1. Greaves M. Molecular genetics, natural history and the demise of child-hood leukaemia. Eur J Cancer 1999; 35: 1941–1953.
2. Seewald L, Taub JW, Maloney KW, et al. Acute leukemias in children with Down syndrome. Mol Genet Metab 2012; 107: 25–30.
3. Inaba H, Greaves M, Mullighan CG. Acute lymphoblastic leukaemia. Lancet 2013; 381: 1943–1955.
4. Greaves M. Infection, immune responses and the aetiology of childhood leukaemia. Nat Rev Cancer 2006; 6: 193–203.
5. Preston DL, Kusumi S, Tomonaga M, et al. Cancer incidence in atomic bomb survivors. Part III. Leukemia, lymphoma and multiple myeloma, 1950–1987. Radiat Res 1994; 137: S68–S97.
6. Doll R, Wakeford R. Risk of childhood cancer from fetal irradiation. Br J Radiol 1997; 70: 130–139.
7. Bartram T, Burkhardt B, Wossmann W, et al. Childhood acute lympho-blastic leukemia-associated risk-loci IKZF1, ARID5B and CEBPE and risk of pediatric non-Hodgkin lymphoma: a report from the Berlin-Frankfurt--Munster Study Group. Leuk Lymphoma 2014: 1–3.
8. Migliorini G, Fiege B, Hosking FJ, et al. Variation at 10p12.2 and 10p14 influences risk of childhood B-cell acute lymphoblastic leukemia and phenotype. Blood 2013; 122: 3298–3307.
9. Perez-Andreu V, Roberts KG, Harvey RC, et al. Inherited GATA3 variants are associated with Ph-like childhood acute lymphoblastic leukemia and risk of relapse. Nat Genet 2013; 45: 1494–1498.
10. Ford AM, Ridge SA, Cabrera ME, et al. In utero rearrangements in the trithorax-related oncogene in infant leukaemias. Nature 1993; 363: 358–360.
11. Wiemels JL, Cazzaniga G, Daniotti M, et al. Prenatal origin of acute lymphoblastic leukaemia in children. Lancet 1999; 354: 1499–1503.
12. Greaves MF, Maia AT, Wiemels JL, et al. Leukemia in twins: lessons in natural history. Blood 2003; 102: 2321–2333.
13. Gruhn B, Taub JW, Ge Y, et al. Prenatal origin of childhood acute lymphoblastic leukemia, association with birth weight and hyperdiploidy. Leukemia 2008; 22: 1692–1697.
14. Smith MT, McHale CM, Wiemels JL, et al. Molecular biomarkers for the study of childhood leukemia. Toxicol Appl Pharmacol 2005; 206: 237–245.
15. Taub JW, Konrad MA, Ge Y, et al. High frequency of leukemic clones in newborn screening blood samples of children with B-precursor acute lymphoblastic leukemia. Blood 2002; 99: 2992–2996.
16. Burjanivova T, Madzo J, Muzikova K, et al. Prenatal origin of childhood AML occurs less frequently than in childhood ALL. BMC Cancer 2006; 6: 100.
17. Wiemels JL, Xiao Z, Buffler PA, et al. In utero origin of t(8;21) AML1--ETO translocations in childhood acute myeloid leukemia. Blood 2002; 99: 3801–3805.
18. McHale CM, Wiemels JL, Zhang L, et al. Prenatal origin of child-hood acute myeloid leukemias harboring chromosomal rearrangements t(15;17) and inv(16). Blood 2003; 101: 4640–4641.
19. Wiemels J, Kang M, Greaves M. Backtracking of leukemic clones to birth. Methods Mol Biol 2009; 538: 7–27.
20. Wiemels JL, Ford AM, Van Wering ER, et al. Protracted and variable latency of acute lymphoblastic leukemia after TEL-AML1 gene fusion in utero. Blood 1999; 94: 1057–1062.
21. Mori H, Colman SM, Xiao Z, et al. Chromosome translocations and covert leukemic clones are generated during normal fetal development. Proc Natl Acad Sci U S A 2002; 99: 8242–8247.
22. Zuna J, Madzo J, Krejci O, et al. ETV6/RUNX1 (TEL/AML1) is a frequent prenatal first hit in childhood leukemia. Blood 2011; 117: 368–369; author reply 370–361.
