ライフサイエンスコーパス: leukemic stem cell

1 oved understanding of the immunophenotype of leukemic stem cells.

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

3 HSCs for terminal tumor transformation into leukemic stem cells.

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

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

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

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

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

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

10 and potential therapeutic target in treating leukemic stem cells.

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

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

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

14 idative crisis and ferroptotic cell death of leukemic stem cells.

15 howing its preferential cytotoxic effects on leukemic stem cells.

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

17 with their microenvironment and maintaining leukemic stem cells.

18 current chemotherapeutic regimens to target leukemic stem cells.

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

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

21 n of NCAM1 is involved in the maintenance of leukemic stem cells and confers stress resistance, likel

22 Despite success, targeting leukemic stem cells and overcoming drug resistance remai

23 An amino acid dropout screen on primary leukemic stem cells and progenitor populations revealed

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

25 Notably, CLL1CART reduce the number of leukemic stem cells and serial transplantability in vivo

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

27 therapy exhibited cytotoxicity against both leukemic stem cells and, to a lesser extent, monocytes e

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

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

30 stant mutations, as well as immunophenotypic leukemic stem cells, and reduced leukemic engraftment in

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

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

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

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

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

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

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

38 MRD is a result of leukemic stem cells being retained in bone marrow protec

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

40 ted leukemic differentiation and reduced the leukemic stem cell burden in bone marrow but also induce

41 1, have demonstrated functions in normal and leukemic stem cells but are rarely mutated in leukemia.

42 ocus on AML, we observe csNPM1 on blasts and leukemic stem cells but not on normal hematopoietic stem

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

44 ere, we demonstrate that LSCs, HSCs, and pre-leukemic stem cells can be identified and molecularly pr

45 (CD45(+)) as well as chemotherapy resistance leukemic stem cells (CD45(+)Lin(-)CD34(+)CD38(-)), which

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

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

48 increase in RNA binding activity of MSI2 in leukemic stem cells compared with normal hematopoietic s

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

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

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

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

53 hat the HIF2alpha stemness pathway maintains leukemic stem cells downstream of MYC in human and mouse

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

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

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

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

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

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

60 myeloid leukemia (AML) and is essential for leukemic stem cell function and AML growth, but dispensa

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

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

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

64 and a more thorough characterization of the leukemic stem cell have provided insights that should le

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

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

67 riving the self-renewal of hematopoietic and leukemic stem cells (HSCs/LSCs).

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

69 Leukemic stem cells in chronic phase chronic myelogenous

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

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

72 ddC also targeted leukemic stem cells in secondary AML xenotransplantation

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

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

75 eceptor directed against IL1RAP expressed by leukemic stem cells in the context of CML.

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

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

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

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

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

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

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

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

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

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

86 Employing machine-learning, we identified leukemic stem cell (LSC) and natural killer (NK) cell ge

87 s (miRNAs) in regulating drug resistance and leukemic stem cell (LSC) fate, we performed global trans

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

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

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

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

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

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

94 cell populations previously shown to contain leukemic stem cell (LSC) potential.

95 However, the role of K3 in leukemic stem cell (LSC) retention and growth in the rem

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

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

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

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

100 The impact of IL2RA on the properties of leukemic stem cells (LSC) and on leukemogenesis were que

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

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

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

104 Eliminating leukemic stem cells (LSC) is a sought after therapeutic

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

106 Leukemic stem cells (LSC) rely on mitochondrial metaboli

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

108 ylation (OxPhos) is a potential weakness for leukemic stem cells (LSC) that can be exploited for ther

109 The AHR pathway is suppressed in leukemic stem cells (LSC), therefore activating AHR sign

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

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

112 1 KO in the malignant counterparts of HSCs - leukemic stem cells (LSCs) - accelerated MLL-AF9- and Me

113 c myeloid leukemia (CML), the persistence of leukemic stem cells (LSCs) after treatment with tyrosine

114 , we demonstrated varied clonal evolution of leukemic stem cells (LSCs) and further dissected subclon

