ライフサイエンスコーパス: leukemic stem cell

1 i-1 in regulating self-renewal of normal and leukemic stem cells.

2 nce suggests that leukemias are sustained by leukemic stem cells.

3 and potential therapeutic target in treating leukemic stem cells.

4 ent model for assessment of human normal and leukemic stem cells.

5 o blast crisis is supported by self-renewing leukemic stem cells.

6 e to therapy-resistant, disease-reinitiating leukemic stem cells.

7 kemia (AML) arises from a rare population of leukemic stem cells.

8 with their microenvironment and maintaining leukemic stem cells.

9 current chemotherapeutic regimens to target leukemic stem cells.

10 sis, prolonged survival, and reduced myeloid leukemic stem cells.

11 ver 90% of AML patient myeloid blasts and in leukemic stem cells.

12 oved understanding of the immunophenotype of leukemic stem cells.

13 hat models increased signaling in normal and leukemic stem cells.

14 HSCs for terminal tumor transformation into leukemic stem cells.

15 X3Y-encoded H-Y antigen is also expressed in leukemic stem cells.

16 e self-renewal potential and may function as leukemic stem cells.

17 normal beta-catenin activity can function as leukemic stem cells.

18 y have utility in sensitizing drug-resistant leukemic stem cells.

19 be explored as a novel approach to eradicate leukemic stem cells and residual disease in chronic phas

20 ritical for the maintenance and expansion of leukemic stem cells and therefore provides a possible me

21 ocompatibility antigens shared by normal and leukemic stem cells, and is mediated predominantly by CD

22 th, identifying and characterizing potential leukemic stem cells, and permitting preclinical studies

23 -ABL1 was expressed and active in Stat5-null leukemic stem cells, and Stat5 deletion did not prevent

24 to identify self-renewing cells as candidate leukemic stem cells, and the dependence of self-renewal

25 could also be involved in immortalization of leukemic stem cells, and thus represent attractive drug

26 However, leukemic stem cells are insensitive to tyrosine kinase i

27 ying the transformation of normal cells into leukemic stem cells are still poorly understood.

28 ary AML specimen and contained self-renewing leukemic stem cells, as demonstrated by secondary transp

29 Determining how normal and leukemic stem cells behave in vivo, in a dynamic and non

30 results provide new insights with regard to leukemic stem cell biology and suggest possibilities for

31 1, have demonstrated functions in normal and leukemic stem cells but are rarely mutated in leukemia.

32 l in mice transplanted with MLL-AF9-positive leukemic stem cells by modulating AKT and 4E-BP1 phospho

33 Myelodysplastic and leukemic stem cell clones that evolve in children and ad

34 failure and selection of TNF-alpha-resistant leukemic stem cell clones.

35 le pathways that are aberrantly regulated in leukemic stem cells compared with normal HSC.

36 ial to specifically target and eliminate the leukemic stem cell compartment, which is likely to impro

37 istic for both hematopoietic progenitors and leukemic stem cells; cyclopamine preferentially reduced

38 These results show that BCR-ABL-expressing leukemic stem cells depend to a greater extent on CD44 f

39 capability by myeloid progenitors to become leukemic stem cells during myeloid leukemia development

40 otential therapeutic target against immature leukemic stem cell-enriched cell fractions in MDS and AM

41 mary human leukemic cells including immature leukemic stem cell-enriched populations.

42 niche into a permissive environment favoring leukemic stem cell expansion over normal HSC maintenance

43 s between healthy hematopoietic and diseased leukemic stem cells for core circadian transcription fac

44 transcription-factor genes demonstrated that leukemic stem-cell formation in AML could directly be ca

45 y genes whose dysregulation is essential for leukemic stem cell function and that are targets for the

46 mmac-deficient mice, we confirmed that human leukemic stem cells, functionally defined by us as SCID

47 and mTORC2 differentially control normal and leukemic stem cell functions.

48 e a novel role for CDK6 in hematopoietic and leukemic stem cells (hematopoietic stem cells [HSCs] and

49 ly, has been implicated in hematopoietic and leukemic stem cell homing.

50 eing pursued in many human malignancies, the leukemic stem cells in acute myeloid leukemia (AML) are

51 Leukemic stem cells in chronic phase chronic myelogenous

52 We investigated whether leukemic stem cells in CML also use the beta-catenin pat

53 The resistance of leukemic stem cells in response to targeted therapies su

54 ddC also targeted leukemic stem cells in secondary AML xenotransplantation

55 -term suspension culture and the survival of leukemic stem cells in short-term cultures.

56 term TKI therapy may reduce the abundance of leukemic stem cells in some patients.

57 expressing cells that is the major source of leukemic stem cells in the full leukemic stage.

58 in (IL1RAP; IL1R3) is expressed on candidate leukemic stem cells in the majority of AML patients, but

59 self-renewal and promote differentiation of leukemic stem cells in the MLL-translocated molecular su

60 lock and decreases the proliferation rate of leukemic stem cells in vivo.

