ライフサイエンスコーパス: myeloblast

1 duce terminal differentiation of FLT3-mutant myeloblasts.

2 trophils as that of the original FLT3-mutant myeloblasts.

3 neutrophilic infiltrates without evidence of myeloblasts.

4 d by replacement of the thymus with leukemic myeloblasts.

5 d sarcoma is an extramedullary malignancy of myeloblasts.

6 3 nor H2B become significantly acetylated in myeloblasts.

7 A) were 2.7-fold lower in DS than for non-DS myeloblasts.

8 ne 5'-triphosphate (ara-CTP) than non-DS AML myeloblasts.

9 tic/molecular abnormalities and/or increased myeloblasts.

10 d 2.6-fold higher in DS compared with non-DS myeloblasts.

11 ration to terminal differentiation of normal myeloblasts.

12 tion with an arrest at the stage of immature myeloblasts.

13 advised for patients with >/=10% bone marrow myeloblasts.

14 ne, cystathionine-beta-synthase (CBS), in DS myeloblasts.

15 ore binding factor 1 (CBF1) in 32D (clone 3) myeloblasts.

16 rodimerize with Hox proteins and immortalize myeloblasts.

17 fusion protein, C/EBPalphaWT-ER, in 32D cl3 myeloblasts.

18 the transactivation of the promoter in Kcl22 myeloblasts.

19 rate that serum, urine, marrow aspirate, and myeloblast 2-HG levels are significantly higher in IDH-m

20 w-risk myelodysplastic syndrome (< 5% marrow myeloblasts), 3-year survivals of 65-75% are achievable

21 tion, cell death, or UPR induction in murine myeloblast 32D and human promyelocytic NB4 cells.

22 d clearance or near clearance of bone marrow myeloblasts after 27 (range 21-84) days with evidence of

23 igher in DS myeloblasts compared with non-DS myeloblasts after incubation with 5 micromol/L ara-C (62

24 ciated with certain leukemias blocked at the myeloblast and promyelocyte stages of differentiation.

25 tic differentiation, with an accumulation of myeloblasts and an absence of mature granulocytes, where

26 lated by E2a-Pbx1 in NIH 3T3 fibroblasts and myeloblasts and by a DNA-binding mutant of E2a-Pbx1 in N

27 nia 2 (ANKRD26-RT) with elevated bone marrow myeloblasts and dysmegakaryopoiesis, without somatic gen

28 GF and one or both receptors was detected in myeloblasts and immature myeloid elements, whereas eryth

29 erns of CBS gene expression in DS and non-DS myeloblasts and may, in part, explain the greater sensit

30 ities characterized by increased bone marrow myeloblasts and myelocytes, as well as extramedullary my

31 Differential priming between malignant myeloblasts and normal hematopoietic stem cells supports

32 nhibition of its expression in HL-60 and NB4 myeloblasts and promyelocytes decreased their proliferat

33 g class IV G-CSFR had greater percentages of myeloblasts and promyelocytes than controls (53% +/- 13%

34 mmature (Mac-1(lo)) myeloid cells, including myeloblasts and promyelocytes, constitutively expressed

35 The highest mRNA levels were observed in myeloblasts and promyelocytes, similar to myeloperoxidas

36 geneity in A1E fusion transcripts in t(8;21) myeloblasts and suggest that synthesis of alternate A1E

37 nificantly higher in DS compared with non-DS myeloblasts, and CBS transcript levels correlated with i

38 cytogenetic abnormalities, percentage of BM myeloblasts, and number of cytopenias; for survival, in

39 Globotriaosylceramide expression on myeloblasts, and possibly myeloid stem cells, may have i

40 e primary human acute myeloid leukemia (AML) myeloblasts, and this heterogeneity decreased in chemoth

41 tein levels significantly increased rates of myeloblast apoptosis two to threefold in response to ser

42 and promoted peripheralization of primitive myeloblasts as early as 2.5 weeks after transplantation.

