ライフサイエンスコーパス: LSC

1 LSC maintenance is related, at least in part, to signals

2 LSCs are defined by their capacity to initiate leukaemia

3 LSCs exhibit a unique metabolic profile and contain meta

4 LSCs have predominantly been studied at the transcript l

5 LSCs home in bone marrow areas at low oxygen tension, wh

6 LSCs, which are resistant to chemotherapy and serve as r

7 ps; unremarkable retina, 294 ps; P < 0.001; LSC: lesion, 404 ps; unremarkable retina, 316 ps; P < 0.

8 3-siRNA (small interfering RNA) in CTLA-4(+) LSCs in vivo, which mobilized LSCs in the BM, induced di

9 Furthermore, the activated Co(3) O(4) /LSC exhibits the best catalytic activities for CO oxidat

10 m cell drives its transformation to become a LSC.

11 Additionally, LSC-Sec and LSC-Exo exhibit superior therapeutic benefit

12 ibility, and direct IKZF2 binding in MLL-AF9 LSCs demonstrate that IKZF2 regulates a HOXA9 self-renew

13 nd with particularly strong activity against LSCs.

14 esent a potential therapeutic target against LSCs.

15 our study shows that IKZF2 regulates the AML LSC program and provides a rationale to therapeutically

16 the key scientific findings pertinent to AML LSC targeting and to consider methods of clinical evalua

17 human acute myeloid leukemia stem cells (AML LSCs) was first reported nearly 2 decades ago through th

18 tics, and clinical associations of human AML LSCs and discuss critical questions that need to be addr

19 to venetoclax in relapsed and refractory AML LSCs mediated by nicotinamide metabolism.

20 These AML LSCs were shown to reside at the apex of a cellular hier

21 nd genetic and cellular heterogeneity to AML LSCs not observed in most cases of CML.

22 In AML, LSCs can arise from multiple cell types through the acti

23 noncoding RNAs in the regulation of HSC and LSC function and identify miR-99 as a critical regulator

24 al functions of ALKBH5 in leukemogenesis and LSC/LIC self-renewal/maintenance and highlight the thera

25 ed AML before therapy and after relapse, and LSC frequency was assessed by limiting dilution analyses

26 Additionally, LSC-Sec and LSC-Exo exhibit superior therapeutic benefits than their

27 Analysis reveals that LSC-Sec and LSC-Exo treatments could attenuate and resolve bleomycin

28 Average particle size of HSC, WSC and LSC based nano-particles were 322.7, 559.2 and 615.6 nm

29 atin accessibility as regulators of HSCs and LSCs, and suggest that targeting HMGN1 or its downstream

30 was independently confirmed in both HSCs and LSCs.

31 R-99 regulates self-renewal in both HSCs and LSCs.

32 t, abnormal clusters of colocalized MSCs and LSCs form but disappear upon Cxcl12 deletion.

33 (IL6) beta2SP(+/-) LSCs not only exhibited nuclear localization of Twist an

34 NFkappaB in (IL6) beta2SP(+/-) LSCs was activated by transforming growth factor beta (T

35 with interleukin-6 (pIL6; (IL6) beta2SP(+/-) LSCs) were highly tumorigenic and metastatic, whereas th

36 ilarities and differences that exist between LSCs in CML and AML and examine the therapeutic strategi

37 sts and healthy HSPCs, we validate candidate LSC markers and highlight novel and potentially targetab

38 binds both CD3 and CD123 eliminates CD123(+) LSCs in a T cell-dependent manner both in vivo and in vi

39 CD133(+) LSCs derived from preneoplastic livers of beta2SP(+/-) m

40 TAK1-NFkappaB signaling cascade in CD133(+) LSCs, and this program interacts with deficient TGFbeta

41 Within CD34(-) and CD34(+) LSC-containing populations, LSC frequencies are similar;

42 CD36(+) LSCs have unique metabolic properties, are strikingly en

43 f which are enriched for leukemia stem cell (LSC) activity.

44 ferentiation and enhance leukemia stem cell (LSC) activity.

45 ting drug resistance and leukemic stem cell (LSC) fate, we performed global transcriptome profiling i

46 is characterized by high leukemia stem cell (LSC) frequency, an aberrant leukemia-specific GPR56 (hig

47 required for maintaining leukemia stem cell (LSC) function but is dispensable for normal hematopoiesi

48 als are integrated to regulate LM stem cell (LSC) function.

