New biological and genetic classification and therapeutically relevant categories in childhood B-cell precursor acute lymphoblastic leukemia

. 2018 ; 7 () : . [epub] 20180928

Jazyk angličtina Země Anglie, Velká Británie Médium electronic-ecollection

Typ dokumentu časopisecké články, práce podpořená grantem, přehledy

Perzistentní odkaz   https://www.medvik.cz/link/pmid30345005

Traditionally, genetic abnormalities detected by conventional karyotyping, fluorescence in situ hybridization, and polymerase chain reaction divided childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL) into well-established genetic subtypes. This genetic classification has been prognostically relevant and thus used for the risk stratification of therapy. Recently, the introduction of genome-wide approaches, including massive parallel sequencing methods (whole-genome, -exome, and -transcriptome sequencing), enabled extensive genomic studies which, together with gene expression profiling, largely expanded our understanding of leukemia pathogenesis and its heterogeneity. Novel BCP-ALL subtypes have been described. Exact identification of recurrent genetic alterations and their combinations facilitates more precise risk stratification of patients. Discovery of targetable lesions in subsets of patients enables the introduction of new treatment modalities into clinical practice and stimulates the transfer of modern methods from research laboratories to routine practice.

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Pui CH, Relling MV, Downing JR: Acute lymphoblastic leukemia. N Engl J Med. 2004;350(15):1535–48. 10.1056/NEJMra023001 PubMed DOI

Harrison CJ, Haas O, Harbott J, et al. : Detection of prognostically relevant genetic abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: recommendations from the Biology and Diagnosis Committee of the International Berlin-Frankfürt-Münster study group. Br J Haematol. 2010;151(2):132–42. 10.1111/j.1365-2141.2010.08314.x PubMed DOI

Iacobucci I, Mullighan CG: Genetic Basis of Acute Lymphoblastic Leukemia. J Clin Oncol. 2017;35(9):975–83. 10.1200/JCO.2016.70.7836 PubMed DOI PMC

Lilljebjörn H, Fioretos T: New oncogenic subtypes in pediatric B-cell precursor acute lymphoblastic leukemia. Blood. 2017;130(12):1395–401. 10.1182/blood-2017-05-742643 PubMed DOI

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(2):125–34. 10.1016/S1470-2045(08)70339-5 PubMed DOI PMC

Mullighan CG, Su X, Zhang J, et al. : Deletion of IKZF1 and prognosis in acute lymphoblastic leukemia. N Engl J Med. 2009;360(5):470–80. 10.1056/NEJMoa0808253 PubMed DOI PMC

Boer JM, Steeghs EM, Marchante JR, et al. : Tyrosine kinase fusion genes in pediatric BCR-ABL1-like acute lymphoblastic leukemia. Oncotarget. 2017;8(3):4618–28. 10.18632/oncotarget.13492 PubMed DOI PMC

Imamura T, Kiyokawa N, Kato M, et al. : Characterization of pediatric Philadelphia-negative B-cell precursor acute lymphoblastic leukemia with kinase fusions in Japan. Blood Cancer J. 2016;6:e419. 10.1038/bcj.2016.28 PubMed DOI PMC

Reshmi SC, Harvey RC, Roberts KG, et al. : Targetable kinase gene fusions in high-risk B-ALL: a study from the Children's Oncology Group. Blood. 2017;129(25):3352–61. 10.1182/blood-2016-12-758979 PubMed DOI PMC

Roberts KG, Li Y, Payne-Turner D, et al. : Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia. N Engl J Med. 2014;371(11):1005–15. 10.1056/NEJMoa1403088 PubMed DOI PMC

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(2):153–66. 10.1016/j.ccr.2012.06.005 PubMed DOI PMC

Roberts KG, Reshmi SC, Harvey RC, et al. : Genomic and outcome analyses of Ph-like ALL in NCI standard-risk patients: a report from the Children's Oncology Group. Blood. 2018;132(8):815–24. 10.1182/blood-2018-04-841676 PubMed DOI PMC

