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Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán

2009, Número 3

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Rev Invest Clin 2009; 61 (3)


La leucemia mieloide crónica en el siglo XXI: biología y tratamiento

Chávez-González MA, Ayala-Sánchez M, Mayani H

Idioma: Español
Referencias bibliográficas: 81
Paginas: 221-232
Archivo PDF: 391.04 Kb.


RESUMEN

La Leucemia Mieloide Crónica (LMC) es una enfermedad clonal, originada en las células troncales hematopoyéticas y caracterizada por la presencia del cromosoma Philadelphia (Ph) y su producto oncoproteico p210Bcr-Abl. Esta proteína presenta una incrementada y constitutiva actividad tirosina cinasa, esencial para la transformación maligna, la cual altera propiedades celulares como la adhesión, proliferación y apoptosis. Históricamente la LMC ha sido tratada con diferentes agentes, que van desde arsénico hasta trasplante de células hematopoyéticas, pasando por diversas sustancias químicas (busulfán, hidroxiurea, citarabina), biomoduladores (IFN-α, IFNα-PEG) y moléculas generadas por diseño (imatinib, nilotinib, dasatinib). Todas estas moléculas ejercen actividades específicas sobre las células hematopoyéticas y conducen a diversas respuestas clínicas y biológicas. En esta revisión se pretende dar una visión general sobre la hematopoyesis en LMC y sus implicaciones en las principales opciones de tratamiento.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Rowley JD. Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature 1973; 243: 290-3.

  2. Piller G. Leukaemia – a brief historical review from ancient times to 1950. Br J Haematology 2001; 112: 282-92.

  3. Jorgensen H, Holyoake T. A comparison of normal and leukemic stem cell biology in chronic myeloid leukemia. Hematol Oncol 2001; 19: 89-106.

  4. Mayani H, Guilbert LJ, Janowska-Wieczorek A. Biology of the hemopoietic microenvironment. Eur J Haematol 1992; 49: 225-33.

  5. Deininger M, Druker B. Specific targeted therapy of chronic myelogenous leukemia with Imatinib. Pharmacol Rev 2003; 55: 401-23.

  6. Deininger M, Bose S, Gora-Tybor J, Yan X, Goldman J, Melo J. Selective induction of leukemia-associated fusion genes by high-dose ionizing radiation. Cancer Res 1998; 58: 421-5.

  7. Sawyers C. Chronic Myeloid Leukemia. N Engl J Med 1999; 340: 1330-40.

  8. Arico M, Biondi A. Myelodysplastic Syndromes and Chronic Myeloproliferative Disorders. In: Ching-Hon P (ed.). Childhood Luekemias. Cambridge University Press; 1999, p. 345-7.

  9. Cross N, Reiter A. Tyrosine kinase fusion genes in chronic myeloproliferative diseases. Leukemia 2002; 16: 1207-12.

  10. Biernaux C, Sels A, Huez G, Stryckmans P. Very low level of major BCR-ABL expression in blood of some healthy individuals. Bone Marrow Transplant 1996; 17: S45-S47.

  11. Clarkson B, Strife A, Wisniewski D, Lambek C, Liu C. Chronic myelogenous leukemia as a paradigm of early cancer and possible curative strategies. Leukemia 2003; 17: 1211-62.

  12. Deininger M, Vieira S, Mendiola R, Schultheis B, Goldman J, Melo J. BCR-ABL Tyrosine Kinase Activity Regulates the expression for multiple genes implicated in the pathogenesis of chronic myeloid leukemia. Cancer Res 2000; 60: 2049-55.

  13. Sawyers C. The bcr-abl gene in chronic myelogenous leukaemia. Cancer Surv 1992; 15: 37-51.

  14. Wang J. Regulation of cell death by the Abl tyrosine kinase. Oncogene 2000; 19: 5643-50.

  15. Diekmann D, Brill S, Garrett M, Totty N, Hsuan J, Manfres C, Hall A. Bcr encodes a GTPase-activating protein for p21 rac. Nature 1991; 351: 400-02.