23. Trka J, Zuna J, Hrusak O, et al. Impact of TEL/AML1-positive patients on age distribution of childhood acute lymphoblastic leukemia in the Czech Republic. Pediatric Hematology Working Group in the Czech Republic. Leukemia 1998; 12: 996–997.
24. Greaves MF, Alexander FE. An infectious etiology for common acute lymphoblastic leukemia in childhood? Leukemia 1993; 7: 349–360.
25. Hrusak O, Trka J, Zuna J, et al. Acute lymphoblastic leukemia incidence during socioeconomic transition: selective increase in children from 1 to 4 years. Leukemia 2002; 16: 720–725.
26. Pandolfi A, Barreyro L, Steidl U. Concise review: preleukemic stem cells: molecular biology and clinical implications of the precursors to leukemia stem cells. Stem Cells Transl Med 2013; 2: 143–150.
27. Shlush LI, Minden MD. Preleukemia: the normal side of cancer. Curr Opin Hematol 2015, in press.
28. Shlush LI, Zandi S, Mitchell A, et al. Identification of pre-leukaemic hae-matopoietic stem cells in acute leukaemia. Nature 2014; 506: 328–333.
29. Kusec R, Laczika K, Knobl P, et al. AML1/ETO fusion mRNA can be detected in remission blood samples of all patients with t(8;21) acute myeloid leukemia after chemotherapy or autologous bone marrow transplantation. Leukemia 1994; 8: 735–739.
30. Miyamoto T, Nagafuji K, Akashi K, et al. Persistence of multipotent progenitors expressing AML1/ETO transcripts in long-term remission patients with t(8;21) acute myelogenous leukemia. Blood 1996; 87: 4789–4796.
31. Preudhomme C, Philippe N, Macintyre E, et al. Persistence of AML1//ETO fusion mRNA in t(8;21) acute myeloid leukemia (AML) in prolonged remission: is there a consensus? Leukemia 1996; 10: 186–188.
32. Zuna J, Burjanivova T, Mejstrikova E, et al. Covert preleukemia driven by MLL gene fusion. Genes Chromosomes Cancer 2009; 48: 98–107.
33. Ford AM, Fasching K, Panzer-Grumayer ER, et al. Origins of „late“ relapse in childhood acute lymphoblastic leukemia with TEL-AML1 fusion genes. Blood 2001; 98: 558–564.
34. Zuna J, Ford AM, Peham M, et al. TEL deletion analysis supports a novel view of relapse in childhood acute lymphoblastic leukemia. Clin Cancer Res 2004; 10: 5355–5360.
35. Bateman CM, Alpar D, Ford AM, et al. Evolutionary trajectories of hyperdiploid ALL in monozygotic twins. Leukemia 2015; 29: 58–65.
36. Hong D, Gupta R, Ancliff P, et al. Initiating and cancer-propagating cells in TEL-AML1-associated childhood leukemia. Science 2008; 319: 336–339.
37. Felix CA. Leukemias related to treatment with DNA topoisomerase II inhibitors. Med Pediatr Oncol 2001; 36: 525–535.
38. Joannides M, Grimwade D. Molecular biology of therapy-related leu-kaemias. Clin Transl Oncol 2010; 12: 8–14.
39. Anderson K, Lutz C, van Delft FW, et al. Genetic variegation of clonal architecture and propagating cells in leukaemia. Nature 2011; 469: 356–361.
40. Ding L, Ley TJ, Larson DE, et al. Clonal evolution in relapsed acute myeloid leukaemia revealed by whole-genome sequencing. Nature 2012; 481: 506–510.
41. Zuna J, Cave H, Eckert C, et al. Childhood secondary ALL after ALL treatment. Leukemia 2007; 21: 1431–1435.
42. Romana SP, Mauchauffe M, Le Coniat M, et al. The t(12;21) of acute lymphoblastic leukemia results in a tel-AML1 gene fusion. Blood 1995; 85: 3662–3670.
43. Ford AM, Palmi C, Bueno C, et al. The TEL-AML1 leukemia fusion gene dysregulates the TGF-beta pathway in early B lineage progenitor cells. J Clin Invest 2009; 119: 826–836.
44. Zaliova M, Madzo J, Cario G, et al. Revealing the role of TEL/AML1 for leukemic cell survival by RNAi-mediated silencing. Leukemia 2011; 25: 313–320.
45. Bhojwani D, Pei D, Sandlund JT, et al. ETV6-RUNX1-positive childhood acute lymphoblastic leukemia: improved outcome with contemporary therapy. Leukemia 2012; 26: 265–270.