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(27):3012–20. 10.1200/JCO.2014.55.4105 PubMed DOI PMC

Zaliova M, Moorman AV, Cazzaniga G, et al. : Characterization of leukemias with ETV6-ABL1 fusion. Haematologica. 2016;101(9):1082–93. 10.3324/haematol.2016.144345 PubMed DOI PMC

Boer JM, Marchante JR, Evans WE, et al. : BCR-ABL1-like cases in pediatric acute lymphoblastic leukemia: a comparison between DCOG/Erasmus MC and COG/St. Jude signatures. Haematologica. 2015;100(9):e354–7. 10.3324/haematol.2015.124941 PubMed DOI PMC

Arber DA, Orazi A, Hasserjian R, et al. : The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. Blood. 2016;127(20):2391–405. 10.1182/blood-2016-03-643544 PubMed DOI

Roberts KG, Yang YL, Payne-Turner D, et al. : Oncogenic role and therapeutic targeting of ABL-class and JAK-STAT activating kinase alterations in Ph-like ALL. Blood Adv. 2017;1(20):1657–71. PubMed PMC

Lilljebjörn H, Henningsson R, Hyrenius-Wittsten A, et al. : Identification of ETV6-RUNX1-like and DUX4-rearranged subtypes in paediatric B-cell precursor acute lymphoblastic leukaemia. Nat Commun. 2016;7:11790. 10.1038/ncomms11790 PubMed DOI PMC

Zaliova M, Kotrova M, Bresolin S, et al. : ETV6/RUNX1-like acute lymphoblastic leukemia: A novel B-cell precursor leukemia subtype associated with the CD27/CD44 immunophenotype. Genes Chromosomes Cancer. 2017;56(8):608–16. 10.1002/gcc.22464 PubMed DOI

Vaskova M, Mejstrikova E, Kalina T, et al. : Transfer of genomics information to flow cytometry: expression of CD27 and CD44 discriminates subtypes of acute lymphoblastic leukemia. Leukemia. 2005;19(5):876–8. 10.1038/sj.leu.2403706 PubMed DOI

Mullighan CG, Miller CBS, Su X, et al. : ERG Deletions Define a Novel Subtype of B-Progenitor Acute Lymphoblastic Leukemia. Blood.(ASH Annual Meeting Abstracts).2007;110(11):691 Reference Source

Yeoh EJ, Ross ME, Shurtleff SA, et al. : Classification, subtype discovery, and prediction of outcome in pediatric acute lymphoblastic leukemia by gene expression profiling. Cancer Cell. 2002;1(2):133–43. 10.1016/S1535-6108(02)00032-6 PubMed DOI

Liu YF, Wang BY, Zhang WN, et al. : Genomic Profiling of Adult and Pediatric B-cell Acute Lymphoblastic Leukemia. EBioMedicine. 2016;8:173–83. 10.1016/j.ebiom.2016.04.038 PubMed DOI PMC

Yasuda T, Tsuzuki S, Kawazu M, et al. : Recurrent DUX4 fusions in B cell acute lymphoblastic leukemia of adolescents and young adults. Nat Genet. 2016;48(5):569–74. 10.1038/ng.3535 PubMed DOI

Zhang J, McCastlain K, Yoshihara H, et al. : Deregulation of DUX4 and ERG in acute lymphoblastic leukemia. Nat Genet. 2016;48(12):1481–9. 10.1038/ng.3691 PubMed DOI PMC

Clappier E, Auclerc MF, Rapion J, et al. : An intragenic ERG deletion is a marker of an oncogenic subtype of B-cell precursor acute lymphoblastic leukemia with a favorable outcome despite frequent IKZF1 deletions. Leukemia. 2014;28(1):70–7. 10.1038/leu.2013.277 PubMed DOI