49 Using publicly available leukemic stem cell (LSC) gene expression profiles and gene expression data g

50 ent mechanisms governing leukemia stem cell (LSC) generation have not been elucidated.

51 he knowledge gained into leukemic stem cell (LSC) niche dependencies might be exploited to devise nov

52 wal in the heterogeneous leukemia stem cell (LSC) pool determine aggressiveness of acute myeloid leuk

53 fective targeting of the leukemic stem cell (LSC) population remains one of several obstacles in trea

54 wever, the role of K3 in leukemic stem cell (LSC) retention and growth in the remodeled tumor-promoti

55 , transforming it into a leukemic stem cell (LSC) that self-renews, proliferates, and differentiates

56 represents a potential leukaemia stem cell (LSC)-directed therapy which may compliment tyrosine kina

57 CD123(+) leukemic stem or initiating cells (LSC), resembles NPM1c(+) AML from patients.

58 RA on the properties of leukemic stem cells (LSC) and on leukemogenesis were queried.

59 se most patients retain leukemic stem cells (LSC) and their progenitors in bone marrow and relapse fo

60 Eliminating leukemic stem cells (LSC) is a sought after therapeutic paradigm for the trea

61 imited efficacy against leukemia stem cells (LSC) responsible for disease propagation, and most CML p

62 rized subpopulations of leukemia stem cells (LSC) that drive chemoresistance and leukemia relapse.

63 Relapse is caused by leukemia stem cells (LSC), the cells with self-renewal capacity.

64 athway is suppressed in leukemic stem cells (LSC), therefore activating AHR signaling is a potential

65 ukemia do not eliminate leukemic stem cells (LSC).

66 f-renewal of leukemia stem/initiating cells (LSCs/LICs) but not essential for normal hematopoiesis.

67 f-renewal of leukemia stem/initiation cells (LSCs/LICs).

68 n in the human limbal stem/progenitor cells (LSCs) in vitro by using small molecules.

69 or to the emergence of leukaemic stem cells (LSCs) and the development of acute myeloid leukaemia.

70 round of firefighting, leukemic stem cells (LSCs) are the embers remaining after completion of tradi

71 HSCs) and acute myeloid leukemia stem cells (LSCs) compared with their differentiated progeny.

72 Leukemic stem cells (LSCs) drive progression of chronic myeloid leukemia (CML

73 r the survival of human leukemia stem cells (LSCs) from patients with acute myeloid leukemia (AML).

74 new study reveals that leukemia stem cells (LSCs) in acute myeloid leukemia downregulate natural kil

75 For two decades, leukaemia stem cells (LSCs) in chronic myeloid leukaemia (CML) and acute myelo

76 ously demonstrated that leukemia stem cells (LSCs) in de novo acute myeloid leukemia (AML) patients a

77 via the elimination of leukemia stem cells (LSCs) in mice.

78 into therapy-resistant leukemia stem cells (LSCs) in secondary acute myeloid leukemia (AML).

79 L-AF9 (MA9)-transformed leukemia stem cells (LSCs) in vivo.

80 small number of MLL-AF9 leukemia stem cells (LSCs) in vivo.

81 n of genetically defective liver stem cells (LSCs) into highly metastatic liver cancer cells in prema

82 ment and maintenance of leukemic stem cells (LSCs) is important to reveal new therapeutic opportuniti

83 Eradication of leukemia stem cells (LSCs) is the ultimate goal of treating acute myeloid leu

84 nd high Wnt activity in leukemic stem cells (LSCs) maintains this pathway activated in malignancies.

85 nate therapy-persistent leukemic stem cells (LSCs) may result in disease relapse.

86 s contain a population of limbal stem cells (LSCs) that continuously renew the corneal epithelium.

87 Leukaemia stem cells (LSCs) underlie cancer therapy resistance but targeting t

88 Here, we found that leukemic stem cells (LSCs) were highly differentiated, and leukemia progressi

89 effectively eradicate leukaemia stem cells (LSCs)(1).

90 chemotherapy-resistant leukaemic stem cells (LSCs)(2,3).

