1. Bennett JH: Case of hypertrophy of the spleen and liver in which death took place from suppuration of the blood. Edinb Med Surg J 64:413, 1845.

2. Virchow R: Weisses Blut. Frorieps Notizen 36:151, 1845.

3. Nowell P, Hungerford D: A minute chromosome in human chronic granulocytic leukemia. Science 132: 1497, 1960.

4. Daley GQ, Van Etten RA, Baltimore D: Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome. Science 247:824, 1990.

5. 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 344:1031, 2001.

6. Cervantes F, Hernandez-Boluda JC, Ferrer A, et al.: The changing profile of Ph-positive chronic myeloid leukemia at presentation: possible impact of earlier diagnosis on survival. Haematologica 84:324, 1999.

7. Lichtman, MA: Chronic myelogenous leukemia and related disorders. In Williams WJ, Beutler E, Erslev A, Lichtman MA (eds.) Hematology, 4th ed. New York: McGraw-Hill; 1991:202.

8. Buesche G, Georgii A, Duensing A, et al.: Evaluating the volume ratio of bone marrow affected by fibrosis: a parameter crucial for the prognostic significance of marrow fibrosis in chronic myeloid leukemia. Hum Pathol 34:391,2003.

9. Aguayo A, Kantarjian H, Manshouri T, et al.: Angiogenesis in acute and chronic leukemias and myelodysplastic syndromes. Blood 96:2240, 2000.

10. Kantarjian HM, Talpaz M: Definition of the accelerated phase of chronic myelogenous leukemia. J Clin Oncol 6:180, 1988.

11. Talpaz M, Silver RT, Druker BJ, et al.: Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia: results of a phase 2 study. Blood 99:1928, 2002.

12. Favre G, Passweg J, Hoffmann T, et al.: Immunophenotype of blast crisis in chronic myeloid leukemia. Schweiz Med Wochenschr 128:1624, 1998.

13. Cervantes F, Villamor N, Esteve J, et al.: "Lymphoid" blast crisis of chronic myeloid leukaemia is associated with distinct clinicohaematological features. Br J Haematol 100:123, 1998.

14. Rowley JD: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature 243:290, 1973.

15. Bartram CR, de Klein A, Hagemeijer A, et al.: Translocation of c-abl oncogene correlates with the presence of a Philadelphia chromosome in chronic myelocytic leukaemia. Nature 306:277, 1983.

16. Groffen J, Stephenson JR, Heisterkamp N, et al.: Philadelphia chromosomal breakpoints are clustered within a limited region, bcr, on chromosome 22. Cell 36:93, 1984.

17. Vardiman JW, Pierre R, Thiele J, et al.: Chronic myelo-proliferative diseases. In: Jaffe ES, Harris NL, Stein H, Vardiman JW (eds.) Tumors of Haematopoietic and Lymphoid Tissues. Lyon, France: IARC Press; 2001:15.

18. Schoch C, Schnittger S, Bursch S, et al.: Comparison of chromosome banding analysis, interphase- and hyper-metaphase-FISH, qualitative and quantitative PCR for diagnosis and for follow-up in chronic myeloid leukemia: a study on 350 cases. Leukemia 16:53, 2002.

19. Le Gouill S, Talmant P, Milpied N, et al.: Fluorescence in situ hybridization on peripheral-blood specimens is a reliable method to evaluate cytogenetic response in chronic myeloid leukemia. J Clin Oncol 18:1533, 2000.

20. Reinhold U, Hennig E, Leiblein S, et al.: FISH for BCR-ABL on interphases of peripheral blood neutrophils but not of unselected white cells correlates with bone marrow cytogenetics in CML patients treated with imatinib. Leukemia 17:1925, 2003.

21. Chase A, Grand F, Zhang JG, et al.: Factors influencing the false positive and negative rates of BCR-ABL fluorescence in situ hybridization. Genes Chromosomes Cancer 18:246, 1997.

22. 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 98:1732, 2001.

23. 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 95:738, 2000.

24. 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 102:2205, 2003.

25. Kolomietz E, Marrano P, Yee K, et al.: Quantitative PCR identifies a minimal deleted region of 120 kb extending from the Philadelphia chromosome ABL translocation breakpoint in chronic myeloid leukemia with poor outcome. Leukemia 17:1313, 2003.

