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REFERENCES

  • 1
    Melo JV. BCR-ABL gene variants. Baillière Clin Haematol 1997;10:203222.
  • 2
    van der Plas DC, Soekarman D, van Gent AM, Grosveld G, Hagemeijer A. bcr-abl mRNA lacking abl exon a2 detected by polymerase chain reaction in a chronic myelogenous leukemia patient. Leukemia 1991;5:457461.
  • 3
    Páldi-Haris P, Barta A, Lengyel L, et al. Molecular background of a new case of chronic myelogenous leukemia with bcr-abl chimera mRNA lacking the A2 exon. Leukemia 1994;8:1791.
  • 4
    Iwata S, Mizutani S, Nakazawa S, Yata J. Heterogeneity of the breakpoint in the ABL gene in cases with BCR/ABL transcript lacking ABL exon a2. Leukemia 1994;8:16961702.
  • 5
    Polák J, Zemanová Z, Michalová K, Klamová H, Čermák J, Haškovec C. A new case of chronic myeloid leukemia (CML) in myeloid blast crisis with an atypical (b3/a3) junction of the BCR/ABL gene. Leukemia 1998;12:250.
  • 6
    Amabile M, Martinelli G, Terragna C, Montefusco V, Tabilio A, Tura S. An atypical (b3a3) junction of the bcr/abl gene lacking abl exon a2 in a patient with chronic myeloid leukemia. Haematologica 1999;84:573575.
  • 7
    Martinelli G, Amabile M, Terragna C, et al. Concomitant expression of the rare E1/A3 and B2/A3 types of BCR/ABL transcript in a chronic myeloid leukemia (CML) patient. Leukemia 1999;13:14631464.
  • 8
    Tiribelli M, Tonso A, Ferrero D, et al. Lack of SH3 domain does not imply a more severe clinical course in Ph+ chronic myeloid leukemia patients. Blood 2000;95:40194020.
  • 9
    Wilson GA, Vandenberghe EA, Pollitt RC, et al. Are aberrant BCR-ABL transcripts more common than previously thought? Br J Haematol 2000;111:11091111.
  • 10
    Roman J, Jimenez A, Barrios M, Castillejo JA, Maldonado J, Torres A. E1A3 as a unique, naturally occurring BCR-ABL transcript in an indolent case of chronic myeloid leukaemia. Br J Haematol 2001;114:635637.
  • 11
    Al-Ali H-K, Leiblein S, Kovacs I, Henning E, Niederwieser D, Deininger MWN. CML with an e1a3 BCR-ABL fusion: rare, benign, and a potential diagnostic pitfall. Blood 2002;100:10921093.
  • 12
    Soekarman D, van Denderen J, Hoefsloot L, et al. A novel variant of the bcr-abl fusion product in Philadelphia chromosome-positive acute lymphoblastic leukemia. Leukemia 1990;4:397403.
  • 13
    Jeffs AR, Wells E, Morris CM Nonrandom distribution of interspersed repeat elements in the BCR and ABL1 genes and its relation to breakpoint cluster regions. Genes Chromosomes Cancer 2001;32:144154.
  • 14
    Skorski T, Nieborowska-Skorska M, Wlodarski P, et al. The SH3 domain contributes to BCR/ABL-dependent leukemogenesis in vivo: role in adhesion, invasion, and homing. Blood 1998;91:406418.
  • 15
    Nieborowska-Skorska M, Wasik MA, Slupianek A, et al. Signal transducer and activator of transcription (STAT) 5 activation by BCR/ABL is dependent on intact Src homology (SH) 3 and SH2 domains of BCR/ABL and is required for leukemogenesis. J Exp Med 1999;189:12291242.
  • 16
    Gross AW, Zhang X, Ren R. Bcr-Abl with an SH3 deletion retains the ability to induce a myeloproliferative disease in mice, yet c-Abl activated by an SH3 deletion induces only lymphoid malignancy. Mol Cell Biol 1999;19:69186928.