Zaliova M, Zimmermannova O, Dörge 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(1):182–5. 10.1038/leu.2013.282 PubMed DOI

Slamova L, Starkova J, Fronkova E, et al. : CD2-positive B-cell precursor acute lymphoblastic leukemia with an early switch to the monocytic lineage. Leukemia. 2014;28(3):609–20. 10.1038/leu.2013.354 PubMed DOI

Gu Z, Churchman M, Roberts K, et al. : Genomic analyses identify recurrent MEF2D fusions in acute lymphoblastic leukaemia. Nat Commun. 2016;7:13331. 10.1038/ncomms13331 PubMed DOI PMC

Hirabayashi S, Ohki K, Nakabayashi K, et al. : ZNF384-related fusion genes define a subgroup of childhood B-cell precursor acute lymphoblastic leukemia with a characteristic immunotype. Haematologica. 2017;102(1):118–29. 10.3324/haematol.2016.151035 PubMed DOI PMC

McClure BJ, Heatley SL, Kok CH, et al. : Pre-B acute lymphoblastic leukaemia recurrent fusion, EP300-ZNF384, is associated with a distinct gene expression. Br J Cancer. 2018;118(7):1000–4. 10.1038/s41416-018-0022-0 PubMed DOI PMC

Gocho Y, Kiyokawa N, Ichikawa H, et al. : A novel recurrent EP300-ZNF384 gene fusion in B-cell precursor acute lymphoblastic leukemia. Leukemia. 2015;29(12):2445–8. 10.1038/leu.2015.111 PubMed DOI

Hrusak O, de Haas V, Stancikova J, et al. : International cooperative study identifies treatment strategy in childhood ambiguous lineage leukemia. Blood. 2018;132(3):264–76. 10.1182/blood-2017-12-821363 PubMed DOI

Shago M, Abla O, Hitzler J, et al. : Frequency and outcome of pediatric acute lymphoblastic leukemia with ZNF384 gene rearrangements including a novel translocation resulting in an ARID1B/ZNF384 gene fusion. Pediatr Blood Cancer. 2016;63(11):1915–21. 10.1002/pbc.26116 PubMed DOI

Herglotz J, Unrau L, Hauschildt F, et al. : Essential control of early B-cell development by Mef2 transcription factors. Blood. 2016;127(5):572–81. 10.1182/blood-2015-04-643270 PubMed DOI

Suzuki K, Okuno Y, Kawashima N, et al. : MEF2D-BCL9 Fusion Gene Is Associated With High-Risk Acute B-Cell Precursor Lymphoblastic Leukemia in Adolescents. J Clin Oncol. 2016;34(28):3451–9. 10.1200/JCO.2016.66.5547 PubMed DOI

Harewood L, Robinson H, Harris R, et al. : Amplification of AML1 on a duplicated chromosome 21 in acute lymphoblastic leukemia: a study of 20 cases. Leukemia. 2003;17(3):547–53. 10.1038/sj.leu.2402849 PubMed DOI

Slater R, Smit E, Kroes W, et al. : A non-random chromosome abnormality found in precursor-B lineage acute lymphoblastic leukaemia: dic(9;20)(p1?3;q11). Leukemia. 1995;9(10):1613–9. PubMed

Russell LJ, Enshaei A, Jones L, et al. : IGH@ translocations are prevalent in teenagers and young adults with acute lymphoblastic leukemia and are associated with a poor outcome. J Clin Oncol. 2014;32(14):1453–62. 10.1200/JCO.2013.51.3242 PubMed DOI

Hunger SP, Ohyashiki K, Toyama K, et al. : Hlf, a novel hepatic bZIP protein, shows altered DNA-binding properties following fusion to E2A in t(17;19) acute lymphoblastic leukemia. Genes Dev. 1992;6(9):1608–20. 10.1101/gad.6.9.1608 PubMed DOI