  16. Deininger M, Goldman J, Melo J. The molecular biology of chronic myeloid leukemia. Blood 2000; 96: 3343-56.

  17. Dash A, Williams I, Kutok J, Tomasson M, Anastasiadou E, Lindahi K, et al. A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9. PNAS 2002; 99: 7622-7.

  18. Calabretta B, Perrotti D. The biology of CML blast crisis. Blood 2004; 103: 4010-22.

  19. Verfaillie C, Hurley R, Lundell B, Zhao C, Bathia R. Integrin-mediated regulation of hematopoiesis: do Bcr/Abl- induced defects in integrin function underlie the abnormal circulation and proliferation of CML progenitors? Acta Hematol 1997; 97: 40-52.

  20. Sawyers C, McLaughin J, Witte O. Genetic requirement for Ras in the transformation of fibroblasts and hematopoietic cells by the BCR/ABL oncogene. J Exp Med 1995; 181: 307-13.

  21. Horita M, Andrew E, Benito A, Arbona C, Sans C, Beet I, 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 ob Bcl-xL. J Exp Med 2000; 191: 977-84.

  22. Reuther J, Reuther G, Cortez D, Pendergast A, Baldwin A. A requirement for NF-kappaB activation in BCR/ABL- mediated transformation. Genes Dev 1998; 12: 968-81.

  23. Shet A, Jahagirdar B, Verfaillie C. Chronic myelogenous leukemia: mechanisms underlying disease progression. Leukemia 2002; 8: 1402-11.

  24. Amarante Mendes G, Naekyung C, Liu L, Huang Y, Perkins C, Green D, Bhalla K. Bcr-Abl exerts its antiapoptotic effect against diverse apoptotic stimuli through blockage of mitochondrial release of cytochrome C and activation of caspase-3. Blood 1998; 91: 1700-05.

  25. Gutierrez-Castellanos S, Cruz M, Rabelo L, Godinez R, Reyes E, Riebeling-Navarro C. Differences in BCL-XL expression and STAT5 phosphorylation in chronic myeloid leukaemia patients. Eur J Haematol 2004; 72: 231-8.

  26. Jennings B, Mills K. C-myc locus amplification and the acquisition of trisomy 8 in the evolution of chronic myeloid leukemia. Leuk Res 1998; 22: 849-903.

  27. Schutte J, Opalka B, Becher R, Bardenheuer W, Szimansky S, Lux A, Seeber S. Analysis of p53 gene in patients with isochromosome 17q and Ph-positive or-negative myeloid leukemia. Leuk Res 1993; 17: 533-9.

  28. Sill H, Goldman J, Cross N. Homozygous deletion of the p16 tumor-suppressor gene are associated with lymphoid transformation of chronic myeloid leukemia. Blood 1995; 85: 2013-6.

  29. Coulombel L, Kalousek D, Eaves C, Gupta C, Eaves A. Longterm marrow culture reveals chromosomally normal hematopoietic progenitor cells in patients with Philadelphia chromosome-positive chronic myelogenous leukemia. N Engl J Med 1983; 308: 1493-8.

  30. Udomsakdi C, Eaves C, Swolin B, Reid D, Barnett M, Eaves A. Rapid decline of chronic myeloid leukemic cells in long term culture due to a defect at the leukemic stem cell level. Proc Natl Acad Sci USA 1992; 89: 6192-6.

  31. Verfaillie C, Miller W, Boylan K, McGlave P. Selection of benign primitive hematopoietic progenitors in chronic myelogenous leukemia on the bases of HLA-DR antigen expression. Blood 1992; 79: 1003-10.

  32. Chávez-González A, Rosas-Cabral A, Vela-Ojeda J, González J, Mayani H. Severe functional alterations in vitro in CD34(+) cell subpopulations from patients with chronic myeloid leukemia. Leuk Res 2004; 28: 639-47.

  33. Holyoake T, Jiang X, Eaves C, Eaves A. Isolation of a highly quiescent subpopulation of primitive leukemic cells in chronic myeloid leukemia. Blood 1999; 94: 2056-64.

  34. Holyoake T, Jiang X, Drummond M, Eaves A, Eaves C. Elucidating critical mechanisms of deregulated stem cell turnover in the chronic phase of chronic myeloid leukemia. Leukemia 2002; 16: 549-58.