61 , curing B-ALL and CML mice requires killing leukemic stem cells insensitive to both imatinib and das

62 XCR4/SDF-1 axis is an important mechanism of leukemic stem cell interaction with marrow stroma, we te

63 A fundamental property of leukemic stem cells is clonal dominance of the bone marr

64 In leukemic stem cells, knockdown of Kdm2b/Jhdm1b impairs t

65 Human leukemic stem cells, like other cancer stem cells, are h

66 clonal disorders of hematopoiesis wherein a leukemic stem cell (LSC) acquires mutations that confer

67 he that impairs normal hematopoiesis, favors leukemic stem cell (LSC) function, and contributes to BM

68 Using publicly available leukemic stem cell (LSC) gene expression profiles and ge

69 t Wnt/beta-catenin signaling is required for leukemic stem cell (LSC) maintenance in chronic myeloid

70 d finally, (5) how the knowledge gained into leukemic stem cell (LSC) niche dependencies might be exp

71 prognosis, and ineffective targeting of the leukemic stem cell (LSC) population remains one of sever

72 urrent models suggest transformation creates leukemic stem cell (LSC) populations arrested at a proge

73 Interestingly, the leukemic stem cell (LSC) shares many characteristics wit

74 al. (2016) reveal metabolic heterogeneity in leukemic stem cell (LSC) subpopulations and show that ch

75 emopoietic stem cell, transforming it into a leukemic stem cell (LSC) that self-renews, proliferates,

76 ntified a 30-gene cluster that characterizes leukemic stem cell (LSC)-depleted cells and a 25-gene cl

77 t yet curative, because most patients retain leukemic stem cells (LSC) and their progenitors in bone

78 iesis and provide experimental evidence that leukemic stem cells (LSC) can reside at the LT-HSC stage

79 mal human hematopoietic stem cells (HSC) and leukemic stem cells (LSC) from patients with acute myelo

80 The major challenge in targeting leukemic stem cells (LSC) is finding therapies that larg

81 r both scientific and therapeutic endeavors, leukemic stem cells (LSC) represent a critical area of i

82 of chronic myeloid leukemia do not eliminate leukemic stem cells (LSC).

83 and results in an increase in the number of leukemic stem cells (LSC).

84 ion of Hif-2alpha accelerates development of leukemic stem cells (LSCs) and shortens AML latency init

85 Hematopoietic stem cells (HSCs) and leukemic stem cells (LSCs) are both capable of self-rene

86 Here, we show that a subpopulation of leukemic stem cells (LSCs) can utilize gonadal adipose t

87 Leukemic stem cells (LSCs) drive progression of chronic

88 kemia (AML) samples studied, indicating that leukemic stem cells (LSCs) express this antigen.

89 biomarker that phenotypically distinguishes leukemic stem cells (LSCs) from normal hematopoietic ste

90 eta-catenin is required for establishment of leukemic stem cells (LSCs) in acute myeloid leukemia (AM

91 cytotoxic antileukemic response to eliminate leukemic stem cells (LSCs) in acute myeloid leukemia (AM

92 encoding B-lymphoid kinase) through c-Myc in leukemic stem cells (LSCs) in CML mice and that Blk func

93 ification, and the role of OBs in regulating leukemic stem cells (LSCs) is not well studied.

94 the failure to eliminate therapy-persistent leukemic stem cells (LSCs) may result in disease relapse

95 Although leukemic stem cells (LSCs) show a symbiotic relationship

96 te myeloid leukemias (AMLs) are sustained by leukemic stem cells (LSCs) that generate through aberran

97 rmal hematopoietic tissue initiated by a few leukemic stem cells (LSCs) that undergo an aberrant and

98 alizability of HSCT use, and the survival of leukemic stem cells (LSCs) within protective areas of th

99 Cells of this nature, herein referred to as leukemic stem cells (LSCs), have been documented for nea

100 se of the inability to effectively eradicate leukemic stem cells (LSCs), the self-renewing component

101 g factors in realizing the goal of targeting leukemic stem cells (LSCs).

102 THSCs are heterogeneous in their capacity as leukemic stem cells (LSCs).

103 the aberrant function of disease-initiating leukemic stem cells (LSCs).

104 L) largely depends on the eradication of CML leukemic stem cells (LSCs).

105 et differentiated cells and do not eliminate leukemic stem cells (LSCs).

106 k for relapse remains, due to persistence of leukemic stem cells (LSCs).

107 ltiple signaling pathways deregulated in MLL leukemic stem cells (LSCs).

108 id leukemia (AML) is driven by self-renewing leukemic stem cells (LSCs).

109 m cells (hematopoietic stem cells [HSCs] and leukemic stem cells [LSCs]) that exceeds its function as

110 ent (pre-leukemic haematopoietic stem cells, leukemic stem cells [LSCs], and leukemic blasts).

111 CD25 is a leukemic stem cell marker and a conspicuous prognostic m

112 expression is restricted to preleukemic and leukemic stem cell populations in this model, providing

113 Therapeutic targeting of pre-leukemic stem cells (pre-LSCs) may be a viable strategy

114 These results establish that BCR-ABL1(+) leukemic stem cells rely to a greater extent on selectin

115 However, the effect of TKIs on leukemic stem cells remains incompletely understood.

116 regulating hematopoietic stem cell (HSC) and leukemic stem cell self-renewal and functions in the con

117 animals revealed a loss of the hematopoietic/leukemic stem cell self-renewal program and an increase

118 The determinants of normal and leukemic stem cell self-renewal remain poorly characteri

119 ated Gene (ERG) is a component of normal and leukemic stem cell signatures and high ERG expression is

120 the complex signaling pathways critical for leukemic stem cell survival.

121 isoform signatures unique to patient-derived leukemic stem cells that constitute a therapeutic Achill

122 gy to exploit differences between normal and leukemic stem cells that may be beneficial in autologous

123 may have limited efficacy in eradicating the leukemic stem cells that sustain the human MPN.

124 estration in the bone marrow niche may allow leukemic stem cells to evade exposure to drugs.

125 e an environment supporting the emergence of leukemic stem cells, we tested the leukemia-promoting ef

126 Furthermore, leukemic stem cells within the CD34(+)/CD38(-) compartme