115 disorder comprising a hierarchy of quiescent leukemic stem cells (LSCs) and proliferating blasts with

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

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

118 ished from an initial round of firefighting, leukemic stem cells (LSCs) are the embers remaining afte

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

120 Leukemic stem cells (LSCs) drive progression of chronic

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

122 Leukemic stem cells (LSCs) from miR-142(-/-)BCR-ABL mice

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

124 Leukemic stem cells (LSCs) fuel acute myeloid leukemia (

125 Leukemic stem cells (LSCs) in acute myeloid leukemia (AM

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

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

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

129 ic phase (CP) chronic myeloid leukemia (CML) leukemic stem cells (LSCs) into blast crisis (BC) LSCs.

130 regulate the development and maintenance of leukemic stem cells (LSCs) is important to reveal new th

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

132 stitutive low Notch and high Wnt activity in leukemic stem cells (LSCs) maintains this pathway activa

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

134 drug resistance and the enduring presence of leukemic stem cells (LSCs) remain formidable barriers to

135 myeloid leukemia (AML) patients is driven by leukemic stem cells (LSCs) resulting in high rates of re

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

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

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

139 BCR::ABL1+ clones, ratio of TKI-insensitive leukemic stem cells (LSCs) to residual hematopoietic ste

140 In acute myeloid leukemia (AML), leukemic stem cells (LSCs) underlie mortality but are di

141 Here, we found that leukemic stem cells (LSCs) were highly differentiated, a

142 , patients harbour a population of quiescent leukemic stem cells (LSCs) which can emerge from quiesce

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

144 IKZF2 is highly expressed in leukemic stem cells (LSCs), and its deficiency results i

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

146 s primarily caused by chemotherapy-resistant leukemic stem cells (LSCs), it is essential to eradicate

147 TKIs do not eliminate disease-propagating leukemic stem cells (LSCs), suggesting a deeper understa

148 r these diseases, they generally do not kill leukemic stem cells (LSCs), the cancer-initiating cells

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

150 residual disease is maintained by persistent leukemic stem cells (LSCs), which drive tyrosine kinase

151 a (AML) are often ineffective in eliminating leukemic stem cells (LSCs), which perpetuate the disease

152 id differentiation, generating self-renewing leukemic stem cells (LSCs).

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

154 eukemia (AML) is maintained by self-renewing leukemic stem cells (LSCs).

155 -3373 have preferential cytotoxic effects on leukemic stem cells (LSCs).

156 s, they fail to eradicate disease-initiating leukemic stem cells (LSCs).

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

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

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

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

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

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

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

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

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

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

167 ind increased H3K4 trimethylation in MLL1(F)-leukemic stem cells (MLL1(F)-LSCs), following loss of th

168 referentially engage ADGRE2(pos)CLEC12A(pos) leukemic stem cells over ADGRE2(low)CLEC12A(neg) normal

169 on markedly decreased CD34+CD38-CD90-CD45RA+ leukemic stem cell population and alone or in combinatio

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

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

172 BCR-ABL leukemias result from leukemic stem cell/progenitor transformation and represe

173 m, was stable through relapse, and induced a leukemic stem cell program.

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

175 CML), issues of drug resistance and residual leukemic stem cells remain.

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

177 w (BM) niche in which chemotherapy-resistant leukemic stem cells reside.

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

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

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

181 ibition (PSTKi) impaired AML cell growth and leukemic stem cell self-renewal.

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

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

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

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

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

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

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

189 ensive chemotherapy often fails to eradicate leukemic stem cells, which are protected by the bone mar

190 stigation into the eradication of persistent leukemic stem cells, which rely on neither the presence

191 icts that stimulating the differentiation of leukemic stem cells while applying TKI therapy can signi

192 tment, targeting both blasts and the pivotal leukemic stem cells while sparing normal bone marrow cel

193 g the metabolic rewiring required by myeloid-leukemic stem cells with that required for hematopoiesis

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