|
1) Izraeli S, Rainis L, Hertzberg L, et al. Trisomy of chromosome 21 in leukemogenesis. Blood Cells Mol Dis. 2007; 39: 156-9
|
|
|
|
2) Ito E. The role of GATA1 mutation in acute megakaryocytic leukemia. Rinsho Ketsueki. 2006; 47: 1415-22
|
|
|
|
|
3) Malinge S, Izraeli S, Crispino JD. Insights into the manifestations, outcomes, and mechanisms of leukemogenesis in Down syndrome. Blood. 2009; 113: 2619-28
|
|
|
|
|
|
4) Wechsler J, Greene M, McDevitt MA, et al. Acquired mutations in GATA 1 in the megakaryoblastic leukemia of Down syndrome. Nat Genet. 2002; 32: 148-52
|
|
|
|
|
|
5) Xu G, Nagano M, Kanezaki R, et al. Frequent mutations in the GATA-1 gene in the transient myeloproliferative disorder of Down syndrome. Blood. 2003; 102: 2960-8
|
|
|
|
|
|
6) Mundschau G, Gurbuxani S, Gamis AS, et al. Mutagenesis of GATA1 is an initiating 1event in Down syndrome leukemogenesis. Blood. 2003; 101: 4298-300
|
|
|
|
|
|
7) Hitzler JK, Cheung J, Li Y, et al. GATA1 mutations in transient leukemia and acute megakaryoblastic leukemia of Down syndrome. Blood. 2003; 101: 4301-4
|
|
|
|
|
|
8) Groet J, Mulligan C, Spinelli M, et al. Independent clones at separable stages of differentiation, bearing different GATA1 mutations, in the same TMD patient with Down syndrome. Blood. 2005; 106: 1887-8
|
|
|
|
|
|
9) Rainis L, Bercovich D, Strehl S, et al. Mutations in exon 2 of GATA1 are early events in megakaryocytic malignancies associated with trisomy 21. Blood. 2003; 102: 981-6
|
|
|
|
|
|
10) Ahmed M, Sternberg A, Hall G, et al. Natural history of GATA1 mutations in Down syndrome. Blood. 2004; 103: 2480-9
|
|
|
|
|
|
11) Hama A, Yagasaki H, Muramatsu H, et al. Gene alterations and expression of hematopoietic transcription factors in pediatric acute megakaryoblastic leukemia (AMKL): A comparison of Down syndrome (DS)-associated AMKL with non-DS-AMKL. Blood(ASH Annual Meeting Abstracts). 2008; 112: 2261
|
|
|
|
|
|
12) Shimada A, Xu G, Toki T, et al. Fetal origin of the GATA1 mutation in identical twins with transient myeloproliferative disorder and acute megakaryoblastic leukemia accompanying Down syndrome. Blood. 2004; 103: 366
|
|
|
|
|
|
13) Pine SR, Guo Q, Yin C, et al. Incidence and clinical implications of GATA1 mutations in newborns with Down syndrome. Blood. 2007; 110: 2128-31
|
|
|
|
|
|
14) Walters DK, Mercher T, Gu TL, et al. Activating alleles of JAK3 in acute megakaryoblastic leukemia. Cancer Cell. 2006; 10: 65-75
|
|
|
|
|
|
15) Klusmann JH, Reinhardt D, Hasle H, et al. Janus kinase mutations in the development of acute megakaryoblastic leukemia in children with and without Down's syndrome. Leukemia. 2007; 21: 1584-7
|
|
|
|
|
|
16) Hama A, Yagasaki H, Takahashi Y, et al. Mutations of JAK2, JAK3 and GATA1 in acute megakaryoblastic leukemia of Down syndrome. Blood. 2008; 111: 2493-4
|
|
|
|
|
|
17) Lange B. The management of neoplastic disorders of haematopoiesis in children with Down's syndrome. Br J Haematol. 2000; 110: 512-24
|
|
|
|
|
|
18) Miyauchi J, Ito Y, Kawano T, et al. Unusual diffuse liver fibrosis accompanying transient myeloproliferative disorder in Down's syndrome: a report of four autopsy cases and proposal of a hypothesis. Blood. 1992; 80: 1521-7
|
|
|
|
|
|
19) Massey GV, Zipursky A, Chang MN, et al. A prospective study of the natural history of transient leukemia (TL) in neonates with Down syndrome (DS): Children's Oncology Group (COG) study POG-9481. Blood. 2006; 107: 4606-13
|
|
|
|
|
|
20) Klusmann JH, Creutzig U, Zimmermann M, et al. Treatment and prognostic impact of transient leukemia in neonates with Down syndrome. Blood. 2008; 111: 2991-8
|
|
|
|
|
|