26. Reid AG, Nacheva EP: A potential role for PRDM12 in the pathogenesis of chronic myeloid leukaemia with derivative chromosome 9 deletion. Leukemia 18:178, 2004.

27. Muller C, Hennig E, Franke C, et al.: The BCR/ABL-extra signal fluorescence in situ hybridization system reliably detects deletions upstream of the ABL locus: implications for reporting of results and followup of chronic myelogenous leukemia patients. Cancer Genet Cytogenet 136:149, 2002.

28. Huntly BJ, Bench AJ, Delabesse E, et al.: Derivative chromosome 9 deletions in chronic myeloid leukemia: poor prognosis is not associated with loss of ABL-BCR expression, elevated BCR-ABL levels, or karyotypic instability. Blood 99:4547, 2002.

29. Melo JV, Gordon DE, Cross NC, et al.: The ABL-BCR fusion gene is expressed in chronic myeloid leukemia. Blood 81:158, 1993.

30. Huntly BJP, Bench A, Green AR: Double jeopardy from a single translocation: deletions of the derivative chromosome 9 in chronic myeloid leukemia. Blood 102:1160, 2003.

31. Reid AG, Huntly BJ, Grace C, et al.: Survival implications of molecular heterogeneity in variant Philadelphia-positive chronic myeloid leukaemia. Br J Haematol 121:419, 2003.

32. Mitelman F: The cytogenetic scenario of chronic myeloid leukemia. Leuk Lymphoma 11(suppl 1):11, 1993.

33. Johansson B, Fioretos T, Mitelman F: Cytogenetic and molecular genetic evolution of chronic myeloid leukemia. Acta Haematol 107:76, 2002.

34. Johansson B, Mertens F, Mitelman F: Geographic heterogeneity of neoplasia-associated chromosome aberrations. Genes Chromosomes Cancer 3:1, 1991.

35. Bumm T, Muller C, Al Ali HK, et al.: Emergence of clonal cytogenetic abnormalities in Ph— cells in some CML patients in cytogenetic remission to imatinib but restoration of polyclonal hematopoiesis in the majority. Blood 101:1941, 2003.

36. Deininger MW, Goldman JM, Melo JV: The molecular biology of chronic myeloid leukemia. Blood 96:3343, 2000.

37. Melo JV, Myint H, Galton DA, et al.: P190 BCR-ABL chronic myeloid leukaemia: the missing link with chronic myelomonocytic leukaemia? Leukemia 8:208, 1994.

38. Melo JV: The diversity of BCR-ABL fusion proteins and their relationship to leukemia phenotype. Blood 88:2375, 1996.

39. Pane F, Frigeri F, Sindona M, et al.: Neutrophilic chronic myeloid leukemia: a distinct disease with a specific molecular marker (BCR/ABL with C3/A2 junction). Blood 88:2410, 1996.

40. Hochhaus A, Reiter A, Skladny H, et al.: A novel BCR-ABL fusion gene (e6a2) in a patient with Philadelphia chromosome-negative chronic myelogenous leukemia. Blood 88:2236, 1996.

41. Al Ali HK, Leiblein S, Kovacs I, et al.: CML with an e1a3 BCR-ABL fusion: rare, benign, and a potential diagnostic pitfall. Blood 100:1092, 2002.

42. Reinhold U, Hennig E, Leiblein S, et al.: FISH for BCR-ABL on interphases of peripheral blood neutrophils but not of unselected white cells correlates with bone marrow cytogenetics in CML patients treated with imatinib. Leukemia 17:1925, 2003.

43. Garicochea B, Chase A, Lazaridou A, et al.: T lymphocytes in chronic myelogenous leukaemia (CML): no evidence of the BCR/ABL fusion gene detected by fluorescence in situ hybridization in 14 patients. Leukemia 8:1197, 1994.

44. Takahashi N, Miura I, Saitoh K, et al.: Lineage involvement of stem cells bearing the Philadelphia chromosome in chronic myeloid leukemia in the chronic phase as shown by a combination of fluorescence-activated cell sorting and fluorescence in situ hybridization. Blood 92:4758, 1998.

45. Gunsilius E, Duba HC, Petzer AL, et al.: Evidence from a leukaemia model for maintenance of vascular endothelium by bone-marrow-derived endothelial cells. Lancet 355:1688, 2000.

