ライフサイエンスコーパス: leukaemic

1 ations of white blood cells, both normal and leukaemic.

2 is feasible, safe, and mediates potent anti-leukaemic activity in children and young adults with che

3 ectively inhibits Mediator kinases, has anti-leukaemic activity in vitro and in vivo, and disproporti

4 oxyprogesterone acetate (BaP) has shown anti-leukaemic activity in vitro and in vivo.

5 these SE-associated genes, yet also has anti-leukaemic activity.

6 be the case, then the cell type that becomes leukaemic and the chromosomal/molecular changes that occ

7 the haematopoietic stem cell lineage causes leukaemic and tumoural diseases but not neurodegenerativ

8 how that low-level expression of the gene in leukaemic blast cells and granulocytes does not associat

9 Apaf-1 protein deficiency occurs in human leukaemic blasts and confers resistance to cytochrome-c-

10 ne in c-Kit(mid)CD3(+)Lin(-) LSCs and CD3(+) leukaemic blasts, recapitulating a subset of human T-ALL

11 myelopoiesis and myeloid differentiation of leukaemic blasts, which protects mice from death related

12 n occur within the Apaf-1 promoter region in leukaemic blasts.

13 diated resistance to cytochrome c in primary leukaemic blasts.

14 t correlate with Apaf-1 mRNA levels in human leukaemic blasts.

15 of drug resistance and the minimal residual leukaemic burden providing effective strategies for futu

16 kinase (BTK) blocks AML blast proliferation, leukaemic cell adhesion to bone marrow stromal cells as

17 meter flowcytometry capable of detecting one leukaemic cell among 10,000 normal cells.

18 of actionable molecular targets by studying leukaemic cell and host genetics, precise risk stratific

19 Genome-wide profiling of germline and leukaemic cell DNA has identified novel submicroscopic s

20 Little is known about the mechanism of leukaemic cell infiltration of the CNS, despite its clin

21 als in human erythroleukaemia (HEL) cells, a leukaemic cell line of platelet-megakaryocyte lineage.

22 za2dc) increased the sensitivity of the K562 leukaemic cell line to UV light-induced apoptosis in ass

23 n global gene expression in t(8;21)-positive leukaemic cell lines and in primary AML blasts using cDN

24 efficacy against human and murine MLL-fusion leukaemic cell lines, through the induction of early cel

25 to determine optimal assay conditions using leukaemic cell lines.

26 mature (MT) Smac genes into the K562 and CEM leukaemic cell lines.

27 Leukaemic cell populations showed clonal rearrangements

28 xpression of miR-22 significantly suppresses leukaemic cell viability and growth in vitro, and substa

29 A higher degree of marrow infiltration by leukaemic cells (> or = 0.1%) in week 14 samples identif

30 ed standard was tested using ex vivo patient leukaemic cells (n=5).

31 Leukaemic cells also show an elevated percentage of Ras

32 lts in cell cycle arrest, differentiation of leukaemic cells and failure to establish leukaemia in im

33 at was based on genetic abnormalities of the leukaemic cells and measurements of minimal residual dis

34 isk stratification by biological features of leukaemic cells and response to treatment, treatment mod

35 However, failure to completely eradicate leukaemic cells and the escape of these cells from previ

36 Immunological detection of residual leukaemic cells at any point in the treatment course is

37 Molecular cytogenetic analysis of leukaemic cells by banded karyotype and FISH revealed a

38 Further studies revealed that circulating leukaemic cells can engraft around these vessels, sugges

39 pecifically targeting the genetic defects of leukaemic cells could revolutionise management of this d

40 Inhibition of JAK2 activity in human leukaemic cells decreases both the expression of the hae

41 The presence of AML1-ETO in leukaemic cells does not prevent this disassembly.

42 Some leukaemic cells expressed high levels of Apaf-1 mRNA but

43 Resistant leukaemic cells expressed high levels of Bruton's tyrosi

44 In t(8;21) leukaemic cells expressing the aberrant fusion protein A

45 Leukaemic cells from 239 patients with T-ALL enrolled at

46 ions, we performed a genome-wide analysis of leukaemic cells from 242 paediatric ALL patients using h

47 Here we show that primary leukaemic cells from children with NF1 show a selective

48 cal significance of submicroscopic levels of leukaemic cells in bone-marrow aspirates from children w

49 Fusions are not observed in leukaemic cells in these patients.

50 therapeutic effects against murine and human leukaemic cells in vitro and in vivo.

51 te relapses might represent new mutations in leukaemic cells not eliminated by conventional therapy.

52 slocation, t(8;21)(q22;q22), observed in the leukaemic cells of approximately 40% of patients with th

53 a fusion oncogene in hard to transfect human leukaemic cells raising the possibility of targeting mal

54 rentially expressed genes were identified in leukaemic cells that were secondarily resistant to STI57

55 unresponsiveness of PLZF-RARalpha-expressing leukaemic cells to RA.

56 sion could be used to predict sensitivity of leukaemic cells to STI571.