  35. Traycoff C, Halstead B, Rice S, McMahel J, Srour E, Cornetta K. Chronic myelogenous leukaemia CD34+ cells exit G0/G1 phases of cell cycle more rapidly than normal marrow CD34+ cells. Br J Haematol 1998; 102: 759-67.

  36. Jonuleit T, Peschel C, Schwab R, Van Der Kuip H, Buchdunger E, Fischer T, et al. Bcr-Abl kinase promotes cell cycle entry of primary myeloid CML cells in the absence of growth factors. Br J Haematol 1998; 100: 295-303.

  37. Jiang X, Lopez A, Holyoake T, Eaves C, Eaves A. Autocrine production and action of IL-3 and granulocyte colony-stimulating factor in chronic myeloid leukemia. Proc Natl Acad Sci USA 1999; 96: 12804-09.

  38. Holyoake T, Jiang X, Jorgensen H, Graham S, Alcorn M, Laird C, et al. Primitive quiescent leukemic cells from patients with chronic myeloid leukemia spontaneously initiate factor-independent growth in vitro in association with up-regulation of expression of interleukin-3. Blood 2001; 97: 720-8.

  39. Inukai T, Sugita K, Mitsui K, Lijima K, Goi K, Tezuka T, et al. Participation of granulocyte colony-stimulating factor in the growth regulation of leukemia cells from Philadelphia chromosome- positive acute leukemia and blast crisis of chronic myeloid leukemia. Leukemia 2000; 14: 1386-95.

  40. Lundell B, McCarthy J, Kovach N, Verfaillie C. Activation of beta 1 integrins on CML progenitors reveals cooperation between beta 1 integrins and CD44 in the regulation of adhesion and proliferation. Leukemia 1997; 11: 822-9.

  41. Petzer A, Gunsilius E. Hematopoietic Stem Cells in Chronic Myeloid Leukemia. Arch Med Res 2003; 34: 496-506.

  42. Zhao Z, Tang X, You Y, Li W, Liu F, Zou P. Assessment of bone marrow mesenchymal stem cell biological characteristics and support hemopoiesis function in patients with chronic myeloid leukemia. Leuk Res 2006; 30: 993-1003.

  43. Druker B. Signal transduction inhibition: results from phase I clinical trials in chronic myeloid leukemia. Semin Hematol 2001; 38(Suppl. 8): 9-14.

  44. Fausel C. Targeted chronic myeloid leukemia therapy. Seeking a cure. Am J Health Syst Pharm 2007; 15: S9-S15.

  45. Tsao A, Kantarjian H, Talpaz M. STI-571 in Chronic Myelogenous Leukemia. Br J Haematol 2002; 119: 15-24.

  46. Dowding C, Gordon M, Guo A, Maison D, Osterholz J, Siezkowski M, Goldman J. Potential mechanisms of action of interferon- alpha in CML. Leuk Lymphoma 1993; 11: S185-S191.

  47. Cornelissen J, Ploemacher R, Wognum B, Borsboom A, Kluin- Nelemans H, Hagemeijer A, Lowenberg B. An in vitro model for cytogenetic conversion in CML. Interferon-alpha preferentially inhibits the outgrowth of malignant stem cells preserved in long-term culture. J Clin Invest 1998; 102: 976-83.

  48. Després D, Goldschmitt J, Aulitzky W, Huber C, Peschel C. Differential effect of type I interferons on hematopoietic progeni tor cells: failure of interferon’s to inhibit IL-3-stimulated normal and CML myeloid progenitors. Exp Hematol 1995; 23: 1431-8.

  49. Marley S, Deininger M, Davidson J, Goldman J, Gordon M. The tyrosine kinase inhibitors STI561, like interferon-alpha, preferentially reduces the capacity for amplification of granulocyte- macrophage progenitors from patients with chronic myeloid leukemia. Exp Hematol 2000; 28: 551-7.

  50. Gabriele L, Borghi P, Rozera C, Sestili P, Andreotti M, Guarini A, et al. IFN-alpha promotes the rapid differentiation of monocytes from patients with chronic myeloid leukemia into activated dendritic cells tuned to undergo full maturation after LPS treatment. Blood 2004; 103: 980-7.