46. Deininger M: Src kinases in Ph+ lymphoblastic leukemia. Nat Genet 36:440, 2004.

47. Talpaz M, Kantarjian H, Kurzrock R, et al.: Interferonalpha produces sustained cytogenetic responses in chronic myelogenous leukemia. Philadelphia chromosome-positive patients. Ann Intern Med 114:532, 1991.

48. McGlave PB, De Fabritiis P, Deisseroth A, et al.: Autologous transplants for chronic myelogenous leukaemia: results from eight transplant groups. Lancet 343:1486,1994.

49. Petzer AL, Eaves CJ, Barnett MJ, et al.: Selective expansion of primitive normal hematopoietic cells in cytokine-supplemented cultures of purified cells from patients with chronic myeloid leukemia. Blood 90:64, 1997.

50. Petzer AL, Eaves CJ, Lansdorp PM, et al.: Characterization of primitive subpopulation of normal and leukemic cells present in the blood of patients with newly diagnosed as well as established chronic myeloid leukemia. Blood 88:2162, 1996.

51. Bergamaschi G, Podesta M, Frassoni F, et al.: Restoration of normal polyclonal haemopoiesis in patients with chronic myeloid leukaemia autografted with Ph-negative peripheral stem cells. Br J Haematol 87:867, 1994.

52. Carella A, Lerma E, Corsetti MT, et al.: Autografting with Philadelphia chromosome-negative mobilized hematopoietic progenitor cells in chronic myeloge-nous leukemia. Blood 93:1534, 1999.

53. Vickers M: Estimation of the number of mutations necessary to cause chronic myeloid leukaemia from epidemiological data. Br J Haematol 94:1, 1996.

54. Raskind WH, Ferraris AM, Najfeld V, et al.: Further evidence for the existence of a clonal Ph-negative stage in some cases of Ph-positive chronic myelocytic leukemia. Leukemia 7:1163, 1993.

55. Biernaux C, Loos M, Sels A, et al.: Detection of major bcr-abl gene expression at a very low level in blood cells of some healthy individuals. Blood 86:3118, 1995.

56. Bose S, Deininger M, Gora-Tybor J, et al.: The presence of BCR-ABL fusion genes in leukocytes of normal individuals: implications for the assessment of minimal residual disease. Blood 92:3362, 1998.

57. O'Dwyer ME, Gatter KM, Loriaux M, et al.: Demonstration of Philadelphia chromosome negative abnormal clones in patients with chronic myeloge-nous leukemia during major cytogenetic responses induced by imatinib mesylate. Leukemia 17:481, 2003.

58. Terre C, Eclache V, Rousselot P, et al.: Report of 34 patients with clonal chromosomal abnormalities in

Philadelphia-negative cells during imatinib treatment of Philadelphia-positive chronic myeloid leukemia. Leukemia 18:1340, 2004.

59. Daley GQ, Van Etten RA, Jackson PK, et al.: Nonmyristoylated Abl proteins transform a factor-dependent hematopoietic cell line. Mol Cell Biol 12:1864, 1992.

60. Hantschel O, Nagar B, Guettler S, et al.: A myristoyl/ phosphotyrosine switch regulates c-Abl. Cell 112:845, 2003.

61. Nagar B, Hantschel O, Young MA, et al.: Structural basis for the autoinhibition of c-Abl tyrosine kinase. Cell 112:859, 2003.

62. Pendergast AM: The Abl family kinases: mechanisms of regulation and signaling. Adv Cancer Res 85:51, 2002.

63. Van Etten RA: Cycling, stressed-out and nervous: cellular functions of c-Abl. Trends Cell Biol 9:179, 1999.

64. Sawyers CL, McLaughlin J, Goga A, et al.: The nuclear tyrosine kinase c-Abl negatively regulates cell growth. Cell 77:121, 1994.

65. Gong JG, Costanzo A, Yang HQ, et al.: The tyrosine kinase c-Abl regulates p73 in apoptotic response to cis-platin-induced DNA damage. Nature 399:806, 1999.

66. Kharbanda S, Ren R, Pandey P, et al.: Activation of the c-Abl tyrosine kinase in the stress response to DNA-damaging agents. Nature 376:785, 1995.