91 is highly expressed in leukemic stem cells (LSCs), and its deficiency results in defective LSC funct

92 chemotherapy-resistant leukemic stem cells (LSCs), it is essential to eradicate LSCs to improve pati

93 ate disease-propagating leukemic stem cells (LSCs), suggesting a deeper understanding of niche-depend

94 y generally do not kill leukemic stem cells (LSCs), the cancer-initiating cells that compete with nor

95 but fails to eradicate leukaemic stem cells (LSCs), which maintain CML.

96 ccumb to chemoresistant leukemia stem cells (LSCs), which persist and reinitiate disease years after

97 on but not in targeting leukemia stem cells (LSCs), which sustain minimal residual disease and are re

98 g the goal of targeting leukemic stem cells (LSCs).

99 the eradication of CML leukemic stem cells (LSCs).

100 ls and do not eliminate leukemic stem cells (LSCs).

101 , due to persistence of leukemic stem cells (LSCs).

102 n by a rare fraction of leukemia stem cells (LSCs).

103 us in their capacity as leukemic stem cells (LSCs).

104 enerating self-renewing leukemic stem cells (LSCs).

105 matopoietic stem cells, leukemic stem cells [LSCs], and leukemic blasts).

106 are activated in stem and progenitor cells, LSCs expanded under chemotherapy-induced stress.

107 ness to enrich and functionally characterize LSCs.

108 ivated beta-catenin levels in chemoresistant LSCs and reduced LSC tumorigenic activity.

109 se, and additional approaches to deplete CML LSC are needed to enhance the possibility of discontinui

110 ntified a molecular network critical for CML LSC survival and propose that simultaneously targeting t

111 signaling contributes to maintenance of CML LSC following TKI treatment and that IL-1 blockade with

112 m the BMM contributes to preservation of CML LSC following TKI treatment.

113 the number and self-renewal capacity of CML LSC in vitro.

114 -1RA enhances elimination of TKI-treated CML LSC.

115 covery in patients almost 2 decades ago, CML LSCs have become a well-recognized exemplar of the cance

116 isms that promote the survival of the CP CML LSCs and how they can be a source of new gene coding mut

117 tifying therapeutic targets to eradicate CML LSCs may be a strategy to cure CML.

118 tein translation, selectively eradicates CML LSCs both in vitro and in a xenotransplantation model of

119 xpression of PRMT5 was observed in human CML LSCs.

120 we searched for such vulnerabilities in CML LSCs.

121 tanding of niche-dependent regulation of CML LSCs is required to eradicate disease.

122 is PGE1-EP4 pathway specifically targets CML LSCs and that the combination of PGE1/misoprostol with c

123 Strong evidence now shows that CML LSCs are resistant to the effects of TKIs and persist in

124 We recently showed that CML LSCs depend on Tcf1 and Lef1 factors for self-renewal.

125 phocyte-associated antigen 4 (CTLA-4) on CML-LSCs but not normal hematopoietic stem cells and this en

126 By comparing LSCs to leukemic blasts and healthy HSPCs, we validate c

127 Despite these complexities, LSCs in both diseases share biological features, making

128 terials for luminescent solar concentrators (LSCs) as they can be engineered for providing highly tun

129 e thin-film luminescent solar concentrators (LSCs) featuring high absolute photoluminescence quantum

130 to HSPCs; this subset of genes constitutes "LSC-specific" genes in human AML.

131 blood volume); and a laser speckle contrast (LSC) channel for imaging perfusion (i.e., cerebral blood

132 (SSC; 18,758 bp) and one large single copy (LSC; 89,132 bp).

133 activity by a liquid scintillation counter (LSC), the compounds can be quantified using gas chromato

134 that loss of JMJD1C substantially decreased LSC frequency and caused differentiation of MLL-AF9- and

135 lial cell-specific Cxcl12 deletion decreases LSC proliferation, suggesting niche-specific effects.

136 Cs), and its deficiency results in defective LSC function.

137 rsf2, whose upregulation in Ythdf2-deficient LSCs primes cells for apoptosis.

138 enting a valuable resource helping to design LSC-directed therapies.

139 Given the role of cysteine in driving LSC energy production, we tested cysteine depletion as a

140 erapeutic target for selectively eliminating LSCs in MLL-rearranged AML.