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(11):1243–6. 10.1038/ng.469 PubMed DOI PMC

Russell LJ, Capasso M, Vater I, et al. : Deregulated expression of cytokine receptor gene, CRLF2, is involved in lymphoid transformation in B-cell precursor acute lymphoblastic leukemia. Blood. 2009;114(13):2688–98. 10.1182/blood-2009-03-208397 PubMed DOI

Mullighan CG, Goorha S, Radtke I, et al. : Genome-wide analysis of genetic alterations in acute lymphoblastic leukaemia. Nature. 2007;446(7137):758–64. 10.1038/nature05690 PubMed DOI

Rand V, Parker H, Russell LJ, et al. : Genomic characterization implicates iAMP21 as a likely primary genetic event in childhood B-cell precursor acute lymphoblastic leukemia. Blood. 2011;117(25):6848–55. 10.1182/blood-2011-01-329961 PubMed DOI

Hunger SP, Mullighan CG: Redefining ALL classification: toward detecting high-risk ALL and implementing precision medicine. Blood. 2015;125(26):3977–87. 10.1182/blood-2015-02-580043 PubMed DOI PMC

Morak M, Attarbaschi A, Fischer S, et al. : Small sizes and indolent evolutionary dynamics challenge the potential role of P2RY8-CRLF2-harboring clones as main relapse-driving force in childhood ALL. Blood. 2012;120(26):5134–42. 10.1182/blood-2012-07-443218 PubMed DOI PMC

Ensor HM, Schwab C, Russell LJ, et al. : Demographic, clinical, and outcome features of children with acute lymphoblastic leukemia and CRLF2 deregulation: results from the MRC ALL97 clinical trial. Blood. 2011;117(7):2129–36. 10.1182/blood-2010-07-297135 PubMed DOI

Jain N, Lu X, Daver N, et al. : Co-occurrence of CRLF2-rearranged and Ph+ acute lymphoblastic leukemia: a report of four patients. Haematologica. 2017;102(12):e514–e517. 10.3324/haematol.2016.161000 PubMed DOI PMC

Heerema NA, Carroll AJ, Devidas M, et al. : Intrachromosomal amplification of chromosome 21 is associated with inferior outcomes in children with acute lymphoblastic leukemia treated in contemporary standard-risk children's oncology group studies: a report from the children's oncology group. J Clin Oncol. 2013;31(27):3397–402. 10.1200/JCO.2013.49.1308 PubMed DOI PMC

Moorman AV, Robinson H, Schwab C, et al. : Risk-directed treatment intensification significantly reduces the risk of relapse among children and adolescents with acute lymphoblastic leukemia and intrachromosomal amplification of chromosome 21: a comparison of the MRC ALL97/99 and UKALL2003 trials. J Clin Oncol. 2013;31(27):3389–96. 10.1200/JCO.2013.48.9377 PubMed DOI

Fischer U, Forster M, Rinaldi A, et al. : Genomics and drug profiling of fatal TCF3-HLF-positive acute lymphoblastic leukemia identifies recurrent mutation patterns and therapeutic options. Nat Genet. 2015;47(9):1020–9. 10.1038/ng.3362 PubMed DOI PMC

Schwab C, Nebral K, Chilton L, et al. : Intragenic amplification of PAX5: a novel subgroup in B-cell precursor acute lymphoblastic leukemia? Blood Adv. 2017;1(19):1473–7. 10.1182/bloodadvances.2017006734 PubMed DOI PMC

Boer JM, den Boer ML: BCR-ABL1-like acute lymphoblastic leukaemia: From bench to bedside. Eur J Cancer. 2017;82:203–18. 10.1016/j.ejca.2017.06.012 PubMed DOI

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(1):252–7. 10.1073/pnas.0911726107 PubMed DOI PMC

