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Haematological Malignancies


(V617F) mutation status, granulocyte activatin, and constitutive mobilization of CD34+ cells into peripheral blood in myeloproliferative disorders, Blood, 2006;107(9): 3676–82.


17. Barosi G, Bergamaschi G, Marchetti M, et al., JAK2 V617F mutational status predicts progression to large splenomegaly and leukaemic transformation in primary myelofibrosis, Blood, 2007;110(12):4030–6.


18. Thoennissen NH, Krug UO, Lee DH, et al., Prevalence and prognostic impact of allelic imbalances associated with leukaemic transformation of Philadelphia chromosome- negative myeloproliferative neoplasms, Blood, 2010;115(14): 2882–90.


19. Campbell PJ, Baxter EJ, Beer PA, et al., Mutation of JAK2 in the myeloproliferative disorders: timing, clonality studies, cytogenetic associations, and role in leukaemic transformation, Blood, 2006;108(10):3548–55.


20. Theocharides A, Boissinot M, Girodon F, et al., Leukemic blasts in transformed JAK2-V617F-positive myeloproliferative disorders are frequently negative for the JAK2-V617F mutation, Blood, 2007;110(1):375–9.


21. Tam CS, Nussenzveig RM, Popat U, et al., The natural history and treatment outcome of blast phase BCR-ABL- myeloproliferative neoplasms, Blood, 2008;112(5):1628–37.


22. Gaidano G, Guerrasio A, Serra A, et al., Mutations of the P53 and RAS family genes are associated with tumor progression of BCR/ABL negative chronic myeloproliferative disorders, Leukemia, 1993;7(7):946–53.


23. Gaidano G, Pastore C, Santini V, et al., Genetic lesions associated with blastic transformation of polycythemia vera and essential thrombocythemia, Genes Chromosomes Cancer, 1997;19(4):250–5.


24. Pedersen-Bjergaard J, Rowley JD, The balanced and the unbalanced chromosome aberrations of acute myeloid leukaemia may develop in different ways and may contribute differently to malignant transformation, Blood, 1994;83:2780.


25. Sterkers Y, Preudhomme C, Lai JL, et al., Acute myeloid leukaemia and myelodysplastic syndromes following essential thrombocythemia treated with hydroxyurea: high proportion of cases with 17p deletion, Blood, 1998;91(2):616–22.


26. Beer PA, Delhommeau F, LeCouédic JP, et al., Two routes to leukaemic transformation after a JAK2 mutation-positive myeloproliferative neoplasm, Blood, 2010;115(14):2891–900.


27. Kiladjian JJ, Rain JD, Bernard JF, et al., Long-term incidence of hematological evolution in three French prospective studies of hydroxyurea and pipobroman in polycythemia vera and essential thrombocytothemia, Semin Thromb Hemost, 2006;32: 417–21.


28. Burkitt MJ, Raafat A, Nitric oxide generation from hydroxyurea: signifiance and implications for leukemogenesis in the management of myeloproliferative disorders, Blood,


2006;107(6):2219–22.


29. Negrini S, Gorgoulis VG, Halazonetis TD, Genomic instability – an evolving hallmark of cancer, Nat Rev Mol Cell Biol, 2010;11(3): 220–8.


30. Aurer I, Labar B, Nemet D, et al., High incidence of conservative RAS mutations in myeloid leukaemia, Acta Haematol, 1994;92(3):123–5.


31. Braun BS, Tuveson DA, Kong N, et al., Somatic activation of oncogenic Kras in hematopoietic cells initiates a rapidly fatal myeloproliferative disorder, Proc Natl Acad Sci U S A, 2004;101(2):597–602.


32. Reilly JT, Wilson G, Barnett D, et al., Karyotypic and ras gene mutational analysis in idiopathic myelofibrosis, Br J Haematol, 1994;88(3):575–81.


33. Mavrogianni D, Viniou N, Michali E, et al., Leukemogenic risk of hydroxyurea therapy as a single agent in polycythemia vera and essential thrombocythemia: N- and K-ras mutations and microsatellite instability in chromosomes 5 and 7 in 69 patients, Int J Hematol, 2002;75(4):394–400.


34. Ding Y, Harada Y, Imagawa J, et al., AML1/RUNX1 point mutation possibly promotes leukaemic tranformation in myeloproliferative neoplasms, Blood, 2009;114(25):5201–5.


35. Wattel E, Preudhomme C, Hecquet B, et al., p53 mutations are associated with resistance to chemotherapy and short survival in hemataologic malignancies, Blood, 1994;84(9): 3148–57.