141 whether it contributes at all to endogenous LSC function.

142 rosine kinase inhibitors (TKIs) to eradicate LSC in chronic phase (CP) chronic myeloid leukaemia (CML

143 that approaches to treatment must eradicate LSCs for cure.

144 In contrast, ven/aza fails to eradicate LSCs in relapsed/refractory (R/R) patients, suggesting a

145 m cells (LSCs), it is essential to eradicate LSCs to improve patient survival.

146 eroid cell-secretome (LSC-Sec) and exosomes (LSC-Exo) by inhalation to treat different models of lung

147 s uniquely found within the JAM-C-expressing LSC compartment.

148 key self-renewal genes and is essential for LSC self-renewal in a subset of AML.

149 cysteine may be of particular importance for LSC survival.

150 ized doped CQWs are excellent candidates for LSCs.

151 drive OXPHOS, thereby providing a means for LSCs to circumvent the cytotoxic effects of ven/aza ther

152 Furthermore, LSCs from both AML and CML can be refractory to standard

153 Furthermore, LSCs suppressed a set of FICZ-responsive AHR target gene

154 s9 significantly reduced the CD34(+)GPR56(+) LSC compartment of primary human triple-mutated AML cell

155 1 is expressed by cell populations with high LSC activity, and that the cell surface expression of IL

156 In contrast, CD36(High) LSCs were unable to transplant leukemia but were highly

157 itution assays resealed that only CD69(High) LSCs were capable of self-renewal and were poorly prolif

158 so differentially expressed in primary human LSCs and normal human HSPCs.

159 apeutic approach to selectively target human LSCs.

160 activity may not eradicate the most immature LSCs.

161 Importantly, LSC subpopulations with myeloid and proliferative molecu

162 ntrols Src family kinase (SFK) activation in LSC and that LIC with exacerbated SFK activation was uni

163 L blasts and preferentially downregulated in LSC-enriched populations within leukemias.

164 BMPR1b expression and in BMP4 expression in LSC from TKI-resistant patients in comparison with diagn

165 iptional regulators previously implicated in LSC function.

166 We demonstrate a 9- to 90-fold increase in LSC frequency between diagnosis and relapse.

167 genetic protein (BMP) pathway is involved in LSC and progenitor expansion.

168 ive to explore the mechanisms that result in LSC survival and develop new therapeutic approaches.

169 toring Notch and Wnt deregulated activity in LSCs attenuates disease progression.

170 rtly elicited the gene expression changes in LSCs caused by Tcf1/Lef1 deficiency.

171 w directions for deployment of doped CQWs in LSCs for advanced solar light harvesting technologies.

172 specifically identify novel dependencies in LSCs, we screened a bespoke library of small hairpin RNA

173 lf-renewal and proliferation are distinct in LSCs as they often are in normal stem cells and suggest

174 n and self-renewal are separate functions in LSCs as they often are in HSCs.

175 ese functions are also separate functions in LSCs, then antiproliferative therapies may fail to targe

176 g-term culture-initiating cells (LTC-ICs) in LSCs from CML patients.

177 set of AHR targets are uniquely repressed in LSCs across diverse genetic AML subtypes.

178 multiple immune checkpoints specifically in LSCs, including PD-L1, TIM3 and CD24.

179 e decisions in HSCs and could be targeted in LSCs to normalize leukemic myeloid cell production.

180 ler subset of these genes was upregulated in LSCs relative to HSPCs; this subset of genes constitutes

181 r, MSC-specific deletion of Cxcl12 increases LSC elimination by TKI treatment.

182 Moreover, miR-99 inhibition induced LSC differentiation and depletion in an MLL-AF9-driven m

183 Large-area (ca. 75 cm(2) ) infrared LSCs were achieved with a high optical conversion effici

184 is drug combination to eliminate FLT3/ITD(+) LSCs and reduce the rate of relapse in AML patients with

185 y, the drug combination depletes FLT3/ITD(+) LSCs in a genetic mouse model of AML, and prolongs survi

186 te FLT3/internal tandem duplication (ITD)(+) LSCs.

