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1 ed transient myeloproliferative disorder and acute megakaryoblastic leukemia.
2 erative disorder, and increased incidence of acute megakaryoblastic leukemia.
3 RBM15-megakaryoblastic leukemia 1 fusion in acute megakaryoblastic leukemia.
4 ner with MKL in the t(1;22) translocation of acute megakaryoblastic leukemia.
5 ote transient myeloproliferative disease and acute megakaryoblastic leukemia.
6 t(1;22) is the principal translocation of acute megakaryoblastic leukemias.
7 scoveries that human GATA1 mutations promote acute megakaryoblastic leukemia, a clonal malignancy wit
8 at a significant proportion of children with acute megakaryoblastic leukemia acquire a translocation
9 have a markedly increased risk of developing acute megakaryoblastic leukemia (AMKL) and acute lymphob
10 ndrome (DS) have a greatly increased risk of acute megakaryoblastic leukemia (AMKL) and acute lymphob
11 clinical and biologic features of pediatric acute megakaryoblastic leukemia (AMKL) and to identify p
12 t all cases of Down syndrome (DS)-associated acute megakaryoblastic leukemia (AMKL) and transient leu
14 ting factor 1 receptor (CSF1R) kinase in the acute megakaryoblastic leukemia (AMKL) cell line MKPL-1.
17 r, early death and subsequent development of acute megakaryoblastic leukemia (AMKL) have been reporte
25 pment of pediatric non-Down's syndrome (DS), acute megakaryoblastic leukemia (AMKL), a malignancy wit
26 own syndrome (DS) are predisposed to develop acute megakaryoblastic leukemia (AMKL), characterized by
27 t of leukemia that closely phenocopied human acute megakaryoblastic leukemia (AMKL), reflected by flo
36 ed rates of acute lymphoblastic leukemia and acute megakaryoblastic leukemia (AMKL); DS newborns pres
37 ubset of hematologic malignancies, including acute megakaryoblastic leukemia and a subset of myelopro
39 Srf, is part of the t(1;22) translocation in acute megakaryoblastic leukemia, and plays a critical ro
40 on oncoprotein, which is found in aggressive acute megakaryoblastic leukemia, confers megakaryocytic
41 tected in the vast majority of patients with acute megakaryoblastic leukemia (DS-AMKL) and in nearly
42 wn syndrome (DS) are at high risk to develop acute megakaryoblastic leukemia (DS-AMKL) and the relate
43 tal restriction is achieved in Down syndrome acute megakaryoblastic leukemia (DS-AMKL), characterized
47 o called transient leukemia) and the related acute megakaryoblastic leukemia (DS-AMKL, also called DS
48 lastic syndrome with erythroid features, and acute megakaryoblastic leukemia (FAB M7) and are charact
49 otein formed by the t(1;22) translocation of acute megakaryoblastic leukemia had a markedly increased
50 ond, children with Down syndrome who develop acute megakaryoblastic leukemia harbor mutations in GATA
51 Dysregulation of GATA-2 is a hallmark of acute megakaryoblastic leukemia in children with Down sy
53 art of the t(1;22) translocation specific to acute megakaryoblastic leukemia, is highly expressed in
54 application involving 14 cases of pediatric acute megakaryoblastic leukemia, MIST more robustly iden
55 including pediatric Down syndrome-associated acute megakaryoblastic leukemia, myelodysplastic syndrom
56 e the mutation spectrum in non-Down syndrome acute megakaryoblastic leukemia (non-DS-AMKL), we perfor
58 ll and platelet counts, more antecedent MDS, acute megakaryoblastic leukemia or undifferentiated AML,
59 our method to gene expression profiling for acute megakaryoblastic leukemia shows that our method de
60 We establish a model of CBFA2T3-GLIS2 driven acute megakaryoblastic leukemia that allows the distinct
61 LIS2 is a fusion oncogene found in pediatric acute megakaryoblastic leukemia that is associated with
62 current t(1;22) chromosomal translocation in acute megakaryoblastic leukemia, the mechanisms by which
63 tions contribute to Diamond-Blackfan anemia, acute megakaryoblastic leukemia, transient myeloprolifer
64 nd other preleukemic disorders together with acute megakaryoblastic leukemia, whereas quantitative or