67. Shafman T, Khanna KK, Kedar P, et al.: Interaction between ATM protein and c-Abl in response to DNA damage. Nature 387:520, 1997.

68. Yuan ZM, Huang Y, Ishiko T, et al.: Regulation of Rad51 function by c-Abl in response to DNA damage. J Biol Chem 273:3799, 1998.

69. Yuan ZM, Huang Y, Whang Y, et al.: Role for c-Abl tyrosine kinase in growth arrest response to DNA damage. Nature 382:272, 1996.

70. Yuan ZM, Shioya H, Ishiko T, et al.: p73 is regulated by tyrosine kinase c-Abl in the apoptotic response to DNA damage. Nature 399:814, 1999.

71. Lewis JM, Baskaran R, Taagepera S, et al.: Integrin regulation of c-Abl tyrosine kinase activity and cytoplasmic-nuclear transport. Proc Natl Acad Sci U S A 93:15174, 1996.

72. Lewis JM, Schwartz MA: Integrins regulate the association and phosphorylation of paxillin by c-Abl. J Biol Chem 273:14225, 1998.

73. Plattner R, Irvin BJ, Guo S, et al.: A new link between the c-Abl tyrosine kinase and phosphoinositide signalling through PLC-gamma1. Nat Cell Biol 5:309, 2003.

74. Schwartzberg PL, Stall AM, Hardin JD, et al.: Mice homozygous for the ablm1 mutation show poor viability and depletion of selected B and T cell populations. Cell 65:1165, 1991.

75. Tybulewicz VL, Crawford CE, Jackson PK, et al.: Neonatal lethality and lymphopenia in mice with a homozygous disruption of the c-abl proto-oncogene. Cell 65:1153, 1991.

76. Koleske AJ, Gifford AM, Scott ML, et al.: Essential roles for the Abl and Arg tyrosine kinases in neurulation. Neuron 21:1259, 1998.

77. Wen ST, Van ER: The PAG gene product, a stress-induced protein with antioxidant properties, is an Abl

SH3-binding protein and a physiological inhibitor of c-Abl tyrosine kinase activity. Genes Dev 11:2456, 1997.

78. Voncken JW, van Schaick H, Kaartinen V, et al.: Increased neutrophil respiratory burst in bcr-null mutants. Cell 80:719, 1995.

79. Lugo TG, Pendergast AM, Muller AJ, et al.: Tyrosine kinase activity and transformation potency of bcr-abl oncogene products. Science 247:1079, 1990.

80. Wertheim JA, Forsythe K, Druker BJ, et al.: BCR-ABL-induced adhesion defects are tyrosine kinase-indepen-dent. Blood 99:4122, 2002.

81. McWhirter JR, Galasso DL, Wang JY: A coiled-coil oligomerization domain of Bcr is essential for the transforming function of Bcr-Abl oncoproteins. Mol Cell Biol 13:7587, 1993.

82. Papadopoulos P, Ridge SA, Boucher CA, et al.: The novel activation of ABL by fusion to an ets-related gene, TEL. Cancer Res 55:34, 1995.

83. He Y, Wertheim JA, Xu L, et al.: The coiled-coil domain and Tyr177 of bcr are required to induce a murine chronic myelogenous leukemia-like disease by bcr/abl. Blood 99:2957, 2002.

84. 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 91:406, 1998.

85. Gaston I, Johnson KJ, Oda T, et al.: Coexistence of phosphotyrosine-dependent and -independent interactions between Cbl and Bcr-Abl. Exp Hematol 32:113, 2004.

86. Salgia R, Sattler M, Pisick E, et al.: p210BCR/ABL induces formation of complexes containing focal adhesion proteins and the protooncogene product p120c-Cbl. Exp Hematol 24:310, 1996.

87. Cortez D, Reuther GW, Pendergast AM: The BCR-ABL tyrosine kinase activates mitotic signaling pathways and stimulates G1-to-S phase transition in hematopoi-etic cells. Oncogene 15:2333, 1997.

88. Skorski T, Kanakaraj P, Nieborowska Skorska M, et al.: Phosphatidylinositol-3 kinase activity is regulated by BCR/ABL and is required for the growth of Philadelphia chromosome-positive cells. Blood 86:726, 1995.