187 ighlights AHR signaling suppression as a key LSC-regulating control mechanism and provides proof of c

188 fetimes in short (SSC; 498-560 nm) and long (LSC; 560-720 nm) spectral channels.

189 critical role and mechanisms of Foxm1 in MA9-LSCs, and indicates that FOXM1 is a potential therapeuti

190 ) in CTLA-4(+) LSCs in vivo, which mobilized LSCs in the BM, induced disease remission, and prolonged

191 sease relapse requires identification of new LSC-selective target(s) that can be exploited therapeuti

192 es that accompany the evolution of these new LSC populations.

193 egies that aim at disrupting essential niche-LSC interactions or improve the regenerative ability of

194 hort (498-560 nm, SSC) and long (560-720 nm, LSC) spectral channels.

195 by accelerating the transformation of normal LSCs to metastatic cancer stem cells (mCSCs).

196 Overall, our data establish HLF as a novel LSC regulator in this genetically defined high-risk AML

197 Transcriptional analysis of LSC and leukemic cells confirms similarity of the de nov

198 that contribute to the overall integrity of LSC function, including the tumor necrosis factor recept

199 n in leukemia development and maintenance of LSC function.

200 nregulation of Cited2, a master regulator of LSC quiescence.

201 le factor-1 (HIF-1), a critical regulator of LSC survival, on the maintenance of CML stem cell potent

202 O1 protein complex as critical regulators of LSC maintenance.

203 nd triggers more electrons in oxygen site of LSC transferred into lattice of Co(3) O(4) , leading to

204 hes that target metabolic vulnerabilities of LSC to selectively eradicate them.

205 ent impaired the persistence and activity of LSCs in a pre-clinical murine CML model and a xenograft

206 s (ROS), resulting in the differentiation of LSCs via oxidative stress and aberrant activation of unf

207 yme, we demonstrate selective eradication of LSCs, with no detectable effect on normal hematopoietic

208 review, we detail the metabolic features of LSCs and how thetse characteristics promote resistance t

209 nsplants with sufficiently high fractions of LSCs, regardless of the LSC percentage in the donor tiss

210 Thus, disrupting interactions of LSCs with the BM environment is a promising strategy to

211 role in the proliferation and maintenance of LSCs.

212 egulators in a unique ex vivo mouse model of LSCs.

213 arge number of LSCs, while a small number of LSCs required PAR-1 for their efficient growth.

214 liferation when there were a large number of LSCs, while a small number of LSCs required PAR-1 for th

215 he disease-inducing and relapse potential of LSCs.

216 help to sustain the functional properties of LSCs.

217 ed here may enable the rapid purification of LSCs from a heterogeneous population of corneal cells, t

218 eloid leukemia (CML) triggers the release of LSCs from the BM into the circulation and impairs their

219 ulatory mechanism to control self-renewal of LSCs and indicates that PRMT5 may represent a potential

220 sights into the fundamental underpinnings of LSCs are now being made in an era in which drug developm

221 th refined and expanded our understanding of LSCs and intrapatient heterogeneity in AML using improve

222 new curative therapeutic approaches based on LSC eradication.

223 Here, we extend our previous report on LSC proteomes to healthy age-matched hematopoietic stem

224 rally expressed on bulk AML cells but not on LSCs.

225 al CD97 as a promising therapeutic target on LSCs in AML.

226 t 530 degrees C achieved by Hf addition onto LSC.

227 Overall, LSCs exhibit distinct properties of immune resistance th

228 e surface Sr enrichment region in perovskite LSC to activate surface lattice oxygen.

229 haracterized leukemia stem cell populations (LSCs) from a well-defined cohort of patients with acute

230 4(-) and CD34(+) LSC-containing populations, LSC frequencies are similar; there are shared clonal str

231 d to survival of preleukemic stem cells (pre-LSCs) is associated with poor prognosis.

232 Herein, we provide direct evidence that pre-LSCs are much less chemosensitive to existing chemothera

233 But unlike mature precursors, LSCs express multiple normal stem cell transcriptional r

234 hibiting its degradation, thereby preserving LSC quiescence, and promoting LSC self-renewal in MLL-re

235 mbined JAK2 and BCR-ABL1 inhibition prevents LSC self-renewal commensurate with ADAR1 downregulation.

