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1 ansient myeloproliferative disease and acute megakaryoblastic leukemia.
2 nsient myeloproliferative disorder and acute megakaryoblastic leukemia.
3 e disorder, and increased incidence of acute megakaryoblastic leukemia.
4 in the pathogenesis of trisomy 21-associated megakaryoblastic leukemia.
5 -megakaryoblastic leukemia 1 fusion in acute megakaryoblastic leukemia.
6 th MKL in the t(1;22) translocation of acute megakaryoblastic leukemia.
7 ;22) is the principal translocation of acute megakaryoblastic leukemias.
8 um response factor (SRF) and its coactivator megakaryoblastic leukemia 1 (MKL1) had increased express
12 ocytosis of ACs by splenic MZMs required the megakaryoblastic leukemia 1 (MKL1) transcriptional coact
16 and a mechanosensitive transcription factor, megakaryoblastic leukemia 1 (MKL1), that coordinately re
17 ctivation of the transcriptional coactivator megakaryoblastic leukemia 1 (MKL1), which targets the se
18 regulate Srf in part via a pathway involving megakaryoblastic leukemia 1 (Mkl1, also known as myocard
19 protein 15 (RBM15) is involved in the RBM15-megakaryoblastic leukemia 1 fusion in acute megakaryobla
20 Z macrophages (MZMs), which in turn disrupts megakaryoblastic leukemia 1-mediated (MKL1-mediated) mec
21 g gene with homology to Drosophila spen, and Megakaryoblastic Leukemia-1 (MKL1), a gene encoding an S
22 ogic disruption of the transcription factors megakaryoblastic leukemia-1 (MKL1)/serum response factor
23 ocardin and the related transcription factor megakaryoblastic leukemia-1 (MKL1/MAL/MRTF-A) can strong
24 n the serum response factor (SRF) co-factors Megakaryoblastic Leukemia-1 and -2 (MKL1 and MKL2) and t
25 ctin polymerization, nuclear accumulation of megakaryoblastic leukemia-1 protein, and SRF activation.
26 ies that human GATA1 mutations promote acute megakaryoblastic leukemia, a clonal malignancy with feat
27 ignificant proportion of children with acute megakaryoblastic leukemia acquire a translocation that c
28 markedly increased risk of developing acute megakaryoblastic leukemia (AMKL) and acute lymphoblastic
29 (DS) have a greatly increased risk of acute megakaryoblastic leukemia (AMKL) and acute lymphoblastic
30 cal and biologic features of pediatric acute megakaryoblastic leukemia (AMKL) and to identify prognos
31 cases of Down syndrome (DS)-associated acute megakaryoblastic leukemia (AMKL) and transient leukemia
34 ly death and subsequent development of acute megakaryoblastic leukemia (AMKL) have been reported.
42 ndrome (DS) are predisposed to develop acute megakaryoblastic leukemia (AMKL), characterized by expre
50 es of acute lymphoblastic leukemia and acute megakaryoblastic leukemia (AMKL); DS newborns present wi
51 of hematologic malignancies, including acute megakaryoblastic leukemia and a subset of myeloprolifera
52 wn syndrome (DS) have had significantly more megakaryoblastic leukemia and have experienced better ou
53 s part of the t(1;22) translocation in acute megakaryoblastic leukemia, and plays a critical role in
55 of HPIP in K562 cells, a multipotent erythro-megakaryoblastic leukemia cell line, led to an induction
56 oprotein, which is found in aggressive acute megakaryoblastic leukemia, confers megakaryocytic identi
57 in the vast majority of patients with acute megakaryoblastic leukemia (DS-AMKL) and in nearly every
58 drome (DS) are at high risk to develop acute megakaryoblastic leukemia (DS-AMKL) and the related tran
59 striction is achieved in Down syndrome acute megakaryoblastic leukemia (DS-AMKL), characterized by th
63 ed transient leukemia) and the related acute megakaryoblastic leukemia (DS-AMKL, also called DS-AML M
64 ty of myocardin to physically associate with megakaryoblastic leukemia factor-1 (MKL1) and characteri
66 formed by the t(1;22) translocation of acute megakaryoblastic leukemia had a markedly increased abili
67 hildren with Down syndrome who develop acute megakaryoblastic leukemia harbor mutations in GATA1 that
68 proliferative disease (MPD) with features of megakaryoblastic leukemia in a murine transplant model.
69 sregulation of GATA-2 is a hallmark of acute megakaryoblastic leukemia in children with Down syndrome
72 the t(1;22) translocation specific to acute megakaryoblastic leukemia, is highly expressed in differ
73 cation involving 14 cases of pediatric acute megakaryoblastic leukemia, MIST more robustly identified
75 mutation spectrum in non-Down syndrome acute megakaryoblastic leukemia (non-DS-AMKL), we performed tr
76 platelet counts, more antecedent MDS, acute megakaryoblastic leukemia or undifferentiated AML, and a
77 ethod to gene expression profiling for acute megakaryoblastic leukemia shows that our method detects
78 contribute to Diamond-Blackfan anemia, acute megakaryoblastic leukemia, transient myeloproliferative
80 er preleukemic disorders together with acute megakaryoblastic leukemia, whereas quantitative or quali
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