ライフサイエンスコーパス: megakaryoblastic leukemia

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

9 Megakaryoblastic leukemia 1 (MKL1) is a myocardin-relate

10 Megakaryoblastic leukemia 1 (MKL1) is a myocardin-relate

11 utrophil immunodeficiency disorder caused by megakaryoblastic leukemia 1 (MKL1) mutation.

12 Megakaryoblastic leukemia 1 (MKL1) promotes the regulati

13 ocytosis of ACs by splenic MZMs required the megakaryoblastic leukemia 1 (MKL1) transcriptional coact

14 Moreover, megakaryoblastic leukemia 1 (MKL1), a well-known actor i

15 Megakaryoblastic leukemia 1 (MKL1), also known as MAL or

16 Megakaryoblastic leukemia 1 (MKL1), identified as part o

17 and a mechanosensitive transcription factor, megakaryoblastic leukemia 1 (MKL1), that coordinately re

18 ctivation of the transcriptional coactivator megakaryoblastic leukemia 1 (MKL1), which targets the se

19 regulate Srf in part via a pathway involving megakaryoblastic leukemia 1 (Mkl1, also known as myocard

20 in-related protein 2/3 complex subunit 1B or megakaryoblastic leukemia 1 deficiency also failed to sh

21 protein 15 (RBM15) is involved in the RBM15-megakaryoblastic leukemia 1 fusion in acute megakaryobla

22 long noncoding RNA called inflammatory MKL1 (megakaryoblastic leukemia 1) interacting long noncoding

23 Z macrophages (MZMs), which in turn disrupts megakaryoblastic leukemia 1-mediated (MKL1-mediated) mec

24 g gene with homology to Drosophila spen, and Megakaryoblastic Leukemia-1 (MKL1), a gene encoding an S

25 ogic disruption of the transcription factors megakaryoblastic leukemia-1 (MKL1)/serum response factor

26 ocardin and the related transcription factor megakaryoblastic leukemia-1 (MKL1/MAL/MRTF-A) can strong

27 n the serum response factor (SRF) co-factors Megakaryoblastic Leukemia-1 and -2 (MKL1 and MKL2) and t

28 ctin polymerization, nuclear accumulation of megakaryoblastic leukemia-1 protein, and SRF activation.

29 ies that human GATA1 mutations promote acute megakaryoblastic leukemia, a clonal malignancy with feat

30 ignificant proportion of children with acute megakaryoblastic leukemia acquire a translocation that c

31 markedly increased risk of developing acute megakaryoblastic leukemia (AMKL) and acute lymphoblastic

32 (DS) have a greatly increased risk of acute megakaryoblastic leukemia (AMKL) and acute lymphoblastic

33 cal and biologic features of pediatric acute megakaryoblastic leukemia (AMKL) and to identify prognos

34 cases of Down syndrome (DS)-associated acute megakaryoblastic leukemia (AMKL) and transient leukemia

35 Pediatric acute megakaryoblastic leukemia (AMKL) associated with the CBF

36 actor 1 receptor (CSF1R) kinase in the acute megakaryoblastic leukemia (AMKL) cell line MKPL-1.

37 Acute megakaryoblastic leukemia (AMKL) comprises between 4% an

38 The recurrent t(1;22) translocation in acute megakaryoblastic leukemia (AMKL) encodes the RBM15-MKL1

39 ly death and subsequent development of acute megakaryoblastic leukemia (AMKL) have been reported.

40 Acute megakaryoblastic leukemia (AMKL) is a form of acute myel

41 Acute megakaryoblastic leukemia (AMKL) is a heterogeneous dise

42 Acute megakaryoblastic leukemia (AMKL) is a heterogeneous dise

43 Acute megakaryoblastic leukemia (AMKL) is a rare subtype of AM

44 Acute megakaryoblastic leukemia (AMKL) is a subtype of acute m

45 Acute megakaryoblastic leukemia (AMKL) is a subtype of acute m

46 Acute megakaryoblastic leukemia (AMKL) is more frequently obse

47 of pediatric non-Down's syndrome (DS), acute megakaryoblastic leukemia (AMKL), a malignancy with poor

48 ndrome (DS) are predisposed to develop acute megakaryoblastic leukemia (AMKL), characterized by expre

49 eukemia that closely phenocopied human acute megakaryoblastic leukemia (AMKL), reflected by flow cyto

50 TMD may be a precursor to acute megakaryoblastic leukemia (AMKL), with an estimated 30%

51 is a key event in the pathogenesis of acute megakaryoblastic leukemia (AMKL).

52 ), and 20% to 30% of those progress to acute megakaryoblastic leukemia (AMKL).

53 clonal preleukemia, and/or who develop acute megakaryoblastic leukemia (AMKL).

54 trisomic for Hsa21, are predisposed to acute megakaryoblastic leukemia (AMKL).

55 myeloproliferative disorder (TMD) and acute megakaryoblastic leukemia (AMKL).

