• 1
    Gilliland DG. Molecular genetics of human leukemias: new insights into therapy. Semin Hematol. 2002; 39: 6-11.
  • 2
    Downing JR. The core-binding factor leukemias: lessons learned from murine models. Curr Opin Genet Dev. 2003; 13: 48-54.
  • 3
    Speck NA, Gilliland DG. Core-binding factors in haematopoiesis and leukaemia. Nat Rev Cancer. 2002; 2: 502-513.
  • 4
    Nucifora G, Begy CR, Erickson P, Drabkin HA, Rowley JD. The 3;21 translocation in myelodysplasia results in a fusion transcript between the AML1 gene and the gene for EAP, a highly conserved protein associated with the Epstein-Barr virus small RNA EBER 1. Proc Natl Acad Sci U S A. 1993; 90: 7784-7788.
  • 5
    Mitani K, Ogawa S, Tanaka T, et al. Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia. EMBO J. 1994; 13: 504-510.
  • 6
    Nucifora G, Begy CR, Kobayashi H, et al. Consistent intergenic splicing and production of multiple transcripts between AML1 at 21q22 and unrelated genes at 3q26 in (3;21)(q26;q22) translocations. Proc Natl Acad Sci U S A. 1994; 91: 4004-4008.
  • 7
    Jaffe ES, Harris NL, Stein H, Vardiman JW. World Health Organization classification of tumours. Pathology and genetics of tumours of haematopoietic and lymphoid tissues. Lyon: IARC Press; 2001.
  • 8
    Hao S, Sanger W, Onciu M, Lai R, Schlette EJ, Medeiros LJ. Mantle cell lymphoma with 8q24 chromosomal abnormalities: a report of 5 cases with blastoid features. Mod Pathol. 2002; 15: 1266-1272.
  • 9
    Yin CC, Medeiros LJ, Glassman AB, Lin P. t(8;21)(q22;q22) in blast phase of chronic myelogenous leukemia. Am J Clin Pathol. 2004; 121: 836-842.
  • 10
    Zent C, Kim N, Hiebert S, et al. Rearrangement of the AML1/CBFA2 gene in myeloid leukemia with the 3;21 translocation: expression of co-existing multiple chimeric genes with similar functions as transcriptional repressors, but with opposite tumorigenic properties. Curr Top Microbiol Immunol. 1996; 211: 243-252.
  • 11
    Senyuk V, Chakraborty S, Mikhail FM, Zhao R, Chi Y, Nucifora G. The leukemia-associated transcription repressor AML1/MDS1/EVI1 requires CtBP to induce abnormal growth and differentiation of murine hematopoietic cells. Oncogene. 2002; 21: 3232-3240.
  • 12
    Senyuk V, Sinha KK, Chakraborty S, Buonamici S, Nucifora G. P/CAF and GCN5 acetylate the AML1/MDS1/EVI1 fusion oncoprotein. Biochem Biophys Res Commun. 2003; 307: 980-986.
  • 13
    Helbling D, Mueller BU, Timchenko NA, et al. The leukemic fusion gene AML1-MDS1-EVI1 suppresses CEBPA in acute myeloid leukemia by activation of calreticulin. Proc Natl Acad Sci U S A. 2004; 101: 13312-13317.
  • 14
    Fears S, Mathieu C, Zelezni-Le N, Huang S, Rowley JD, Nucifora G. Intergenic splicing of MDS1 and EVI1 occurs in normal tissues as well as in myeloid leukemia and produces a new member of the PR domain family. Proc Natl Acad Sci U S A. 1996; 93: 1642-1647.
  • 15
    Sood R, Talwar-Trikha A, Chakrabarti SR., Nucifora G. MDS1/EVI1 enhances TGF-beta1 signaling and strengthens its growth-inhibitory effect but the leukemia-associated fusion protein AML1/MDS1/EVI1, product of the t(3;21), abrogates growth-inhibition in response to TGF-beta1. Leukemia. 1999; 13: 348-357.
  • 16
    Morishita K, Suzukawa K, Taki T, Ihle JN, Yokota J. EVI-1 zinc finger protein works as a transcriptional activator via binding to a consensus sequence of GACAAGATAAGATAAN1–28 CTCATCTTC. Oncogene. 1995; 10: 1961-1967.
  • 17
    Mitani K. Molecular mechanisms of leukemogenesis by AML1/EVI-1. Oncogene. 2004; 23: 4263-4269.
  • 18
    Faderl S, Talpaz M, Estrov Z, O'Brien S, Kurzrock R, Kantarjian HM. The biology of chronic myeloid leukemia. N Engl J Med. 1999; 341: 164-172.
  • 19
    Cortes J, O'Dwyer ME. Clonal evolution in chronic myelogenous leukemia. Hematol Oncol Clin North Am. 2004; 18: 671-684.
  • 20
    Cuenco GM, Ren R. Both AML1 and EVI1 oncogenic components are required for the cooperation of AML1/MDS1/EVI1 with BCR/ABL in the induction of acute myelogenous leukemia in mice. Oncogene. 2004; 23: 569-579.
  • 21
    Andersen MK, Christiansen DH, Pedersen-Bjergaard J. Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML. Leukemia. 2005; 19: 197-200.
  • 22
    Slovak ML, Bedell V, Popplewell L, Arber DA, Schoch C, Slater R. 21q22 balanced chromosome aberrations in therapy-related hematopoietic disorders: report from an international workshop. Genes Chromosomes Cancer. 2002; 33: 379-394.
  • 23
    Pedersen-Bjergaard J, Philip P. Balanced translocations involving chromosome bands 11q23 and 21q22 are highly characteristic of myelodysplasia and leukemia following therapy with cytostatic agents targeting at DNA-topoisomerase II. Blood. 1991; 78: 1147-1148.
  • 24
    Nielsen I, Hasselbalch HC. Acute leukemia and myelodysplasia in patients with a Philadelphia chromosome negative chronic myeloproliferative disorder treated with hydroxyurea alone or with hydroxyurea after busulphan. Am J Hematol. 2003; 74: 26-31.
  • 25
    Bernasconi P, Boni M, Cavigliano PM, et al. Acute myeloid leukemia (AML) having evolved from essential thrombocythemia (ET): distinctive chromosome abnormalities in patients treated with pipobroman or hydroxyurea. Leukemia. 2002; 16: 2078-2083.
  • 26
    Mitelman F. The cytogenetic scenario of chronic myeloid leukemia. Leuk Lymphoma. 1993; 11(Suppl 1): 11-15.
  • 27
    Johansson B, Fioretos T, Garwicz S, Heim S, Mitelman F. t(3;21)(q26;q22) with AML1 rearrangement in a de novo childhood acute monoblastic leukaemia. Br J Haematol. 1996; 92: 429-431.
  • 28
    Morishita K, Parganas E, William CL, et al. Activation of EVI1 gene expression in human acute myelogenous leukemias by translocations spanning 300-400 kilobases on chromosome band 3q26. Proc Natl Acad Sci U S A. 1992; 89: 3937-3941.