sequencing an acute myeloid leukemia genome. N Engl J Med. 2009;361(11):1058–66.

    Article  PubMed  CAS  Google Scholar 

  39. Ding L, et al. Clonal evolution in relapsed acute myeloid leukaemia revealed by whole-genome sequencing. Nature. 2012;481(7382):506–10.

    Article  PubMed  CAS  Google Scholar 

  40. Walter MJ, et al. Clonal architecture of secondary acute myeloid leukemia. N Engl J Med. 2012;366(12):1090–8.

    Article  PubMed  CAS  Google Scholar 

  41. Clinical Trials. 2012. http://clinicaltrials.gov/. Accessed 12 Feb 2012.

  42. Alatrash G, Molldrem JJ. Vaccines as consolidation therapy for myeloid leukemia. Exp Rev Hematol. 2011;4(1):37–50.

    Article  Google Scholar 

  43. Rezvani K, et al. Leukemia-associated antigen-specific T-cell responses following combined PR1 and WT1 peptide vaccination in patients with myeloid malignancies. Blood. 2008;111(1):236–42.

    Article  PubMed  CAS  Google Scholar 

  44. Klisovic RB, et al. Phase I study of GTI-2040, an antisense to ribonucleotide reductase, in combination with high-dose cytarabine in patients with acute myeloid leukemia. Clin Cancer Res. 2008;14(12):3889–95.

    Article  PubMed  CAS  Google Scholar 

  45. Lal D, et al. Aflibercept exerts antivascular effects and enhances levels of anthracycline chemotherapy in vivo in human acute myeloid leukemia models. Mol Cancer Ther. 2010;9:2737–51.

    Article  PubMed  CAS  Google Scholar 

  46. Juckett M, et al. Phase II study of AZD2171 for the treatment of patients with acute myelogenous leukemia, in ASCO Annual Meeting 2011; American Society of Clinical Oncology.

    Google Scholar 

  47. Cortes JE, et al. Safety, pharmacokinetics, and efficacy of BP-100.1.01 (L-Grb-2 antisense oligonucleotide) in patients with refractory or relapsed acute myeloid leukemia (AML), Philadelphia chromosome positive chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL), and myelodysplastic syndrome (MDS). ASH Annu Meeting Abstr. 2011;118(21):3639.

    Google Scholar 

  48. Moore JO, et al. Phase 2 study of Oblimersen sodium (G3139; Bcl-2 antisense; genasense(R)) plus gemtuzumab ozogamcin (Mylotarg(R)) in elderly patients with relapsed acute myeloid leukemia (AML). ASH Annu Meeting Abstr. 2004;104(11):865.

    Google Scholar 

  49. Kolitz JE, et al. P-glycoprotein inhibition using valspodar (PSC-833) does not improve outcomes for patients younger than age 60 years with newly diagnosed acute myeloid leukemia: cancer and leukemia group b study 19808. Blood. 2010;116(9):1413–21.

    Article  PubMed  CAS  Google Scholar 

  50. Raponi M, et al. A 2-gene classifier for predicting response to the farnesyltransferase inhibitor tipifarnib in acute myeloid leukemia. Blood. 2008;111(5):2589–96.

    Article  PubMed  CAS  Google Scholar 

  51. Cripe LD, et al. Zosuquidar, a novel modulator of P-glycoprotein, does not improve the outcome of older patients with newly diagnosed acute myeloid leukemia: a randomized, placebo-controlled trial of the Eastern Cooperative Oncology Group 3999. Blood. 2010;116(20):4077–85.

    Article  PubMed  CAS  Google Scholar 

  52. Garcia-Manero G, et al. Phase II study of vorinostat in combination with idarubicin (Ida) and cytarabine (ara-C) as front line therapy in acute myelogenous leukemia (AML) or higher risk myelodysplastic syndrome (MDS). ASH Annu Meeting Abstr. 2009;114(22):1055.

    Google Scholar 

  53. Castaigne S, et al. Fractionated doses of gemtuzumab ozogamicin (GO) combined to standard chemotherapy (CT) improve event-free and overall survival in newly-diagnosed de novo aml patients aged 50–70 years old. A prospective randomized phase 3 trial from the Acute Leukemia French Association (ALFA). ASH Ann Meeting Abstr. 2011;118(21):6.

    Google Scholar 

  54. Delaunay J, et al. Addition of gemtuzumab ozogamycin to chemotherapy improves event-free survival but not overall survival of AML patients with intermediate cytogenetics not eligible for allogeneic transplantation. Results of the GOELAMS AML 2006 IR Study. ASH Annu Meet Abstr. 2011;118(21):79.

    Google Scholar 

  55. Feldman EJ, et al. Phase III randomized multicenter study of a humanized anti-CD33 monoclonal antibody, lintuzumab, in combination with chemotherapy, versus chemotherapy alone in patients with refractory or first-relapsed acute myeloid leukemia. J Clin Oncol. 2005;23(18):4110–6.