57 c transfectants increased the sensitivity of leukaemic cells to UV light-induced apoptosis and the ac

58 The proportion of patients with detectable leukaemic cells was 23% at remission induction and 17% a

59 The treatment of leukaemic cells with SAHM1 results in genome-wide suppre

60 Here we show that, in human leukaemic cells, AML1-ETO resides in and functions throu

61 over, Lmo2 knock-down impaired the growth of leukaemic cells, and high LMO2 expression at diagnosis c

62 nhibitor of the production of differentiated leukaemic cells, but does not deplete leukaemic stem cel

63 We studied leukaemic cells, collected at diagnosis, to identify cas

64 one marrow in vivo in the proximity of other leukaemic cells, differentiate upon exposure to blue lig

65 y, treatment based on biological features of leukaemic cells, host genetics, and the amount of residu

66 presents the turnover rate of differentiated leukaemic cells, while the second slope of 0.008 per day

67 d co-expressed with HOXA9, in MLL-rearranged leukaemic cells.

68 y leads to a biphasic exponential decline of leukaemic cells.

69 tosis and suppressing proliferation in human leukaemic cells.

70 ucture of the human c-FMS gene in normal and leukaemic cells.

71 ced colony formation and Ki-67 expression in leukaemic cells.

72 ur understanding of their role in normal and leukaemic cells.

73 togenetic clones and without any evidence of leukaemic change.

74 specific DPB1 alleles and two groups of non-leukaemic children, one consisting of children with soli

75 normal lymphocyte development, facilitating leukaemic clonal expansion.

76 yrosine kinase resistance in CML, leading to leukaemic clone escape and disease propagation.

77 This study was to isolate the anti-leukaemic component from edible mushroom Hypsizygus marm

78 Osteoblasts were recently implicated in pre-leukaemic conditions in mice.

79 Our results, obtained using TALL-104 human leukaemic CTLs as a model system, are consistent with th

80 We used TALL-104 human leukaemic cytotoxic T cells as a model system, and stimu

81 R-Cas9-mediated depletion of ENL led to anti-leukaemic effects, including increased terminal myeloid

82 eader domain was essential for ENL-dependent leukaemic growth.

83 th cDNAs representing the RNAs of normal and leukaemic leucocyte populations were sufficiently differ

84 30 patients (12.6%) had leukaemic lymphoblasts with an ETP-related gene-expressi

85 e expression of the CD2-myc transgene in pre-leukaemic mice.

86 Flt3 internal tandem duplication (Flt3(ITD)) leukaemic mutations to accelerate leukaemogenesis, throu

87 'Pre-leukaemic' mutations are thought to promote clonal expan

88 (GMP) behaviour in mice during emergency and leukaemic myelopoiesis.

89 ntonic regulatory element) during normal and leukaemic myelopoiesis.

90 ant cell populations and remotely modulating leukaemic niches.

91 the expression of important mediators of the leukaemic phenotype such as HHEX/PRH.

92 ssion of miR-196b results in more aggressive leukaemic phenotypes and causes much faster leukemogenes

93 )c chromosome with gene dosage optimized for leukaemic potential, showing constrained copy-number lev

94 Granulocytic differentiation from normal and leukaemic precursors is accompanied by loss of transcrip

95 ronic phase of CML the primitive multipotent leukaemic progenitor cells remain growth factor dependen

96 .008 per day represents the turnover rate of leukaemic progenitors.

97 potential therapeutic target for controlling leukaemic progression in Noonan syndrome and for improvi

98 culated that DNA damage might also constrain leukaemic self-renewal and malignant haematopoiesis.

99 way that is necessary for maintenance of the leukaemic state and identify this enzyme as a potential

100 L3 and is implicated in the maintenance of a leukaemic state.

101 d disease management, but fails to eradicate leukaemic stem cells (LSCs), which maintain CML.

102 tiated leukaemic cells, but does not deplete leukaemic stem cells.

103 Can imatinib eradicate leukaemic stem cells?

104 In human Jurkat leukaemic T cells expressing an ER-targeted Ca(2+) indic

105 show here, that expression of TCL1 occurs in leukaemic T cells from A-T patients with chromosome 14 r

106 , these results show that PTEN expression in leukaemic T cells leads to reduced proliferation via an

107 PMCA in shaping Ca2+ signals in Jurkat human leukaemic T cells using single-cell voltage-clamp and ca

108 dhesion signal required for the targeting of leukaemic T-cells into the CNS.

109 hDOT1L contributes to CALM-AF10-mediated leukaemic transformation by preventing nuclear export of

110 2;p13) chromosomal translocation, drives the leukaemic transformation of early B-cell precursors, but

111 p16(INK4A), increases the susceptibility to leukaemic transformation of haematopoietic progenitor ce

112 hat abrogated H3K4me3 binding also abolished leukaemic transformation.

113 fusion is both necessary and sufficient for leukaemic transformation.

114 lation of c-FMS expression may contribute to leukaemic transformation.

115 nction of PAX5 and IKZF1 and readily enabled leukaemic transformation.

116 opoiesis, and an important fusion partner in leukaemic translocations.

117 erted high growth inhibitory effect on human leukaemic U937 cells and sufficient toxicological safety