46. Loh ML, Goldwasser MA, Silverman LB, et al. Prospective analysis of TEL/AML1-positive patients treated on Dana-Farber Cancer Institute Consortium Protocol 95-01. Blood 2006; 107: 4508–4513.
47. Zuna J, Hrusak O, Kalinova M, et al. TEL/AML1 positivity in child-hood ALL: average or better prognosis? Czech Paediatric Haematology Working Group. Leukemia 1999; 13: 22–24.
48. Zuna J, Hrusak O, Kalinova M, et al. Significantly lower relapse rate for TEL/AML1-positive ALL. Leukemia 1999; 13: 1633.
49. Paulsson K, Forestier E, Lilljebjorn H, et al. Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia. Proc Natl Acad Sci U S A 2010; 107: 21719–21724.
50. Paulsson K, Johansson B. High hyperdiploid childhood acute lymphoblastic leukemia. Genes Chromosomes Cancer 2009; 48: 637–660.
51. Paulsson K, Forestier E, Andersen MK, et al. High modal number and triple trisomies are highly correlated favorable factors in childhood B-cell precursor high hyperdiploid acute lymphoblastic leukemia treated according to the NOPHO ALL 1992/2000 protocols. Haematologica 2013; 98: 1424–1432.
52. Holmfeldt L, Wei L, Diaz-Flores E, et al. The genomic landscape of hypodiploid acute lymphoblastic leukemia. Nat Genet 2013; 45: 242–252.
53. Meyer C, Hofmann J, Burmeister T, et al. The MLL recombinome of acute leukemias in 2013. Leukemia 2013; 27: 2165–2176.
54. Meyer C, Kowarz E, Hofmann J, et al. New insights to the MLL recombinome of acute leukemias. Leukemia 2009; 23: 1490–1499.
55. Nowell PC, Hungerford DA. Chromosome studies on normal and leukemic human leukocytes. J Natl Cancer Inst 1960; 25: 85–109.
56. Rowley JD. Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature 1973; 243: 290–293
57. Melo JV. The diversity of BCR-ABL fusion proteins and their relationship to leukemia phenotype. Blood 1996; 88: 2375–2384.
58. Zaliova M, Fronkova E, Krejcikova K, et al. Quantification of fusion transcript reveals a subgroup with distinct biological properties and predicts relapse in BCR/ABL-positive ALL: implications for residual disease monitoring. Leukemia 2009; 23: 944–951.
59. Biondi A, Schrappe M, De Lorenzo P, et al. Imatinib after induction for treatment of children and adolescents with Philadelphia-chromosome--positive acute lymphoblastic leukaemia (EsPhALL): a randomised, open-label, intergroup study. Lancet Oncol 2012; 13: 936–945.
60. Schultz KR, Bowman WP, Aledo A, et al. Improved early event-free survival with imatinib in Philadelphia chromosome-positive acute lymphoblastic leukemia: a children‘s oncology group study. J Clin Oncol 2009; 27: 5175–5181.
61. Schultz KR, Pullen DJ, Sather HN, et al. Risk- and response-based classification of childhood B-precursor acute lymphoblastic leukemia: a combined analysis of prognostic markers from the Pediatric Oncology Group (POG) and Children‘s Cancer Group (CCG). Blood 2007; 109: 926–935.
62. Andersen MK, Autio K, Barbany G, et al. Paediatric B-cell precursor acute lymphoblastic leukaemia with t(1;19)(q23;p13): clinical and cytogenetic characteristics of 47 cases from the Nordic countries treated according to NOPHO protocols. Br J Haematol 2011; 155: 235–243.
63. Mullighan CG, Goorha S, Radtke I, et al. Genome-wide analysis of genetic alterations in acute lymphoblastic leukaemia. Nature 2007; 446: 758–764.
64. Mullighan CG, Miller CB, Radtke I, et al. BCR-ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros. Nature 2008; 453: 110–114.
65. Dorge P, Meissner B, Zimmermann M, et al. IKZF1 deletion is an independent predictor of outcome in pediatric acute lymphoblastic leukemia treated according to the ALL-BFM 2000 protocol. Haematologica 2013; 98: 428–432.
66. Mullighan CG, Su X, Zhang J, et al. Deletion of IKZF1 and prognosis in acute lymphoblastic leukemia. N Engl J Med 2009; 360: 470–480.