    Article  PubMed  CAS  Google Scholar 

  56. Lancet JE, et al. Lintuzumab and low-dose cytarabine compared to placebo and low-dose cytarabine in patients with untreated acute myeloid leukemia (AML) 60 years and older: results of a randomized, double-blinded phase 2b study. ASH Ann Meeting Abstr. 2011;118(21):3613.

    Google Scholar 

  57. Rosenblat T, et al. Sequential cytarabine and alpha-particle immunotherapy with bismuth-213 (213Bi)-labeled-HuM195 (lintuzumab) for acute myeloid leukemia (AML). ASH Annu Meeting Abstr. 2008;112(11):2983.

    Google Scholar 

  58. Jurcic JG, et al. Phase I trial of the targeted alpha-particle nano-generator actinium-225 (225Ac)-lintuzumab (anti-CD33; HuM195) in acute myeloid leukemia (AML). ASH Annu Meeting Abstr. 2011;118(21):768.

    Google Scholar 

  59. Stone R, Fischer T, Paquette R. A phase 1b study of midostaurin (PKC412) in combination with daunorubicin and cytarabine induction and high-dose cytarabine consolidation in patients under age 61 with newly diagnosed de novo acute myeloid leukemia: overall survival of patients whose blasts have FLT3 mutations is similar to those with wild-type FLT3., in 51st ASH Annual Meeting and Exposition New Orleans; 2009.

    Google Scholar 

  60. Stone RM, et al. A randomized phase III study of induction (daunorubicin/cytarabine) and consolidation (high-dose cytarabine) chemotherapy combined with midostaurin or placebo in treatment-naive patients with FLT3 mutated AML, in ASCO Annual Meeting, Chicago, p. TPS199; 2011.

    Google Scholar 

  61. Fischer T, et al. Phase IIB trial of oral midostaurin (PKC412), the FMS-like tyrosine kinase 3 receptor (FLT3) and multi-targeted kinase inhibitor, in patients with acute myeloid leukemia and high-risk myelodysplastic syndrome with either wild-type or mutated FLT3. J Clin Oncol. 2010;28(28):4339–45.

    Article  PubMed  CAS  Google Scholar 

  62. Knapper S, et al. A phase 2 trial of the FLT3 inhibitor lestaurtinib (CEP701) as first-line treatment for older patients with acute myeloid leukemia not considered fit for intensive chemotherapy. Blood. 2006;108(10):3262–70.

    Article  PubMed  CAS  Google Scholar 

  63. Levis M, et al. Results from a randomized trial of salvage chemotherapy followed by lestaurtinib for patients with FLT3 mutant AML in first relapse. Blood. 2011;117(12):3294–301.

    Article  PubMed  CAS  Google Scholar 

  64. Yee KWH, et al. Synergistic effect of SU11248 with cytarabine or daunorubicin on FLT3 ITD—positive leukemic cells. Blood. 2004;104(13):4202–9.

    Article  PubMed  CAS  Google Scholar 

  65. Fiedler W, et al. A phase 1 study of SU11248 in the treatment of patients with refractory or resistant acute myeloid leukemia (AML) or not amenable to conventional therapy for the disease. Blood. 2005;105(3):986–93.

    Article  PubMed  CAS  Google Scholar 

  66. Fiedler W, et al. A phase I/II study combining sunitinib with standard ara-C/daunorubicin chemotherapy in patients 60 years or older with FLT3 mutated AML. ASH Ann Meeting Abstr. 2010;116(21):3285.

    Google Scholar 

  67. Cortes J, et al. A phase I dose escalation study of KW-2449, an oral multi-kinase inhibitor against FLT3, Abl, FGFR1 and Aurora in patients with relapsed/refractory AML, ALL and MDS or resistant/intolerant CML. ASH Ann Meeting Abstr. 2008;112(11):2967.

    Google Scholar 

  68. Lee SH, et al. Complete resolution of leukemia cutis with sorafenib in an acute myeloid leukemia patient with FLT3-ITD mutation. Am J Hematol. 2009;84(10):701–2.

    Article  PubMed  Google Scholar 

  69. Safaian NN, et al. Sorafenib (Nexavar®) induces molecular remission and regression of extramedullary disease in a patient with FLT3-ITD+ acute myeloid leukemia. Leuk Res. 2009;33(2):348–50.

    Article  PubMed  CAS  Google Scholar 

  70. Ravandi F, et al. Phase I/II study of combination therapy with sorafenib, idarubicin, and cytarabine in younger patients with acute myeloid leukemia. J Clin Oncol. 2010;28(11):1856–62.

    Article  PubMed  CAS  Google Scholar 

  71. Serve H, et al. Sorafenib in combination with standard induction and consolidation therapy in elderly AML patients: results from a randomized, placebo-controlled phase II trial. ASH Annu Meeting Abstr. 2010;116(21):333.

    Google Scholar 

  72. Zhang W, et al. Acquired point mutations of TKD are responsible for sorafenib resistance in FLT3-ITD mutant AML. ASH Ann Meeting Abstr. 2011;118(21):3505.

