• 1
    Deininger MW,Goldman JM,Melo JV. The molecular biology of chronic myeloid leukemia. Blood. 2000; 96: 33433356.
  • 2
    Sinclair PB,Nacheva EP,Leversha M, et al. Large deletions at the t(9;22) breakpoint are common and may identify a poor-prognosis subgroup of patients with chronic myeloid leukemia. Blood. 2000; 95: 738743.
  • 3
    Cohen N,Rozenfeld-Granot G,Hardan I, et al. Subgroup of patients with Philadelphia-positive chronic myelogenous leukemia characterized by a deletion of 9q proximal to ABL gene: expression profiling, resistance to interferon therapy, and poor prognosis. Cancer Genet Cytogenet. 2001; 128: 114119.
  • 4
    Huntly BJ,Reid AG,Bench AJ, et al. Deletions of the derivative chromosome 9 occur at the time of the Philadelphia translocation and provide a powerful and independent prognostic indicator in chronic myeloid leukemia. Blood. 2001; 98: 17321738.
  • 5
    Huntly BJ,Bench A,Green AR. Double jeopardy from a single translocation: deletions of the derivative chromosome 9 in chronic myeloid leukemia. Blood. 2003; 102: 11601168.
  • 6
    Huntly BJ,Guilhot F,Reid AG, et al. Imatinib improves but may not fully reverse the poor prognosis of patients with CML with derivative chromosome 9 deletions. Blood. 2003; 102: 22052212.
  • 7
    Quintas-Cardama A,Kantarjian H,Talpaz M, et al. Imatinib mesylate therapy may overcome the poor prognostic significance of deletions of derivative chromosome 9 in patients with chronic myelogenous leukemia. Blood. 2005; 105: 22812286.
  • 8
    Storlazzi CT,Specchia G,Anelli L, et al. Breakpoint characterization of der deletions in chronic myeloid leukemia patients. Genes Chromosomes Cancer. 2002; 35: 271276.
  • 9
    Deininger MW,Goldman JM,Lydon N,Melo JV. The tyrosine kinase inhibitor CGP57148B selectively inhibits the growth of BCR-ABL-positive cells. Blood. 1997; 90: 36913698.
  • 10
    Druker BJ,Talpaz M,Resta DJ, et al. Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N Engl J Med. 2001; 344: 10311037.
  • 11
    Druker BJ,Guilhot F,O'Brien SG, et al. Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. N Engl J Med. 2006; 355: 24082417.
  • 12
    Marin D,Marktel S,Bua M, et al. Prognostic factors for patients with chronic myeloid leukaemia in chronic phase treated with imatinib mesylate after failure of interferon alfa. Leukemia. 2003; 17: 14481453.
  • 13
    Kantarjian HM,Bueso-Ramos CE,Talpaz M, et al. Significance of myelofibrosis in early chronic-phase, chronic myelogenous leukemia on imatinib mesylate therapy. Cancer. 2005; 104: 777780.
  • 14
    Kreil S,Pfirrmann M,Haferlach C, et al. Heterogeneous prognostic impact of derivative chromosome 9 deletions in chronic myelogenous leukemia. Blood. 2007; 110: 12831290.
  • 15
    O'Brien SG,Guilhot F,Larson RA, et al. Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia. N Engl J Med. 2003; 348: 9941004.
  • 16
    Hughes TP,Kaeda J,Branford S, et al. Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia. N Engl J Med. 2003; 349: 14231432.
  • 17
    Kantarjian HM,O'Brien S,Cortes JE, et al. Treatment ofPhiladelphia chromosome-positive, accelerated-phase chronic myelogenous leukemia with imatinib mesylate. Clin Cancer Res. 2002; 8: 21672176.
  • 18
    Castagnetti F,Marzocchi G,Luatti S, et al. Deletions of the derivative chromosome 9 do not influence response to imatinib to early chronic phase chronic myeloid leukemia patients (a GIMEMA Working Party analysis) [ASH Annual Meeting Abstracts]. Blood. 2006; 108. Abstract 2112.
  • 19
    Goldberg Z,Levav Y,Krichevsky S,Fibach E,Haupt Y. Treatment of chronic myeloid leukemia cells with imatinib (STI571) impairs p53 accumulation in response to DNA damage. Cell Cycle. 2004; 3: 11881195.
  • 20
    Vigneri P,Wang JY. Induction of apoptosis in chronic myelogenous leukemia cells through nuclear entrapment of BCR-ABL tyrosine kinase. Nat Med. 2001; 7: 228234.
  • 21
    Fernandez-Luna JL. Bcr-Abl and inhibition of apoptosis in chronic myelogenous leukemia cells. Apoptosis. 2000; 5: 315318.
  • 22
    Horita M,Andreu EJ,Benito A, et al. Blockade of the Bcr-Abl kinase activity induces apoptosis of chronic myelogenous leukemia cells by suppressing signal transducer and activator of transcription 5-dependent expression of Bcl-xL. J Exp Med. 2000; 191: 977984.
  • 23
    Fang G,Kim CN,Perkins CL, et al. CGP57148B (STI-571) induces differentiation and apoptosis and sensitizes Bcr-Abl-positive human leukemia cells to apoptosis due to antileukemic drugs. Blood. 2000; 96: 22462253.
  • 24
    Sattler M,Verma S,Shrikhande G, et al. The BCR/ABL tyrosine kinase induces production of reactive oxygen species in hematopoietic cells. J Biol Chem. 2000; 275: 2427324278.
  • 25
    Slupianek A,Nowicki MO,Koptyra M,Skorski T. BCR/ABL modifies the kinetics and fidelity of DNA double-strand breaks repair in hematopoietic cells. DNA Repair (Amsterdam). 2006; 5: 243250.
  • 26
    Nowicki MO,Falinski R,Koptyra M, et al. BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species-dependent DNA double-strand breaks. Blood. 2004; 104: 37463753.
  • 27
    Penserga ET,Skorski T. Fusion tyrosine kinases: a result and cause of genomic instability. Oncogene. 2007; 26: 1120.