67. van der Veer A, Zaliova M, Mottadelli F, et al. IKZF1 status as a prognostic feature in BCR-ABL1-positive childhood ALL. Blood 2014; 123: 1691–1698.
68. Zaliova M, Zimmermannova O, Dorge P, et al. ERG deletion is associated with CD2 and attenuates the negative impact of IKZF1 deletion in childhood acute lymphoblastic leukemia. Leukemia 2014; 28: 182–185.
69. Mullighan CG, Collins-Underwood JR, Phillips LA, et al. Rearrangement of CRLF2 in B-progenitor- and Down syndrome-associated acute lymphoblastic leukemia. Nat Genet 2009; 41: 1243–1246.
70. Yoda A, Yoda Y, Chiaretti S, et al. Functional screening identifies CRLF2 in precursor B-cell acute lymphoblastic leukemia. Proc Natl Acad Sci U S A 2010; 107: 252–257.
71. Harvey RC, Mullighan CG, Chen IM, et al. Rearrangement of CRLF2 is associated with mutation of JAK kinases, alteration of IKZF1, Hispanic//Latino ethnicity, and a poor outcome in pediatric B-progenitor acute lymphoblastic leukemia. Blood 2010; 115: 5312–5321.
72. Den Boer ML, van Slegtenhorst M, De Menezes RX, et al. A subtype of childhood acute lymphoblastic leukaemia with poor treatment outcome: a genome-wide classification study. Lancet Oncol 2009; 10: 125–134.
73. Roberts KG, Pei D, Campana D, et al. Outcomes of children with BCR--ABL1-like acute lymphoblastic leukemia treated with risk-directed therapy based on the levels of minimal residual disease. J Clin Oncol 2014; 32: 3012–3020.
74. Mullighan CG. Molecular genetics of B-precursor acute lymphoblastic leukemia. J Clin Invest 2012; 122: 3407–3415.
75. Roberts KG, Morin RD, Zhang J, et al. Genetic alterations activating kinase and cytokine receptor signaling in high-risk acute lymphoblastic leukemia. Cancer Cell 2012; 22: 153–166.
76. Meijerink JP. Genetic rearrangements in relation to immunophenotype and outcome in T-cell acute lymphoblastic leukaemia. Best Pract Res Clin Haematol 2010; 23: 307–318.
77. Coustan-Smith E, Mullighan CG, Onciu M, et al. Early T-cell precursor leukaemia: a subtype of very high-risk acute lymphoblastic leukaemia. Lancet Oncol 2009; 10: 147–156.
78. Patrick K, Wade R, Goulden N, et al. Outcome for children and young people with early T-cell precursor acute lymphoblastic leukaemia treated on a contemporary protocol, UKALL 2003. Br J Haematol 2014; 166: 421–424.
79. Patrick K, Vora A. Update on biology and treatment of T-cell acute lymphoblastic leukaemia. Curr Opin Pediatr 2015; 27: 44–49.
80. Ley TJ, Mardis ER, Ding L, et al. DNA sequencing of a cytogenetically normal acute myeloid leukaemia genome. Nature 2008; 456: 66–72.
81. Radtke I, Mullighan CG, Ishii M, et al. Genomic analysis reveals few genetic alterations in pediatric acute myeloid leukemia. Proc Natl Acad Sci U S A 2009; 106: 12944–12949.
82. Renneville A, Roumier C, Biggio V, et al. Cooperating gene mutations in acute myeloid leukemia: a review of the literature. Leukemia 2008; 22: 915–931.
83. Takahashi S. Current findings for recurring mutations in acute myeloid leukemia. J Hematol Oncol 2011; 4: 36.
84. Steffen B, Muller-Tidow C, Schwable J, et al. The molecular pathogenesis of acute myeloid leukemia. Crit Rev Oncol Hematol 2005; 56: 195–221.
85. Downing JR. The AML1-ETO chimaeric transcription factor in acute myeloid leukaemia: biology and clinical significance. Br J Haematol 1999; 106: 296–308.
86. Larson RA, Williams SF, Le Beau MM, et al. Acute myelomonocytic leukemia with abnormal eosinophils and inv(16) or t(16;16) has a favorable prognosis. Blood 1986; 68: 1242–1249.
87. Liu P, Tarle SA, Hajra A, et al. Fusion between transcription factor CBF beta/PEBP2 beta and a myosin heavy chain in acute myeloid leukemia. Science 1993; 261: 1041–1044.