Hertzberg L, Vendramini E, Ganmore I, et al. : Down syndrome acute lymphoblastic leukemia, a highly heterogeneous disease in which aberrant expression of CRLF2 is associated with mutated JAK2: a report from the International BFM Study Group. Blood. 2010;115(5):1006–17. 10.1182/blood-2009-08-235408 PubMed DOI

Bugarin C, Sarno J, Palmi C, et al. : Fine tuning of surface CRLF2 expression and its associated signaling profile in childhood B-cell precursor acute lymphoblastic leukemia. Haematologica. 2015;100(6):e229–32. 10.3324/haematol.2014.114447 PubMed DOI PMC

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(9):936–45. 10.1016/S1470-2045(12)70377-7 PubMed DOI PMC

Andersson AK, Ma J, Wang J, et al. : The landscape of somatic mutations in infant MLL-rearranged acute lymphoblastic leukemias. Nat Genet. 2015;47(4):330–7. 10.1038/ng.3230 PubMed DOI PMC

Holmfeldt L, Wei L, Diaz-Flores E, et al. : The genomic landscape of hypodiploid acute lymphoblastic leukemia. Nat Genet. 2013;45(3):242–52. 10.1038/ng.2532 PubMed DOI PMC

Paulsson K, Lilljebjörn H, Biloglav A, et al. : The genomic landscape of high hyperdiploid childhood acute lymphoblastic leukemia. Nat Genet. 2015;47(6):672–6. 10.1038/ng.3301 PubMed DOI

Zhang J, Mullighan CG, Harvey RC, et al. : Key pathways are frequently mutated in high-risk childhood acute lymphoblastic leukemia: a report from the Children's Oncology Group. Blood. 2011;118(11):3080–7. 10.1182/blood-2011-03-341412 PubMed DOI PMC

Zaliova M, Hovorkova L, Vaskova M, et al. : Slower early response to treatment and distinct expression profile of childhood high hyperdiploid acute lymphoblastic leukaemia with DNA index < 1.16. Genes Chromosomes Cancer. 2016;55(9):727–37. 10.1002/gcc.22374 PubMed DOI

Irving J, Matheson E, Minto L, et al. : Ras pathway mutations are prevalent in relapsed childhood acute lymphoblastic leukemia and confer sensitivity to MEK inhibition. Blood. 2014;124(23):3420–30. 10.1182/blood-2014-04-531871 PubMed DOI PMC

Jerchel IS, Hoogkamer AQ, Ariës IM, et al. : RAS pathway mutations as a predictive biomarker for treatment adaptation in pediatric B-cell precursor acute lymphoblastic leukemia. Leukemia. 2018;32(4):931–40. 10.1038/leu.2017.303 PubMed DOI PMC

Duployez N, Grzych G, Ducourneau B, et al. : NUP214-ABL1 fusion defines a rare subtype of B-cell precursor acute lymphoblastic leukemia that could benefit from tyrosine kinase inhibitors. Haematologica. 2016;101(4):e133–4. 10.3324/haematol.2015.136499 PubMed DOI PMC

Kobayashi K, Miyagawa N, Mitsui K, et al. : TKI dasatinib monotherapy for a patient with Ph-like ALL bearing ATF7IP/PDGFRB translocation. Pediatr Blood Cancer. 2015;62(6):1058–60. 10.1002/pbc.25327 PubMed DOI

Lengline E, Beldjord K, Dombret H, et al. : Successful tyrosine kinase inhibitor therapy in a refractory B-cell precursor acute lymphoblastic leukemia with EBF1-PDGFRB fusion. Haematologica. 2013;98(11):e146–8. 10.3324/haematol.2013.095372 PubMed DOI PMC

Masuzawa A, Kiyotani C, Osumi T, et al. : Poor responses to tyrosine kinase inhibitors in a child with precursor B-cell acute lymphoblastic leukemia with SNX2-ABL1 chimeric transcript. Eur J Haematol. 2014;92(3):263–7. 10.1111/ejh.12234 PubMed DOI