  51. Talpaz M. Interferon-alfa-based treatment of chronic myeloid leukemia and implications of signal transduction inhibition. Semin Hematol 2001; 38: 22-7.

  52. Martín-Henao G, Quiroga R, Sureda A, Gonzalez J, Moreno V, Garcia J. L-selectin expression is low on CD34+ cells from patients with chronic myeloid leukemia and interferon-a up regulates this expression. Haematologica 2000; 85: 139-46.

  53. Belluci R, Sala R, De Porpris M, Cordone I, de Fabritis P. Interferon- alpha and bcr-abl antisense oligodeoxinulceotides in combination enhance the antileukemic effect and the adherence of CML progenitors to preformed stroma. Leuk Lymphoma 1999; 35: 471-81.

  54. Góngora-Bianchi R, Selva-Pallares J, Gómez-Almaguer D, Meillón-García L, Vela-Ojeda L, Espinosa-Larrañaga F. Grupo Colaborativo AMEH/LMV. Declaración Mexicana de posición para el tratamiento de la Leucemia Mieloide Crónica. Revista de Hematología 2005; 6: S1-S11.

  55. Anafi M, Gazit A, Zehavi A, Ben-Neriah Y, Levitzki A. Tyrphostin- induced inhibition of p210 bcr-abl tyrosine kinase activity induces K562 to differentiate. Blood 1993; 82: 3524-9.

  56. Druker B, Lydon N. Lessons learned from the development of an Abl tyrosine kinase inhibitor for chronic myelogenous leukemia. J Clin Invest 2000; 105: 3-7.

  57. Goldman J. Tyrosine-kinase inhibition in treatment of chronic myeloid leukaemia. Lancet 2000; 355: 1031-2.

  58. Sawyers C. Molecular studies in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors. Semin Hematol 2001; 38: 15-21.

  59. Druker B, Tamura S, Buchdunger E, Ohno S, Segal G, Fanning S, et al. Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells. Nat Med 1996; 2: 561-6.

  60. Carroll M, Ohno-Jhones S, Tamura S, Buchdunger E, Zimmermann J, Lydon N, et al. CGP57148, a tyrosine kinase inhibitor, inhibits the growth of cells expressing BCR-ABL, TEL-ABL, and TEL-PDGFR fusion proteins. Blood 1997; 90: 4947-52.

  61. Mow M, Chandra J, Svingen P, Hallgren C, Weisber E, Kottke T, et al. Effects of the Bcr/abl kinase inhibitors STI571 and adaphostin (NSC680410) on CML cells in vitro. Blood 2002; 99: 664-71.

  62. Kindler T, Breitenbuecher F, Kasper S, Stevens T, Carius B, Gschaidmeier H, et al. In BCR-ABL positive cells, STAT5 tyrosine-phosphorylation integrates signal induced by imatinib mesylate and Ara C. Leukemia 2003; 17: 999-1009.

  63. Gambacorti-Passerini C, Barni R, Marchesi E, Verga M, Rossi F, Rossi F, et al. Sensitivity to the abl inhibitor STI571 in fresh leukaemic cells obtained from chronic myelogenous leukaemia patients in different stages of disease. Br J Haematol 2001; 112: 972-4.

  64. Holtz M, Slovak M, Zhang F, Sawyers C, Forman S, Bathia R. Imatinib mesylate (STI571) inhibits growth of primitive malignant progenitors in chronic myelogenous leukemia through reversal of abnormally increased proliferation. Blood 2002; 99: 3792-800.

  65. Graham S, Jorgensen H, Allan E, Pearson C, Alcorn M, Richmond L, Holyoake T. Primitive, quiescent, Philadelphiapositive stem cells from patients with chronic myeloid leukemia are insensitive to STI571 in vitro. Blood 2002; 99: 319-25.

  66. Chávez-González A, Ayala-Sánchez M, Sánchez-Valle E, Ruíz-Sánchez E, Arana-Trejo RM, Vela-Ojeda J, Mayani H. Functional integrity in vitro of hematopoietic progenitor cells from patients with chronic myeloid leukemia that have achieved hematological remission after different therapeutic procedures. Leuk Res 2006; 30: 286-95.