88. Creutzig U, van den Heuvel-Eibrink MM, Gibson B, et al. Diagnosis and management of acute myeloid leukemia in children and adolescents: recommendations from an international expert panel. Blood 2012; 120: 3187–3205.
89. Pollard JA, Alonzo TA, Gerbing RB, et al. Prevalence and prognostic significance of KIT mutations in pediatric patients with core binding factor AML enrolled on serial pediatric cooperative trials for de novo AML. Blood 2010; 115: 2372–2379.
90. Shimada A, Taki T, Tabuchi K, et al. KIT mutations, and not FLT3 internal tandem duplication, are strongly associated with a poor prognosis in pediatric acute myeloid leukemia with t(8;21): a study of the Japanese Childhood AML Cooperative Study Group. Blood 2006; 107: 1806–1809.
91. Huang ME, Ye YC, Chen SR, et al. Use of all-trans retinoic acid in the treatment of acute promyelocytic leukemia. Blood 1988; 72: 567–572.
92. Balgobind BV, Zwaan CM, Pieters R, et al. The heterogeneity of pediatric MLL-rearranged acute myeloid leukemia. Leukemia 2011; 25: 1239–1248.
93. Martelli MP, Sportoletti P, Tiacci E, et al. Mutational landscape of AML with normal cytogenetics: biological and clinical implications. Blood Rev 2013; 27: 13–22.
94. Campana D. Minimal residual disease monitoring in childhood acute lymphoblastic leukemia. Curr Opin Hematol 2012; 19: 313–318.
95. Gaipa G, Basso G, Biondi A, et al. Detection of minimal residual disease in pediatric acute lymphoblastic leukemia. Cytometry B Clin Cytom 2013; 84: 359–369.
96. Kalina T, Flores-Montero J, Lecrevisse Q, et al. Quality assessment program for EuroFlow protocols: Summary results of four-year (2010--2013) quality assurance rounds. Cytometry A 2014.
97. Kalina T, Flores-Montero J, van der Velden VH, et al. EuroFlow standardization of flow cytometer instrument settings and immunophenotyping protocols. Leukemia 2012; 26: 1986–2010.
98. Inaba H, Coustan-Smith E, Cao X, et al. Comparative analysis of different approaches to measure treatment response in acute myeloid leukemia. J Clin Oncol 2012; 30: 3625–3632.
99. Szczepanski T, van der Velden VH, van Dongen JJ. Flow-cytometric immunophenotyping of normal and malignant lymphocytes. Clin Chem Lab Med 2006; 44: 775–796.
100. van der Velden VH, van der Sluijs-Geling A, Gibson BE, et al. Clinical significance of flowcytometric minimal residual disease detection in pediatric acute myeloid leukemia patients treated according to the DCOG ANLL97/MRC AML12 protocol. Leukemia 2010; 24: 1599–1606.
101. Trka J, Kalinova M, Hrusak O, et al. Real-time quantitative PCR detection of WT1 gene expression in children with AML: prognostic significance, correlation with disease status and residual disease detection by flow cytometry. Leukemia 2002; 16: 1381–1389.
102. Willasch AM, Gruhn B, Coliva T, et al. Standardization of WT1 mRNA quantitation for minimal residual disease monitoring in childhood AML and implications of WT1 gene mutations: a European multicenter study. Leukemia 2009; 23: 1472–1479.
103. Szczepanski T, Harrison CJ, van Dongen JJ. Genetic aberrations in paediatric acute leukaemias and implications for management of patients. Lancet Oncol 2010; 11: 880–889.
104. Schiller J, Praulich I, Krings Rocha C, et al. Patient-specific analysis of FLT3 internal tandem duplications for the prognostication and monitoring of acute myeloid leukemia. Eur J Haematol 2012; 89: 53–62.
105. Schnittger S, Kern W, Tschulik C, et al. Minimal residual disease levels assessed by NPM1 mutation-specific RQ-PCR provide important prognostic information in AML. Blood 2009; 114: 2220–2231.
106. Szczepanski T, Flohr T, van der Velden VH, et al. Molecular monitoring of residual disease using antigen receptor genes in childhood acute lymphoblastic leukaemia. Best Pract Res Clin Haematol 2002; 15: 37–57.