89. Sillaber C, Gesbert F, Frank DA, et al.: STAT5 activation contributes to growth and viability in Bcr/Abl-trans-formed cells. Blood 95:2118, 2000.

90. Sawyers CL, Callahan W, Witte ON: Dominant negative MYC blocks transformation by ABL oncogenes. Cell 70:901, 1992.

91. Melo JV, Deininger MW: Biology of chronic myeloge-nous leukemia-signaling pathways of initiation and transformation. Hematol Oncol Clin North Am 18:545-viii, 2004.

92. Pendergast AM, Quilliam LA, Cripe LD, et al.: BCR-ABL-induced oncogenesis is mediated by direct interaction with the SH2 domain of the GRB-2 adaptor protein. Cell 75:175, 1993.

93. Goga A, McLaughlin J, Afar DE, et al.: Alternative signals to RAS for hematopoietic transformation by the BCR-ABL oncogene. Cell 82:981, 1995.

94. Sexl V, Piekorz R, Moriggl R, et al.: Stat5a/b contribute to interleukin 7-induced B-cell precursor expansion, but abl- and bcr/abl-induced transformation are independent of stat5. Blood 96:2277, 2000.

95. Li S, Gillessen S, Tomasson MH, et al.: Interleukin 3 and granulocyte-macrophage colony-stimulating factor are not required for induction of chronic myeloid leukemia-like myeloproliferative disease in mice by BCR/ABL. Blood 97:1442, 2001.

96. Jonuleit T, Peschel C, Schwab R, et al.: Bcr-Abl kinase promotes cell cycle entry of primary myeloid CML cells in the absence of growth factors. Br J Haematol 100:295, 1998.

97. Amos TA, Lewis JL, Grand FH, et al.: Apoptosis in chronic myeloid leukaemia: normal responses by progenitor cells to growth factor deprivation, X-irradiation and glucocorticoids. Br J Haematol 91:387, 1995.

98. Jiang X, Lopez A, Holyoake T, et al.: Autocrine production and action of IL-3 and granulocyte colony-stimulating factor in chronic myeloid leukemia. Proc Natl Acad Sci U S A 96:12804, 1999.

99. Amarante Mendes GP, McGahon AJ, Nishioka WK

et al.: Bcl-2-independent Bcr-Abl-mediated resistance to apoptosis: protection is correlated with up regulation of Bcl-xL. Oncogene 16:1383, 1998.

100. Amarante Mendes GP, Naekyung Kim C, Liu L, et al.: Bcr-Abl exerts its antiapoptotic effect against diverse apoptotic stimuli through blockage of mitochondrial release of cytochrome C and activation of caspase-3. Blood 91:1700, 1998.

101. Bedi A, Barber JP, Bedi GC, et al.: BCR-ABL-mediated inhibition of apoptosis with delay of G2/M transition after DNA damage: a mechanism of resistance to multiple anticancer agents. Blood 86:1148, 1995.

102. Cortez D, Kadlec L, Pendergast AM: Structural and signaling requirements for BCR-ABL-mediated transformation and inhibition of apoptosis. Mol Cell Biol 15:5531, 1995.

103. Kuribara R, Honda H, Matsui H, et al.: Roles of Bim in apoptosis of normal and Bcr-Abl-expressing hematopoietic progenitors. Mol Cell Biol 24:6172, 2004.

104. Gordon MY, Dowding CR, Riley GP, et al.: Altered adhesive interactions with marrow stroma of haematopoietic progenitor cells in chronic myeloid leukaemia. Nature 328:342, 1987.

105. Salgia R, Quackenbush E, Lin J, et al.: The BCR/ABL oncogene alters the chemotactic response to stromal-derived factor-1alpha. Blood 94:4233, 1999.

106. Ramaraj P, Singh H, Niu N, et al.: Effect of mutational inactivation of tyrosine kinase activity on BCR/ABL-induced abnormalities in cell growth and adhesion in human hematopoietic progenitors. Cancer Res 64:5322, 2004.

107. Canitrot Y, Falinski R, Louat T, et al.: p210 BCR/ABL kinase regulates nucleotide excision repair (NER) and resistance to UV radiation. Blood 102:2632, 2003.