43 ne shared hallmark is the arrest of leukemic myeloblasts at an immature and self-renewing stage of de

44 sts, L cell fibroblasts, C2C12 myoblasts, M1 myeloblasts, BALB/MK cells, 70Z/3 preB lymphocytes, and

45 myeloid leukaemias (AMLs) involving immature myeloblasts, but a minority were acute lymphoblastic leu

46 ong 1,215 samples with less than 5% leukemic myeloblasts by morphology, 100 (8.2%) were MRD positive

47 roteins were constitutively expressed in the myeloblast cell line M1, using the retrovirus vector LXS

48 C/EBPalpha-ER induces the 32D cl3 myeloblast cell line to differentiate to granulocytes.

49 3-base pair cDNA clone (HA0683) from a human myeloblast cell line.

50 astic cell lines (U937 and THP-1), the early myeloblast cell lines (ML1, KCL22, MDS92), and the T-cel

51 psilon mRNA decreased when the HL60 and KG-1 myeloblast cell lines were induced to differentiate towa

52 associated with host gene mutations and with myeloblast cell percentages.

53 We utilized 32Dcl3 myeloblast cells to investigate translational regulation

54 Likewise, in 32Dcl3 myeloblast cells, CalDAG-GEF Ia expression increases cel

55 1 as a new WT1 target gene in 32D cl3 murine myeloblast cells.

56 reg(EM) impacted survival independently from myeloblast characteristics, cytopenias, karyotype, and c

57 turation but not proliferation, resulting in myeloblast colony formation.

58 te (ara-CTP) were significantly higher in DS myeloblasts compared with non-DS myeloblasts after incub

59 and secondary-AML samples, regardless of the myeloblast count.

60 HL-60 myeloblasts cultured with RA have developed mutations of

61 -epsilon was cloned from a promyelocyte-late myeloblast-derived lambda gt11 library.

62 ing by the Pbx1 HD is essential for blocking myeloblast differentiation but dispensable for fibroblas

63 ms T lymphoblasts and fibroblasts and blocks myeloblast differentiation.

64 tients with less than 5% marrow myeloblasts, myeloblast dyspoiesis was associated with an increased h

65 Like mature peripheral blood neutrophils, myeloblasts expressed glucosylceramide, lactosylceramide

66 y inhibited the proliferation of primary AML myeloblasts expressing FLT3 ITD but not WT FLT3 protein.

67 8 inhibited the proliferation of primary AML myeloblasts expressing mutant FLT3 ITD but not WT FLT3 p

68 ronic myelogenous leukemia (CML), Bcr-Abl(+) myeloblasts fail to undergo terminal maturation.

69 ric sensitivity assay), compared with non-DS myeloblasts, following exposure to ara-C for 72 hours.

70 n the granulocytic developmental pathway, as myeloblasts from C/EBPalpha-null mice exhibit an early b

71 Myeloblasts from Down syndrome (DS) children with acute

72 vity and metabolism of ara-C was examined in myeloblasts from DS and non-DS patients with AML, DS inf

73 pression of chromosome 21-localized genes in myeloblasts from newly diagnosed AML patients.

74 phosphate (ara-CTP) from ara-C compared with myeloblasts from non-DS patients.

75 tein (P-gp), which is often overexpressed in myeloblasts from refractory or relapsed AML.

76 to disrupt differentiation, as evidenced in myeloblast immortalization, but dispensable for its abil

77 We identified CD25(POS) myeloblasts in 87 patients (13%), of whom 92% had interm

78 and MDS remains, with the presence of >=20% myeloblasts in marrow or peripheral blood generally rega

79 itory fragments potentiated the clearance of myeloblasts in the bone marrow of xenograft-recipient mi

80 ransplantation, 69 patients had less than 5% myeloblasts in the marrow, and 40 patients had more adva

81 persistently active in BH3 mimetic-resistant myeloblasts, including FLT-3 inhibitors and SMAC mimetic

82 tant (TSN) from acute myeloid leukemia (AML) myeloblasts inhibits peripheral blood T cell activation

83 Coincidentally, rapamycin-treated myeloblast Kasumi-1 cells exhibit lower levels of transc

84 n analysis on a set of 34 candidate genes in myeloblast (KG-1 and HL-60), monoblast (U937), and T lym

85 identifying the malignant cell population as myeloblasts, leading to a diagnosis of myeloid sarcoma.

