Page 34 - 2019_05-HaematologicaMondo-web
P. 34

A. Tuval and L.I. Shlush et al.
et al. Minimal residual disease monitoring
based on FLT3 internal tandem duplication in adult acute myeloid leukemia. Leuk Res. 2012;36(3):316-323.
45. Arber DA, Orazi A, Hasserjian R, et al. The 2016 revision to the world health organiza- tion classification of myeloid neoplasms and acute leukemia. Blood. 2016;127(20):2391- 2405.
46. Swerdlow SH, Campo E, Harris NL, et al, editors. WHO classification of tumours of haematopoietic and lymphoid tissues. 4th ed. Lyon: IARC; 2008.
47. Grimwade D, Jovanovic JV, Hills RK, et al. Prospective minimal residual disease moni- toring to predict relapse of acute promyelo- cytic leukemia and to direct pre-emptive arsenic trioxide therapy. J Clin Oncol. 2009;27(22):3650-3658.
48. Jourdan E, Boissel N, Chevret S, et al. Prospective evaluation of gene mutations and minimal residual disease in patients with core binding factor acute myeloid leukemia. Blood. 2013;121(12):2213-2223.
49. Wiemels JL, Xiao Z, Buffler PA, et al. In utero origin of t(8;21) AML1-ETO transloca- tions in childhood acute myeloid leukemia. Blood. 2002;99(10):3801-3805.
50. Jurlander J, Caligiuri MA, Ruutu T, et al. Persistence of the AML1/ETO fusion tran- script in patients treated with allogeneic bone marrow transplantation for t(8;21) leukemia. Blood. 1996;88(6):2183-2191.
51. Miyamoto T, Weissman IL, Akashi K. AML1/ETO-expressing nonleukemic stem cells in acute myelogenous leukemia with 8;21 chromosomal translocation. Proc Natl Acad Sci U S A. 2000;97(13):7521-7526.
52. Chapiro E, Delabesse E, Asnafi V, et al. Expression of T-lineage-affiliated transcripts and TCR rearrangements in acute promye- locytic leukemia: implications for the cellu- lar target of t(15;17). Blood. 2006;108(10): 3484–3493.
53. Ailles LE, Gerhard B, Kawagoe H, Hogge DE. Growth characteristics of acute myel- ogenous leukemia progenitors that initiate
malignant hematopoiesis in nonobese dia- betic/severe combined immunodeficient mice. Blood. 1999;94(5):1761-1772.
54. Grimwade D, Enver T. Acute promyelocytic leukemia: where does it stem from? Leukemia. 2004;18(3):375-384.
Enasidenib in mutant IDH2 relapsed or refractory acute myeloid leukemia. Blood. 2017;130(6):722-731.
65. Krönke J, Bullinger L, Teleanu V, et al. Clonal evolution in relapsed NPM1-mutated acute myeloid leukemia. Blood. 2013;122(1):100-
55. Haferlach T, Löffler H, Nickenig C, et al. Cell 108.
lineage specific involvement in acute promyelocytic leukaemia (APL) using a combination of May-Grunwald-Giemsa staining and fluorescence in situ hybridiza- tion techniques for the detection of the translocation t(15;17)(q22;q12). Br J Haematol. 1998;103(1):93-99.
56. Turhan AG, Lemoine FM, Debert C, et al. Highly purified primitive hematopoietic stem cells are PML-RARA negative and gen- erate nonclonal progenitors in acute promyelocytic leukemia. Blood. 1995;85(8): 2154-2161.
57. SEER program [Internet]. National Cancer Institute. 2018 - [cited 2019 January 10]. Available from: https://seer.cancer.gov/
58. Shlush LI. Age related clonal hematopoiesis. Blood. 2018;131(5):496-504.
59. Berger G, Kroeze LI, Koorenhof-Scheele TN, et al. Early detection and evolution of preleukemic clones in therapy-related myeloid neoplasms following autologous SCT. Blood. 2018;131(16):1846-1857.
60. Zhang W, Deisseroth AB. Conformational change of p53 protein in growth factor-stim- ulated human myelogenous leukemia cells. Leuk Lymphoma. 1994;14(3-4):251-255.
61. Ding L, Ley TJ, Larson DE, et al. Clonal evo- lution in relapsed acute myeloid leukaemia revealed by whole-genome sequencing. Nature. 2012;481(7382):506-510.
62. Parkin B, Ouillette P, Li Y, et al. Clonal evo- lution and devolution after chemotherapy in adult acute myelogenous leukemia. Blood. 2013;121(2):369-377.
63. Di Nardo CD, Stein EM, de Botton S, et al. Durable remissions with ivosidenib in IDH1-mutated relapsed or refractory AML. N Engl J Med. 2018;378(25):2386-2398.
64. Stein EM, Di Nardo CD, Pollyea DA, et al.
66. Ng SW, Mitchell A, Kennedy JA, et al. A 17- gene stemness score for rapid determination of risk in acute leukaemia. Nature. 2016;540(7633):433-437.
67. Pollyea DA, Stevens BM, Jones CL, et al. Venetoclax with azacitidine disrupts energy metabolism and targets leukemia stem cells in patients with acute myeloid leukemia. Nat Med. 2018;24(12):1859-1866.
68. Di Nardo CD, Pratz K, Pullarkat V, et al. Venetoclax combined with decitabine or azacitidine in treatment-naive, elderly patients with acute myeloid leukemia. Blood. 2019;133(1):7-17.
69. Herold S, Sockel K, Sayehli C, et al. Evolution of NPM1-negative therapy-related myelodysplastic syndromes following cura- tive treatment of NPM1- mutant AML. Leukemia. 2017;31(10):2247-2251.
70. Kohlmann A, Nadarajah N, Alpermann T, et al. Monitoring of residual disease by next- generation deep-sequencing of RUNX1 mutations can identify acute myeloid leukemia patients with resistant disease. Leukemia. 2014;28(1):129-137.
71. Webersinke G, Kranewitter W, Deutschbauer S, et al. Switch of the muta- tion type of the NPM1 gene in acute myeloid leukemia (AML): relapse or second- ary AML? Blood Cancer J. 2014;4(6):e221.
72. Engel N, Rovo A, Badoglio M, et al. European experience and risk factor analysis of donor cell-derived leukaemias/MDS fol- lowing haematopoietic cell transplantation. Leukemia. 2019;33(2):508-517.
73. Hahn CN, Ross DM, Feng J, et al. A tale of two siblings: two cases of AML arising from a single pre-leukemic DNMT3A mutant clone. Leukemia. 2015;29(10):2101-2104.
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