Mayfield JR, Czuchlewski DR, Gale JM, et al. : Integration of ruxolitinib into dose-intensified therapy targeted against a novel JAK2 F694L mutation in B-precursor acute lymphoblastic leukemia. Pediatr Blood Cancer. 2017;64(5):e26328. 10.1002/pbc.26328 PubMed DOI PMC

Perwein T, Strehl S, König M, et al. : Imatinib-induced long-term remission in a relapsed RCSD1-ABL1-positive acute lymphoblastic leukemia. Haematologica. 2016;101(8):e332–5. 10.3324/haematol.2015.139568 PubMed DOI PMC

Schwab C, Ryan SL, Chilton L, et al. : EBF1-PDGFRB fusion in pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL): genetic profile and clinical implications. Blood. 2016;127(18):2214–8. 10.1182/blood-2015-09-670166 PubMed DOI

Weston BW, Hayden MA, Roberts KG, et al. : Tyrosine kinase inhibitor therapy induces remission in a patient with refractory EBF1-PDGFRB-positive acute lymphoblastic leukemia. J Clin Oncol. 2013;31(25):e413–6. 10.1200/JCO.2012.47.6770 PubMed DOI

Ding YY, Stern JW, Jubelirer TF, et al. : Clinical efficacy of ruxolitinib and chemotherapy in a child with Philadelphia chromosome-like acute lymphoblastic leukemia with GOLGA5-JAK2 fusion and induction failure. Haematologica. 2018;103(9):e427–e431. 10.3324/haematol.2018.192088 PubMed DOI PMC

Malone A, Langabeer S, O'Marcaigh A, et al. : A doctor(s) dilemma: ETV6-ABL1 positive acute lymphoblastic leukaemia. Br J Haematol. 2010;151(1):101–2. 10.1111/j.1365-2141.2010.08323.x PubMed DOI

Yeung DT, Moulton DJ, Heatley SL, et al. : Relapse of BCR-ABL1-like ALL mediated by the ABL1 kinase domain mutation T315I following initial response to dasatinib treatment. Leukemia. 2015;29(1):230–2. 10.1038/leu.2014.256 PubMed DOI

Zhang Y, Gao Y, Zhang H, et al. : PDGFRB mutation and tyrosine kinase inhibitor resistance in Ph-like acute lymphoblastic leukemia. Blood. 2018;131(20):2256–61. 10.1182/blood-2017-11-817510 PubMed DOI PMC

Slayton WB, Schultz KR, Kairalla JA, et al. : Dasatinib Plus Intensive Chemotherapy in Children, Adolescents, and Young Adults With Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia: Results of Children's Oncology Group Trial AALL0622. J Clin Oncol. 2018;36(22):2306–14. 10.1200/JCO.2017.76.7228 PubMed DOI PMC

Lukes J, Jr, Potuckova E, Sramkova L, et al. : Two novel fusion genes, AIF1L-ETV6 and ABL1-AIF1L, result together with ETV6-ABL1 from a single chromosomal rearrangement in acute lymphoblastic leukemia with prenatal origin. Genes Chromosomes Cancer. 2018;57(9):471–7. 10.1002/gcc.6 PubMed DOI

Zimmermannova O, Doktorova E, Stuchly J, et al. : An activating mutation of GNB1 is associated with resistance to tyrosine kinase inhibitors in ETV6-ABL1-positive leukemia. Oncogene. 2017;36(43):5985–94. 10.1038/onc.2017.210 PubMed DOI PMC

Zuna J, Zaliova M, Muzikova K, et al. : Acute leukemias with ETV6/ABL1 ( TEL/ABL) fusion: poor prognosis and prenatal origin. Genes Chromosomes Cancer. 2010;49(10):873–84. 10.1002/gcc.20796 PubMed DOI