    Google Scholar 

  73. Ferrara F. Tipifarnib and etoposide for older AML patients: from bench to bedside. Blood. 2009;113(20):4824–5.

    Article  PubMed  CAS  Google Scholar 

  74. Karp JE, et al. Phase II trial of tipifarnib as maintenance therapy in first complete remission in adults with acute myelogenous leukemia and poor-risk features. Clin Cancer Res. 2008;14(10):3077–82.

    Article  PubMed  CAS  Google Scholar 

  75. Schlenk R, et al. Interim results of a phase I/II clinical trial of belinostat in combination with idarubicin in patients with AML not suitable for standard intensive therapy. ASH Ann Meeting Abstr. 2008;112(11):1953.

    Google Scholar 

  76. Holkova B, et al. Phase I trial of belinostat and bortezomib in patients with relapsed or refractory acute leukemia, myelodysplastic syndrome, or chronic myelogenous leukemia in blast crisis. ASH Ann Meeting Abstr. 2011;118(21):2598.

    Google Scholar 

  77. Meng F, et al. Synergistic effect of panobinostat and bortezomib on chemoresistant acute myelogenous leukemia cells via Akt/NF-{kappa}B Pathway. ASH Annu Meeting Abstr. 2011;118(21):3621.

    Google Scholar 

  78. Tan PT, et al. Determination of the maximum tolerated dose of panobinostat in combination with a 5-day schedule of azacitidine in high-risk myelodysplastic syndrome and acute myeloid leukemia: planned interim analysis of a phase Ib/II study. ASH Annu Meeting Abstr. 2011;118(21):1529.

    Google Scholar 

  79. Carter BZ, et al. Antagonizing IAPs by SMAC mimetic TL32711 induces apoptosis in AML cells including AML stem/progenitor cells alone and in combination with chemotherapy. ASH Annu Meeting Abstr. 2011; 118(21):66

    Google Scholar 

  80. Meng F, et al. Synergistic effect of panobinostat and bortezomib on chemoresistant acute myelogenous leukemia cells via Akt/NF-κB pathway, in 53rd American Society of Hematology Annual Meeting and Exposition, San Diego; 2011.

    Google Scholar 

  81. Swords RT, et al. MLN4924, a novel first in class small molecule inhibitor of the Nedd8 activating enzyme (NAE), has potent activity in preclinical models of acute myeloid leukemia. ASH Ann Meeting Abstr. 2009; 114(22):1021.

    Google Scholar 

  82. Nawrocki ST, et al. Disrupting NEDD8-mediated protein turnover with MLN4924 significantly augments the efficacy of cytarabine. ASH Annu Meeting Abstr. 2010; 116(21): 3255.

    Google Scholar 

  83. Weidenaar AC, et al. Patterns of bone marrow micro vessel morphology in AML and high risk MDS predict treatment outcome following intensive chemotherapy and bevacizumab. ASH Annu Meeting Abstr. 2011;118(21):1555.

    Google Scholar 

  84. Fiedler W, et al. An open, phase I study of cediranib in patients with acute myeloid leukemia (AML). ASH Annu Meeting Abstr. 2007;110(11):895.

    Google Scholar 

  85. Legros L, et al. Treatment of MDS with excess blasts by bevacizumab is well tolerated and is associated with a decrease of VEGF plasma level. ASH Ann Meeting Abstr. 2009;114(22):2770.

    Google Scholar 

  86. Zahiragic L, et al. Bevacizumab reduces VEGF expression in patients with relapsed and/or refractory acute myeloid leukaemia (AML) without clinical antileukemic activity. ASH Annu Meeting Abstr. 2006;108(11):4543.

    Google Scholar 

  87. Pollard JA, et al. FLT3 internal tandem duplication in CD34+/CD33-precursors predicts poor outcome in acute myeloid leukemia. Blood. 2006;108(8):2764–9.

    Article  PubMed  CAS  Google Scholar 

  88. Shih L-Y, et al. Heterogeneous patterns of FLT3 Asp835 mutations in relapsed de novo acute myeloid leukemia. Clin Cancer Res. 2004;10(4):1326–32.

    Article  PubMed  CAS  Google Scholar 

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Authors and Affiliations

  1. Department of Internal Medicine, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA

    Mithun Vinod Shah

  2. Division of Hematology and Oncology and Penn State Hershey Cancer Institute, Penn State Milton S. Hershey Medical Center, Hershey, PA, 17033, USA

    Amit Barochia & Thomas P. Loughran Jr. M.D. (Professor of Medicine)

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  1. Mithun Vinod Shah
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  2. Amit Barochia
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  3. Thomas P. Loughran Jr. M.D.
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Correspondence to Thomas P. Loughran Jr. M.D. .

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    Wafik S El-Deiry

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Shah, M.V., Barochia, A., Loughran, T.P. (2013). Impact of Genetic Targets on Cancer Therapy in Acute Myelogenous Leukemia. In: El-Deiry, W. (eds) Impact of Genetic Targets on Cancer Therapy. Advances in Experimental Medicine and Biology, vol 779. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-6176-0_19

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