36. Haferlach C, Dicker F, Herholz H, et al., Mutations of the TP53 gene in acute myeloid leukaemia are strongly associated with a complex aberrant karyotype, Leukemia, 2008;22(8):1539–41.


37. Bohlander SK, ETV6: a versatile player in leukemogenesis, Semin Cancer Biol, 2005;15(3):162–74.


38. Pabst T, Mueller BU, Transcriptional dysregulation during myeloid transformation in AML, Oncogene, 2007;26(47): 6829–37.


39. Mitelman F, Kaneko Y, Trent JM, Report of the committee on chromosome changes in neoplasia, Cytogenet Cell Genet, 1990;55(1–4):358–86.


40. Johnson E, Cotter FE, Monosomy 7 and 7q associated with myeloid malignancy, Blood Rev, 1997;11(1):46–55.


41. van den Heuvel-Eibrink MM, Wiemer EA, de Boevere MJ, et al., MDR1 expression in poor-risk acute meloid leukaemia with partial or complete monosomy 7, Leukemia, 2001;15(3): 398–405.


42. Li M, Li Z, Morris DL, et al., Identification of SH2B2beta as an inhibitor for SH2B1- and SH2B2alpha-promoted Janus kinase-2 activation and insulin signaling, Endocrinology, 2007;148(4): 1615–21.


43. Sinclair AM, Lee JA, Goldstein A, et al., Lyphoid apoptosis and myeloid hyperplasia in CCAAT displacement protein mutant mice, Blood, 2001;98(13):3658–67.


44. Passam FH, Tsirakis G, Boula A, et al., Levels of soluble forms of ICAM and VCAM in patients with myelodysplastic syndromes and their prognostic significance, Clin Lab Haematol, 2004;26(6):391–5.


45. Pearl LH, Hsp90 and Cdc37 – a chaperone cancer conspiracy, Curr Opin Genet Dev, 2005;15(1):55–61.


46. Warner JK, Wang JC, Takenaka K, et al., Direct evidence for cooperating genetic events in the leukaemic transformation of normal human hematopopietic cells, Leukemia, 2005;19(10): 1794–1805.


47. Yeh ES, Means AR, PIN1, the cell cycle and cancer, Nat Rev Cancer, 2007;7(5):381–8.


48. Tefferi A, Pardanani A, Lim KH, et al., TET2 mutations and their clinical correlates in polycythemia vera, essential thrombocythemia and myelofibrosis, Leukemia, 2009;23(5): 905–11.


49. Tahiliani M, Koh KP, Shen Y, et al., Conversion of 5- methylcytosine to 5-hydroxymethylcytosine in mammalian DNA by MLL partner TET1, Science, 2009;324(5929):930–5.


50. Carbuccia N, Murati A, Trouplin V, et al., Mutatoins of ASXL1 gene in myeloproliferative neoplasms, Leukemia, 2009;23: 2183–6.


51. Tefferi A, Lasho TL, Abdel-Wahab O, et al., IDH1 and IDH2 mutation studies in 1473 patients with chronic-, fibrotic- or blast-phase essential thrombocythemia, polycythemia vera or myelofibrosis, Leukemia, 2010;24(7):1302–9.


52. Dunbar AJ, Gondek LP, O’Keefe CL, 250K single nucleotide polymorphism array karyotyping identifies acquired uniparental disomy and homozygous mutations, including novel missense substitutions of c-Cbl, in myeloid malignancies, Cancer Res, 2008;68(24):10349–57.


53. Tefferi A, Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH and IKZF1, Leukemia, 2010;24(6): 1128–38.


54. Baxter EJ, Scott LM, Campbell PJ, et al., Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders, Lancet, 2005;365(9464):1054–61.


55. James C, Ugo V, Le Couedic JP, et al., A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera, Nature, 2005;434(7037):1144–8.


56. Kralovics R, Passamonti F, Buser AS, et al., A gain-of-function mutation of JAK2 in myeloproliferative disorders, N Engl J Med, 2005;352(17):1779–90.


57. Levine RL, Wadleigh M, Cools J, et al., Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis, Cancer Cell, 2005;7(4):387–97.


58. Gondek LP, Tiu R, O’Keefe CL, et al., Chromosomal lesions and uniparental disomy detected by SNP arrays in MDS, MDS/MPD, and MDS-derived AML, Blood, 2008;111(3):1534–42.


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EUROPEAN ONCOLOGY & HAEMATOLOGY


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