21) Muramatsu H, Kato K, Watanabe N, et al. Risk factors for early death in neonates with Down syndrome and transient leukaemia. Br J Haematol. 2008; 142: 610-5
|
|
|
|
|
|
22) Hama A, Yagasaki H, Takahashi Y, et al. Acute megakaryoblastic leukaemia (AMKL) in children: a comparison of AMKL with and without Down syndrome. Br J Haematol. 2008; 140: 552-61
|
|
|
|
|
|
23) Forestier E, Izraeli S, Beverloo B, et al. Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome: an iBFM-SG study. Blood. 2008; 111: 1575-83
|
|
|
|
|
|
24) O'Brien MM, Taub JW, Chang MN, et al. Cardiomyopathy in children with Down syndrome treated for acute myeloid leukemia: a report from the Children's Oncology Group Study POG 9421. J Clin Oncol. 2008; 26: 414-20
|
|
|
|
|
|
25) Gamis AS, Woods WG, Alonzo TA, et al. Increased age at diagnosis has a significantly negative effect on outcome in children with Down syndrome and acute myeloid leukemia: a report from the Children's Cancer Group Study 2891. J Clin Oncol. 2003; 21: 3415-22
|
|
|
|
|
|
26) Abildgaard L, Ellebaek E, Gustafsson G, et al. Optimal treatment intensity in children with Down syndrome and myeloid leukaemia: data from 56 children treated on NOPHO-AML protocols and a review of the literature. Ann Hematol. 2006; 85: 275-80
|
|
|
|
|
|
27) Creutzig U, Reinhardt D, Diekamp S, et al. AML patients with Down syndrome have a high cure rate with AML-BFM therapy with reduced dose intensity. Leukemia. 2005; 19: 1355-60
|
|
|
|
|
|
28) Rao A, Hills RK, Stiller C, et al. Treatment for myeloid leukaemia of Down syndrome: population-based experience in the UK and results from the Medical Research Council AML 10 and AML 12 trials. Br J Haematol. 2006; 132: 576-83
|
|
|
|
|
|
29) Kojima S, Sako M, Kato K, et al. An effective chemotherapy regimen for acute myeloid leukemia and myelodysplastic syndrome with Down's syndrome. Leukemia. 2000; 14: 786-91
|
|
|
|
|
|
30) Kudo K, Kojima S, Tabuchi K, et al. Prospective study of a pirarubicin, intermediate-dose cytarabine, and etoposide regimen in children with Down syndrome and acute myeloid leukemia: the Japanese Childhood AML Cooperative Study Group. J Clin Oncol. 2007; 25: 5442-7
|
|
|
|
|
|
31) Kojima S, Kato K, Matsuyama T, et al. Favorable treatment outcome in children with acute myeloid leukemia and Down syndrome. Blood. 1993; 81: 3164
|
|
|
|
|
|
32) Hasle H, Abrahamsson J, Arola M, et al. Myeloid leukemia in children 4 years or older with Down syndrome often lacks GATA1 mutation and cytogenetics and risk of relapse are more akin to sporadic AML. Leukemia. 2008; 22: 1428-30
|
|
|
|
|
|
33) Kawamura M, Kaku H, Taketani T, et al. Mutations of GATA1, FLT3, MLL-partial tandem duplication, NRAS, and RUNX1 genes are not found in a 7-year-old Down syndrome patient with acute myeloid leukemia (FAB-M2) having a good prognosis. Cancer Genet Cytogenet. 2008; 180: 74-8
|
|
|
|
|
|
34) Daifu T, Kato I, Matubara H, et al. Relapsed acute myeloid leukemia with Down syndrome showing long disease-free survival after bone marrow transplantation. Rinsho Ketsueki. 2009; 50: 73-7
|
|
|
|
|
|
35) Zwaan CM, Kaspers GJ, Pieters R, et al. Different drug sensitivity profiles of acute myeloid and lymphoblastic leukemia and normal peripheral blood mononuclear cells in children with and without Down syndrome. Blood. 2002; 99: 245-51
|
|
|
|
|
|
36) Yamada S, Hongo T, Okada S, et al. Distinctive multidrug sensitivity and outcome of acute erythroblastic and megakaryoblastic leukemia in children with Down syndrome. Int J Hematol. 2001; 74: 428-36
|
|
|
|
|
|
37) Ge Y, Stout ML, Tatman DA, et al. GATA1, cytidine deaminase, and the high cure rate of Down syndrome children with acute megakaryocytic leukemia. J Natl Cancer Inst. 2005; 97: 226-31
|
|
|
|
|