Schwartzman O, Savino AM, Gombert M, et al. : Suppressors and activators of JAK-STAT signaling at diagnosis and relapse of acute lymphoblastic leukemia in Down syndrome. Proc Natl Acad Sci U S A. 2017;114(20):E4030–E4039. 10.1073/pnas.1702489114 PubMed DOI PMC

Clappier E, Grardel N, Bakkus M, et al. : IKZF1 deletion is an independent prognostic marker in childhood B-cell precursor acute lymphoblastic leukemia, and distinguishes patients benefiting from pulses during maintenance therapy: results of the EORTC Children's Leukemia Group study 58951. Leukemia. 2015;29(11):2154–61. 10.1038/leu.2015.134 PubMed DOI

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(11):1691–8. 10.1182/blood-2013-06-509794 PubMed DOI

Asai D, Imamura T, Suenobu S, et al. : IKZF1 deletion is associated with a poor outcome in pediatric B-cell precursor acute lymphoblastic leukemia in Japan. Cancer Med. 2013;2(3):412–9. 10.1002/cam4.87 PubMed DOI PMC

Chen IM, Harvey RC, Mullighan CG, et al. : Outcome modeling with CRLF2, IKZF1, JAK, and minimal residual disease in pediatric acute lymphoblastic leukemia: a Children's Oncology Group study. Blood. 2012;119(15):3512–22. 10.1182/blood-2011-11-394221 PubMed DOI PMC

Dörge 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(3):428–32. 10.3324/haematol.2011.056135 PubMed DOI PMC

Kuiper RP, Waanders E, van der Velden VH, et al. : IKZF1 deletions predict relapse in uniformly treated pediatric precursor B-ALL. Leukemia. 2010;24(7):1258–64. 10.1038/leu.2010.87 PubMed DOI

Olsson L, Castor A, Behrendtz M, et al. : Deletions of IKZF1 and SPRED1 are associated with poor prognosis in a population-based series of pediatric B-cell precursor acute lymphoblastic leukemia diagnosed between 1992 and 2011. Leukemia. 2014;28(2):302–10. 10.1038/leu.2013.206 PubMed DOI

Olsson L, Ivanov Öfverholm I, Norén-Nyström U, et al. : The clinical impact of IKZF1 deletions in paediatric B-cell precursor acute lymphoblastic leukaemia is independent of minimal residual disease stratification in Nordic Society for Paediatric Haematology and Oncology treatment protocols used between 1992 and 2013. Br J Haematol. 2015;170(6):847–58. 10.1111/bjh.13514 PubMed DOI

van der Veer A, Waanders E, Pieters R, et al. : Independent prognostic value of BCR-ABL1-like signature and IKZF1 deletion, but not high CRLF2 expression, in children with B-cell precursor ALL. Blood. 2013;122(15):2622–9. 10.1182/blood-2012-10-462358 PubMed DOI PMC

Yamashita Y, Shimada A, Yamada T, et al. : IKZF1 and CRLF2 gene alterations correlate with poor prognosis in Japanese BCR-ABL1-negative high-risk B-cell precursor acute lymphoblastic leukemia. Pediatr Blood Cancer. 2013;60(10):1587–92. 10.1002/pbc.24571 PubMed DOI

Yang YL, Hung CC, Chen JS, et al. : IKZF1 deletions predict a poor prognosis in children with B-cell progenitor acute lymphoblastic leukemia: a multicenter analysis in Taiwan. Cancer Sci. 2011;102(10):1874–81. 10.1111/j.1349-7006.2011.02031.x PubMed DOI PMC

Stanulla M, Dagdan E, Zaliova M, et al. : IKZF1 plus Defines a New Minimal Residual Disease-Dependent Very-Poor Prognostic Profile in Pediatric B-Cell Precursor Acute Lymphoblastic Leukemia. J Clin Oncol. 2018;36(12):1240–9. 10.1200/JCO.2017.74.3617 PubMed DOI

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