86 Here we demonstrated that 32D cells, a myeloblast-like cell line transfected with FLT3-ITD, hav

87 xpression occurring in promyelocyte and late-myeloblast-like cell lines.

88 those that were at the promyelocyte (M3) and myeloblast (M2) stages of development.

89 sylceramide, the parvovirus B19 receptor, on myeloblasts may also explain the association between B19

90 ed in ara-C metabolism between DS and non-DS myeloblasts may lead to improvements in AML therapy.

91 These results elucidate how AML myeloblasts metabolically adapt to BETi by consuming lac

92 Among patients with less than 5% marrow myeloblasts, myeloblast dyspoiesis was associated with a

93 Inducing differentiation of myeloblasts, not cytotoxicity, seems to drive the clinic

94 that express PML-RARalpha or are at the late myeloblast or promyelocyte stage of myeloid development.

95 RNA sequencing of leukemic myeloblasts or CD34(+) cells pooled from healthy donors

96 were no grains specifically associated with myeloblasts or erythroblasts.

97 d 3.8-fold higher in DS compared with non-DS myeloblasts (P <.0001 and P <.0001, respectively).

98 er adjusting for risk factors such as marrow myeloblast percentage and IPSS score.

99 ic Scoring System (IPSS) score or for marrow myeloblast percentage.

100 , such as lactate dehydrogenase, circulating myeloblasts, platelets, and cytogenetics could further s

101 HCT comorbidity index </= 4 and < 5% marrow myeloblasts pre-HCT were randomly assigned to receive MA

102 rpart granulocyte-macrophage progenitors and myeloblast precursors.

103 r interleukin-6 (IL-6), Fos expression in M1 myeloblasts promoted apoptotic cell death, entailing cyt

104 HL-60 cells, a myeloblast/promyelocyte cell line, were cultured in the

105 ased on the acidic motif in Lon protease and myeloblast protein inhibited the binding of nucleolin to

106 in IRS-1 and IRS-2, including Lon protease, myeloblast protein, and nucleolin.

107 Serum and myeloblast samples from patients with IDH-mutant AML con

108 t C/EBP alpha-deficient mice was filled with myeloblasts, similar to human AML, supporting the notion

109 GL-1 was expressed on myeloid cells from the myeloblast stage to the segmented neutrophil, but was no

110 iring lactate utilization rendered resistant myeloblasts susceptible to BET inhibition.

111 ren is linked to increased sensitivity of DS myeloblasts to 1-beta-D-arabinofuranosylcytosine (ara-C)

112 art, to increased in vitro sensitivity of DS myeloblasts to cytosine arabinoside (ara-C) and daunorub

113 marrow, is characterized by the inability of myeloblasts to differentiate into mature cell types.

114 marrow, is characterized by the inability of myeloblasts to differentiate into mature cell types.

115 Lactate utilization allows AML myeloblasts to maintain metabolic integrity and circumve

116 o C/EBPalpha-mediated down-regulation forces myeloblasts to remain in an undifferentiated state.

117 p27, and potentially other factors to induce myeloblasts to undergo granulocytic differentiation and

118 -associated lactate dehydrogenase allows AML myeloblasts to utilize lactate as a metabolic bypass to

119 BETi resistance in AML myeloblasts was found to correlate with maintaining mito

120 DS myeloblasts were approximately 10-fold more sensitive to

121 To study the latter, myeloblasts were collected from patients with acute nonl

122 Primitive myeloblasts were increased to approximately 10% of bone

123 In myeloblasts, where there is a very low level of Lys expr

124 Furthermore, myeloblasts with knocked-down Mer demonstrated decreased

125 , it also enhances the survival of other AML myeloblasts with lower viability.

126 er RNA (mRNA) increases with maturation from myeloblasts with peak level in myelocytes (MC)/metamyelo

127 NOD-SCID-gamma mice transplanted with Nomo-1 myeloblasts with reduced levels of Mer had a significant