  67. Bhatia R, Holtz M, Niu N, Gray R, Snyder D, Sawyers C, et al. Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment. Blood 2003; 101: 4701-07.

  68. Von-Bubnoff N, Peschel C, Duyster J. Resistance of Philadelphia- chromosome positive leukemia towards the kinase inhibitor imatinib (STI571, Glivec): a targeted oncoprotein strikes back. Leukemia 2003; 17: 829-38.

  69. Mahon F, Belloc F, Lagarde V, Chollet C, Moreau-Gaurdry F, Reifers J, et al. MDR1 gene over expression confers resistance to imatinib mesylate in leukemia cell line models. Blood 2003; 101: 2368-73.

  70. Barthe C, Gharbi M, Lagarde V, Chollet C, Cony-Makhoul P, Reiffers J, et al. Mutation in the ATP-binding site of BCR-ABL in a patient with chronic myeloid leukaemia with increasing resistance to STI571. Br J Haematol 2002: 119: 109-11.

  71. Roumiantsev S, Shah N, Gorre M, Nicoll J, Brasher B, Sawers C, Van Etten R. Clinical resistance to the kinase inhibitor STI571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop. Proc Natl Acad Sci USA 2002; 99: 1000-05.

  72. Weisberg E, Maley P, Mestan J, Cowan-Jacob S, Ray A, Griffin J. AMN107 (nilotinib): a novel and selective inhibitor of BCRABL. Br J Cancer 2006; 94: 1675-796.

  73. Weisberg E, Manley PW, Breitestein W, Bruggenn J, Cowan- Jacob S, Ray A, et al. Characterization of AM107, a selective inhibitor of native and mutant Bcr-Abl. Cancer Cell 2005; 7: 129-41.

  74. Copland M, Hamilton A, Elric L, Baird J, Allan E, Jordanides N, et al. Dasatinib (BMS-354825) targets an earlier progenitor population that imatinib in primary CML but does not eliminate the quiescent fraction. Blood 2006; 107: 4532-9.

  75. O’Hare T, Walters D, Stoffregen E, Jia T, Manley P, Mestan J, et al. In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant abl kinase domain mutants. Cancer Res 2005; 65: 4500-05.

  76. Goldman J. How I treat chronic myeloid leukemia in the Imatinib era. Blood 2007; 110: 2828-37.

  77. Ramírez P, Di-Persio J. Therapy options in Imatinib failures. Oncologist 2008; 4: 424-34.

  78. Copland M, Pellicano F, Richmond L, Allan E, Hamilton A, Lee F, et al. BMS-214662 potently induces apoptosis of chronic myeloid leukemia stem and progenitor cells and synergizes with tyrosine kinase inhibitors. Blood 2008; 111: 2843-53.

  79. Ruiz-Argüelles G, Gómez-Almaguer D, Morales-Toquero A, Gutiérrez-Aguirre C, Vela-Ojeda J, Latin American Cooperative Oncohematology Group, et al. The early referral for reduced- intensity stem cell transplantation in patients with Ph1(+) chronic myelogenous leukemia in chronic phase in the imatinib era: results of the Latin American Cooperative Oncohematology Group (LACOHG) prospective multicenter study. Bone Marrow Transplant 2005; 36: 1043-7.

  80. Vela-Ojeda J, Tripp-Villanueva F, Sánchez-Cortés E, Ayala- Sánchez M, Rosas-Cabral A, Esparza M, et al. Allogeneic bone marrow transplantation for chronic myeloid leukemia: a single center experience. Arch Med Res 2000; 31: 206-09.

  81. Ruiz-Arguelles G, Tarin-Arzaga L, González-Carrillo M, Gutiérrez-Riveroll K, Rangel-Malo R, Gutiérrez-Aguirre C, et al. Therapeutic choices in patients with Ph-positive CML living in México in the tyrosine kinase inhibitor era: SCT or TKIs? Bone Marrow Transplant 2008; 42: 23-8.




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