107. van der Velden VH, Cazzaniga G, Schrauder A, et al. Analysis of minimal residual disease by Ig/TCR gene rearrangements: guidelines for interpretation of real-time quantitative PCR data. Leukemia 2007; 21: 604–611.
108. van Dongen JJ, Wolvers-Tettero IL. Analysis of immunoglobulin and T cell receptor genes. Part II: Possibilities and limitations in the diagnosis and management of lymphoproliferative diseases and related disorders. Clin Chim Acta 1991; 198: 93–174.
109. van Dongen JJ, Wolvers-Tettero IL. Analysis of immunoglobulin and T cell receptor genes. Part I: Basic and technical aspects. Clin Chim Acta 1991; 198: 1–91.
110. van der Velden VH, Corral L, Valsecchi MG, et al. Prognostic significance of minimal residual disease in infants with acute lymphoblastic leukemia treated within the Interfant-99 protocol. Leukemia 2009; 23: 1073–1079.
111. Logan AC, Vashi N, Faham M, et al. Immunoglobulin and T cell receptor gene high-throughput sequencing quantifies minimal residual disease in acute lymphoblastic leukemia and predicts post-transplantation relapse and survival. Biol Blood Marrow Transplant 2014; 20: 1307–1313.
112. Wu D, Emerson RO, Sherwood A, et al. Detection of minimal residual disease in B lymphoblastic leukemia by high-throughput sequencing of IGH. Clin Cancer Res 2014; 20: 4540–4548.
113. Thol F, Kolking B, Damm F, et al. Next-generation sequencing for minimal residual disease monitoring in acute myeloid leukemia patients with FLT3-ITD or NPM1 mutations. Genes Chromosomes Cancer 2012; 51: 689–695.
114. van Dongen JJ, Seriu T, Panzer-Grumayer ER, et al. Prognostic value of minimal residual disease in acute lymphoblastic leukaemia in childhood. Lancet 1998; 352: 1731–1738.
115. Conter V, Bartram CR, Valsecchi MG, et al. Molecular response to treatment redefines all prognostic factors in children and adolescents with B-cell precursor acute lymphoblastic leukemia: results in 3184 patients of the AIEOP-BFM ALL 2000 study. Blood 2010; 115: 3206–3214.
116. Eckert C, Henze G, Seeger K, et al. Use of allogeneic hematopoietic stem-cell transplantation based on minimal residual disease response improves outcomes for children with relapsed acute lymphoblastic leukemia in the intermediate-risk group. J Clin Oncol 2013; 31: 2736–2742.
117. Eckert C, von Stackelberg A, Seeger K, et al. Minimal residual disease after induction is the strongest predictor of prognosis in intermediate risk relapsed acute lymphoblastic leukaemia - long-term results of trial ALL-REZ BFM P95/96. Eur J Cancer 2013; 49: 1346–1355.
118. Bader P, Kreyenberg H, Henze GH, et al. Prognostic value of minimal residual disease quantification before allogeneic stem-cell transplantation in relapsed childhood acute lymphoblastic leukemia: the ALL-REZ BFM Study Group. J Clin Oncol 2009; 27: 377–384.
119. Krejci O, van der Velden VH, Bader P, et al. Level of minimal residual disease prior to haematopoietic stem cell transplantation predicts prognosis in paediatric patients with acute lymphoblastic leukaemia: a report of the Pre-BMT MRD Study Group. Bone Marrow Transplant 2003; 32: 849–851.
120. Stentoft J, Hokland P, Ostergaard M, et al. Minimal residual core binding factor AMLs by real time quantitative PCR--initial response to chemotherapy predicts event free survival and close monitoring of peripheral blood unravels the kinetics of relapse. Leuk Res 2006; 30: 389–395.
121. Zhang L, Cao Z, Ruan M, et al. Monitoring the AML1/ETO fusion transcript to predict outcome in childhood acute myeloid leukemia. Pediatr Blood Cancer 2014; 61: 1761–1766.
122. Loken MR, Alonzo TA, Pardo L, et al. Residual disease detected by multidimensional flow cytometry signifies high relapse risk in patients with de novo acute myeloid leukemia: a report from Children‘s Oncology Group. Blood 2012; 120: 1581–1588.
123. Rubnitz JE, Inaba H, Dahl G, et al. Minimal residual disease-directed thera py for childhood acute myeloid leukaemia: results of the AML02 multicentre trial. Lancet Oncol 2010; 11: 543–552.