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Original Articles: Clinical

KIT mutations correlate with adverse survival in children with core-binding factor acute myeloid leukemia

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Pages 829-836 | Received 02 Apr 2017, Accepted 24 Jul 2017, Published online: 09 Aug 2017

References

  • Grimwade D, Walker H, Oliver F, et al. The importance of diagnostic cytogenetics on outcome in AML: analysis of 1,612 patients entered into the MRC AML 10 trial. The Medical Research Council Adult and Children’s Leukaemia Working Parties. Blood. 1998;92:2322–2333.
  • Downing JR. The AML1-ETO chimaeric transcription factor in acute myeloid leukaemia: biology and clinical significance. Br J Haematol. 1999;106:296–308.
  • Byrd JC, Ruppert AS, Mrozek K, et al. Repetitive cycles of high-dose cytarabine benefit patients with acute myeloid leukemia and inv(16)(p13q22) or t(16;16)(p13;q22): results from CALGB 8461. JCO. 2004;22:1087–1094.
  • Paschka P, Marcucci G, Ruppert AS, et al. Adverse prognostic significance of KIT mutations in adult acute myeloid leukemia with inv(16) and t(8;21): a Cancer and Leukemia Group B Study. JCO. 2006;24:3904–3911.
  • Castilla LH, Garrett L, Adya N, et al. The fusion gene Cbfb-MYH11 blocks myeloid differentiation and predisposes mice to acute myelomonocytic leukaemia. Nat Genet. 1999;23:144–146.
  • Hart SM, Foroni L. Core binding factor genes and human leukemia. Haematologica. 2002;87:1307–1323.
  • Kitayama H, Tsujimura T, Matsumura I, et al. Neoplastic transformation of normal hematopoietic cells by constitutively activating mutations of c-kit receptor tyrosine kinase. Blood. 1996;88:995–1004.
  • d'Auriol L, Mattei MG, Andre C, et al. Localization of the human c-kit protooncogene on the q11-q12 region of chromosome 4. Hum Genet. 1988;78:374–376.
  • 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.
  • 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.
  • Faber ZJ, Chen X, Gedman AL, et al. The genomic landscape of core-binding factor acute myeloid leukemias. Nat Genet. 2016;48:1551–1556.
  • Allen C, Hills RK, Lamb K, et al. The importance of relative mutant level for evaluating impact on outcome of KIT, FLT3 and CBL mutations in core-binding factor acute myeloid leukemia. Leukemia. 2013;27:1891–1901.
  • Cairoli R, Beghini A, Grillo G, et al. Prognostic impact of c-KIT mutations in core binding factor leukemias: an Italian retrospective study. Blood. 2006;107:3463–3468.
  • Wang D, Qiao C, Xiao M, et al. Integrative analysis of prognostic factors in Chinese core binding factor leukemia. Biochem Biophys Res Commun. 2012;428:411–415.
  • Krauth MT, Eder C, Alpermann T, et al. High number of additional genetic lesions in acute myeloid leukemia with t(8;21)/RUNX1-RUNX1T1: frequency and impact on clinical outcome. Leukemia. 2014;28:1449–1458.
  • Goemans BF, Zwaan CM, Miller M, et al. Mutations in KIT and RAS are frequent events in pediatric core-binding factor acute myeloid leukemia. Leukemia. 2005;19:1536–1542.
  • Tokumasu M, Murata C, Shimada A, et al. Adverse prognostic impact of KIT mutations in childhood CBF-AML: the results of the Japanese Pediatric Leukemia/Lymphoma Study Group AML-05 trial. Leukemia. 2015;29:2438–2441.
  • Chen W, Xie H, Wang H, et al. Prognostic significance of KIT mutations in core-binding factor acute myeloid leukemia: a systematic review and meta-analysis. PLoS One. 2016;11:e0146614.
  • Gu R-J, Lv S-G, Sun G-X, et al. Childhood acute myeloid leukemia diagnosis and therapy recommendations. Chin J Pediatric. 2006;44:877–879.
  • Shaffer LJM-J, Schmid M. An international system for human cytogenetic nomenclature. Basel (Switzerland): S. Karger AG; 2013.
  • Al-Ali HK, Heinrich MC, Lange T, et al. High incidence of BCR-ABL kinase domain mutations and absence of mutations of the PDGFR and KIT activation loops in CML patients with secondary resistance to imatinib. Hematol J. 2004;5:55–60.
  • Stirewalt DL, Kopecky KJ, Meshinchi S, et al. Size of FLT3 internal tandem duplication has prognostic significance in patients with acute myeloid leukemia. Blood. 2006;107:3724–3726.
  • Thiede C, Steudel C, Mohr B, et al. Analysis of FLT3-activating mutations in 979 patients with acute myelogenous leukemia: association with FAB subtypes and identification of subgroups with poor prognosis. Blood. 2002;99:4326–4335.
  • Ahmad F, Mandava S, Das BR. Mutations of NPM1 gene in de novo acute myeloid leukaemia: determination of incidence, distribution pattern and identification of two novel mutations in Indian population. Hematol Oncol. 2009;27:90–97.
  • Brown P, McIntyre E, Rau R, et al. The incidence and clinical significance of nucleophosmin mutations in childhood AML. Blood. 2007;110:979–985.
  • Gombart AF, Hofmann WK, Kawano S, et al. Mutations in the gene encoding the transcription factor CCAAT/enhancer binding protein alpha in myelodysplastic syndromes and acute myeloid leukemias. Blood. 2002;99:1332–1340.