56 myeloproliferative disorder (TMD), and acute megakaryoblastic leukemia (AMKL).

57 k of developing leukemia, particularly acute megakaryoblastic leukemia (AMKL).

58 es of acute lymphoblastic leukemia and acute megakaryoblastic leukemia (AMKL); DS newborns present wi

59 of hematologic malignancies, including acute megakaryoblastic leukemia and a subset of myeloprolifera

60 wn syndrome (DS) have had significantly more megakaryoblastic leukemia and have experienced better ou

61 JAK inhibitors are selective for acute megakaryoblastic leukemia and significantly prolong surv

62 L as a potential therapy option in erythroid/megakaryoblastic leukemias and highlight an AML subgroup

63 s part of the t(1;22) translocation in acute megakaryoblastic leukemia, and plays a critical role in

64 nuclear abundance of transcription cofactor, megakaryoblastic leukemia, and protein levels of its tar

65 MEG-01 is the human megakaryoblastic leukemia cell line that can be differen

66 megakaryocytic differentiation of the human megakaryoblastic leukemia cell line UT7-MPL.

67 of HPIP in K562 cells, a multipotent erythro-megakaryoblastic leukemia cell line, led to an induction

68 BCL2 or MCL1, for the survival of erythroid/megakaryoblastic leukemia cell lines.

69 toclax as highly effective against erythroid/megakaryoblastic leukemia cell lines.

70 oprotein, which is found in aggressive acute megakaryoblastic leukemia, confers megakaryocytic identi

71 in the vast majority of patients with acute megakaryoblastic leukemia (DS-AMKL) and in nearly every

72 drome (DS) are at high risk to develop acute megakaryoblastic leukemia (DS-AMKL) and the related tran

73 striction is achieved in Down syndrome acute megakaryoblastic leukemia (DS-AMKL), characterized by th

74 of these infants subsequently develop acute megakaryoblastic leukemia (DS-AMKL).

75 ative disorder (TMD) and Down syndrome-acute megakaryoblastic leukemia (DS-AMKL).

76 ttention as a candidate oncogene in DS-acute megakaryoblastic leukemia (DS-AMKL).

77 ed transient leukemia) and the related acute megakaryoblastic leukemia (DS-AMKL, also called DS-AML M

78 syndrome with erythroid features, and acute megakaryoblastic leukemia (FAB M7) and are characterized

79 ty of myocardin to physically associate with megakaryoblastic leukemia factor-1 (MKL1) and characteri

80 d possibly increasing ability to distinguish megakaryoblastic leukemia from lymphoid leukemia.

81 formed by the t(1;22) translocation of acute megakaryoblastic leukemia had a markedly increased abili

82 hildren with Down syndrome who develop acute megakaryoblastic leukemia harbor mutations in GATA1 that

83 tomics of patient samples with erythroid and megakaryoblastic leukemias identified high BCL2L1 expres

84 proliferative disease (MPD) with features of megakaryoblastic leukemia in a murine transplant model.

85 sregulation of GATA-2 is a hallmark of acute megakaryoblastic leukemia in children with Down syndrome

86 to identify chromosome 21 genes that promote megakaryoblastic leukemia in children with DS.

87 ons in which several members developed acute megakaryoblastic leukemia in early childhood.

88 o cooperate with GATA1 mutations to initiate megakaryoblastic leukemia in vivo.

89 the t(1;22) translocation specific to acute megakaryoblastic leukemia, is highly expressed in differ

90 cation involving 14 cases of pediatric acute megakaryoblastic leukemia, MIST more robustly identified

91 Megakaryoblastic leukemia (MKL)/serum-response factor (S

92 ing pediatric Down syndrome-associated acute megakaryoblastic leukemia, myelodysplastic syndromes, ch

93 mutation spectrum in non-Down syndrome acute megakaryoblastic leukemia (non-DS-AMKL), we performed tr

94 Acute megakaryoblastic leukemia of Down syndrome (DS-AMKL) is

95 platelet counts, more antecedent MDS, acute megakaryoblastic leukemia or undifferentiated AML, and a

96 ranscription factor A (Mrtfa), also known as megakaryoblastic leukemia protein (Mkl1/MAL), associates

97 ethod to gene expression profiling for acute megakaryoblastic leukemia shows that our method detects

98 ablish a model of CBFA2T3-GLIS2 driven acute megakaryoblastic leukemia that allows the distinction of

99 s a fusion oncogene found in pediatric acute megakaryoblastic leukemia that is associated with a poor

100 t t(1;22) chromosomal translocation in acute megakaryoblastic leukemia, the mechanisms by which MRTFA

101 contribute to Diamond-Blackfan anemia, acute megakaryoblastic leukemia, transient myeloproliferative

102 in)-box transcriptional co-regulator, Mkl-1 (megakaryoblastic leukemia [translocation] 1).

103 Megakaryoblastic leukemia was unfavorable in others but

104 er preleukemic disorders together with acute megakaryoblastic leukemia, whereas quantitative or quali