108. Canitrot Y, Lautier D, Laurent G, et al.: Mutator phe-notype of BCR—ABL transfected Ba/F3 cell lines and its association with enhanced expression of DNA poly-merase beta. Oncogene 18:2676, 1999.

109. Deutsch E, Dugray A, Abdul Karim B, et al.: BCR-ABL down-regulates the DNA repair protein DNA-PKcs. Blood 97:2084, 2001.

110. Dierov J, Dierova R, Carroll M: BCR/ABL translocates to the nucleus and disrupts an ATR-dependent intra-S phase checkpoint. Cancer Cell 5:275, 2004.

111. Takedam N, Shibuya M, Maru Y: The BCR-ABL oncoprotein potentially interacts with the xeroderma pigmentosum group B protein. Proc Natl Acad Sci U S A 96:203, 1999.

112. Brummendorf TH, Holyoake TL, Rufer N, et al.: Prognostic implications of differences in telomere length between normal and malignant cells from patients with chronic myeloid leukemia measured by flow cytometry. Blood 95:1883, 2000.

113. Hernandez-Boluda JC, Cervantes F, Colomer D, et al.: Genomic p16 abnormalities in the progression of chronic myeloid leukemia into blast crisis: a sequential study in 42 patients. Exp Hematol 31:204, 2003.

114. Sill H, Goldman JM, Cross NC: Homozygous deletions of the p16 tumor-suppressor gene are associated with lymphoid transformation of chronic myeloid leukemia. Blood 85:2013, 1995.

115. Feinstein E, Cimino G, Gale RP, et al.: p53 in chronic myelogenous leukemia in acute phase. Proc Natl Acad Sci U S A 88:6293, 1991.

116. Towatari M, Adachi K, Kato H, et al.: Absence of the human retinoblastoma gene product in the megakary-oblastic crisis of chronic myelogenous leukemia. Blood 78:2178, 1991.

117. Deguchi K, Gilliland DG: Cooperativity between mutations in tyrosine kinases and in hematopoietic transcription factors in AML. Leukemia 16:740, 2002.

118. Dash AB, Williams IR, Kutok JL, et al.: A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9. Proc Natl Acad Sci U S A 99:7622, 2002.

119. Carapeti M, Goldman JM, Cross NC: Overexpression of EVI-1 in blast crisis of chronic myeloid leukemia. Leukemia 10:1561, 1996.

120. Cuenco GM, Ren R: Cooperation of BCR-ABL and AML1/MDS1/EVI1 in blocking myeloid differentiation and rapid induction of an acute myelogenous leukemia. Oncogene 20:8236, 2001.

121. 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 23:569, 2004.

122. 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 101:13312, 2004.

123. Perrotti D, Cesi V, Trotta R, et al.: BCR-ABL suppresses C/EBPalpha expression through inhibitory action of hnRNP E2. Nat Genet 30:48, 2002.

124. Jamieson CH, Ailles LE, Dylla SJ, et al.: Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML. N Engl J Med 351:657, 2004.

125. Gaiger A, Henn T, Hoerth E, et al.: Increase of BCR-ABL chimeric mRNA expression in tumor cells of patients with chronic myeloid leukemia precedes disease progression. Blood 86:2371, 1995.

126. Asimakopoulos FA, Shteper PJ, Krichevsky S, et al.: ABL1 methylation is a distinct molecular event associated with clonal evolution of chronic myeloid leukemia. Blood 94:2452, 1999.

127. Elefanty AG, Cory S: Hematologic disease induced in BALB/c mice by a bcr-abl retrovirus is influenced by the infection conditions. Mol Cell Biol 12:1755, 1992.

128. Pear WS, Miller JP, Xu L, et al.: Efficient and rapid induction of a chronic myelogenous leukemia-like myeloproliferative disease in mice receiving P210 bcr/abl-transduced bone marrow. Blood 92:3780, 1998.

129. Heisterkamp N, Jenster G, Kioussis D, et al.: Human bcr-abl gene has a lethal effect on embryogenesis. Transgenic Res 1:45, 1991.

130. Koschmieder S, Goettgens B, Zhang P, et al.: Inducible chronic phase of myeloid leukemia with expansion of hematopoietic stem cells in a transgenic model of BCR-ABL leukemogenesis. Blood 105:324, 2005.

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