  • Lin LI, Chen CY, Lin DT, et al. Characterization of CEBPA mutations in acute myeloid leukemia: most patients with CEBPA mutations have biallelic mutations and show a distinct immunophenotype of the leukemic cells. Clin Cancer Res. 2005;11:1372–1379.
  • Chen X, Yang Y, Huang Y, et al. WT1 mutations and single nucleotide polymorphism rs16754 analysis of patients with pediatric acute myeloid leukemia in a Chinese population. Leuk Lymphoma. 2012;53:2195–2204.
  • Shih LY, Liang DC, Huang CF, et al. Cooperating mutations of receptor tyrosine kinases and Ras genes in childhood core-binding factor acute myeloid leukemia and a comparative analysis on paired diagnosis and relapse samples. Leukemia. 2008;22:303–307.
  • Klein K, Kaspers G, Harrison CJ, et al. Clinical impact of additional cytogenetic aberrations, cKIT and RAS mutations, and treatment elements in pediatric t(8;21)-AML: results From an International Retrospective Study by the International Berlin-Frankfurt-Munster Study Group. JCO. 2015;33:4247–4258.
  • Cheng Y, Wang Y, Wang H, et al. Cytogenetic profile of de novo acute myeloid leukemia: a study based on 1432 patients in a single institution of China. Leukemia. 2009;23:1801–1806.
  • Appelbaum FR, Kopecky KJ, Tallman MS, et al. The clinical spectrum of adult acute myeloid leukaemia associated with core binding factor translocations. Br J Haematol. 2006;135:165–173.
  • Boissel N, Leroy H, Brethon B, et al. Incidence and prognostic impact of c-Kit, FLT3, and Ras gene mutations in core binding factor acute myeloid leukemia (CBF-AML). Leukemia. 2006;20:965–970.
  • Qin YZ, Zhu HH, Jiang Q, et al. Prevalence and prognostic significance of c-KIT mutations in core binding factor acute myeloid leukemia: a comprehensive large-scale study from a single Chinese center. Leuk Res. 2014;38:1435–1440.
  • Riera L, Marmont F, Toppino D, et al. Core binding factor acute myeloid leukaemia and c-KIT mutations. Oncol Rep. 2013;29:1867–1872.
  • Paschka P, Dohner K. Core-binding factor acute myeloid leukemia: can we improve on HiDAC consolidation? Hematol Am Soc Hematol Educ Prog. 2013;2013:209–219.
  • Park SH, Lee HJ, Kim IS, et al. Incidences and prognostic impact of c-KIT, WT1, CEBPA, and CBL mutations, and mutations associated with epigenetic modification in core binding factor acute myeloid leukemia: a multicenter study in a Korean population. Ann Lab Med. 2015;35:288–297.
  • 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.
  • Kohl TM, Schnittger S, Ellwart JW, et al. KIT exon 8 mutations associated with core-binding factor (CBF)-acute myeloid leukemia (AML) cause hyperactivation of the receptor in response to stem cell factor. Blood. 2005;105:3319–3321.
  • Growney JD, Clark JJ, Adelsperger J, et al. Activation mutations of human c-KIT resistant to imatinib mesylate are sensitive to the tyrosine kinase inhibitor PKC412. Blood. 2005;106:721–724.
  • Schnittger S, Kohl TM, Haferlach T, et al. KIT-D816 mutations in AML1-ETO-positive AML are associated with impaired event-free and overall survival. Blood. 2006;107:1791–1799.
  • Meshinchi S, Stirewalt DL, Alonzo TA, et al. Activating mutations of RTK/ras signal transduction pathway in pediatric acute myeloid leukemia. Blood. 2003;102:1474–1479.
  • Care RS, Valk PJ, Goodeve AC, et al. Incidence and prognosis of c-KIT and FLT3 mutations in core binding factor (CBF) acute myeloid leukaemias. Br J Haematol. 2003;121:775–777.
  • Dohner H, Weisdorf DJ, Bloomfield CD. Acute myeloid leukemia. N Engl J Med. 2015;373:1136–1152.
  • Manara E, Bisio V, Masetti R, et al. Core-binding factor acute myeloid leukemia in pediatric patients enrolled in the AIEOP AML 2002/01 trial: screening and prognostic impact of c-KIT mutations. Leukemia. 2014;28:1132–1134.
  • Lange BJ, Dinndorf P, Smith FO, et al. Pilot study of idarubicin-based intensive-timing induction therapy for children with previously untreated acute myeloid leukemia: Children’s Cancer Group Study 2941. JCO. 2004;22:150–156.
  • Ravindranath Y, Chang M, Steuber CP, et al. Pediatric Oncology Group (POG) studies of acute myeloid leukemia (AML): a review of four consecutive childhood AML trials conducted between 1981 and 2000. Leukemia. 2005;19:2101–2116.
  • Woods WG, Kobrinsky N, Buckley JD, et al. Timed-sequential induction therapy improves postremission outcome in acute myeloid leukemia: a report from the Children’s Cancer Group. Blood. 1996;87:4979–4989.
  • Whitman SP, Archer KJ, Feng L, et al. Absence of the wild-type allele predicts poor prognosis in adult de novo acute myeloid leukemia with normal cytogenetics and the internal tandem duplication of FLT3: a cancer and leukemia group B study. Cancer Res. 2001;61:7233–7239.
  • Pratz KW, Sato T, Murphy KM, et al. FLT3-mutant allelic burden and clinical status are predictive of response to FLT3 inhibitors in AML. Blood. 2010;115:1425–1432.

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