236 c potential and induces apoptosis of primary LSCs from MLL-rearranged AML patients in vitro and in vi

237 and several forms of leukemia, with primary LSCs being particularly sensitive to DJ34.

238 as a potential target to eradicate primitive LSCs in AML.

239 nction, and failed to upregulate a prominent LSC-specific AHR target in HSPCs, suggesting that differ

240 SCs) reduces normal HSC numbers but promotes LSC expansion by increasing self-renewing cell divisions

241 eby preserving LSC quiescence, and promoting LSC self-renewal in MLL-rearranged AML.

242 ubstantial heterogeneity within the putative LSC population in CML at diagnosis and demonstrate diffe

243 m, demonstrated selective eradication of R/R LSCs while sparing normal hematopoietic stem/progenitor

244 istance and a metabolic vulnerability of R/R LSCs.

245 F decreased leukemia development and reduced LSC maintenance.

246 in levels in chemoresistant LSCs and reduced LSC tumorigenic activity.

247 elevated nicotinamide metabolism in relapsed LSCs, which activates both amino acid metabolism and fat

248 d markedly eliminated long-term repopulating LSCs and infiltrating blast cells, conferring a survival

249 ription factor highly expressed in resistant LSC.

250 omplete cytogenetic remission, TKI-resistant LSC and progenitors display high levels of BMPR1b expres

251 n in maintaining quiescence of TKI-resistant LSC populations.

252 ng rationale for targeting therapy-resistant LSCs by PARP1 inhibition, which renders them amenable to

253 s interaction might target therapy-resistant LSCs.

254 correlated to JAM-C expression that reveals LSC heterogeneity.

255 tivity aggregated all in vivo patient sample LSC activity into a single sorted population, tightly co

256 dies utilizing lung spheroid cell-secretome (LSC-Sec) and exosomes (LSC-Exo) by inhalation to treat d

257 The inhibition of PARP1 sensitizes LSCs to immunotherapy, highlighting its potential as a t

258 CQDs that are aimed for full solar spectrum LSCs suffer from moderately low quantum efficiency, intr

259 (HSC), water chestnut (WSC) and lotus stem (LSC) were prepared for nano-encapsulation of catechin.

260 be most effective for identifying successful LSC-directed therapies.

261 is a potential therapeutic option to target LSCs and to treat acute myeloid leukemia.

262 rmining the best strategy by which to target LSCs, with their well-documented heterogeneity and readi

263 emia and discuss opportunities for targeting LSC-specific mechanisms for the prevention or cure of ma

264 tification of molecules capable of targeting LSCs appears therefore of primary importance to aim at C

265 s a therapeutic target of specific targeting LSCs.

266 target whose inhibition selectively targets LSCs while promoting HSC expansion.

267 Analysis reveals that LSC-Sec and LSC-Exo treatments could attenuate and resol

268 More recently, we demonstrated that LSCs in patients with de novo AML rely on amino acid met

269 on medicine strategy providing evidence that LSCs can be eradicated.

270 ition, our data provide strong evidence that LSCs harbor a characteristic energy metabolism, adhesion

271 Together, these findings indicate that LSCs are aberrantly reliant on cysteine to sustain energ

272 The LSC exhibits high photoluminescence quantum yield, low r

273 pproaches that show promise to eradicate the LSC, and future challenges on the path to cure.

274 In summary, our data link the LSC concept to immune escape and provide a strong ration

275 reducing the concentration of and making the LSC more oxidized at its surface.

276 The most TKI-insensitive cells of the LSC compartment can be captured within the CD45RA(-) fra

277 ly high fractions of LSCs, regardless of the LSC percentage in the donor tissue.

278 Cell sorting based on the LSC marker GPR56 allowed isolation of triple-mutated fro

279 c inhibition of PARP1 induces NKG2DLs on the LSC surface but not on healthy or pre-leukaemic cells.

280 A Monte Carlo simulation predicts the LSC to possess exceptionally high optical efficiencies o

281 lysis to define the heterogeneity within the LSC population in chronic phase chronic myeloid leukemia

282 s a new and novel method for eliminating the LSCs that are otherwise not targeted by existing therapi

283 h classic CsPbI(3) NCs, the stability of the LSCs after TPP treatments has been greatly improved, eve

284 maintained the undifferentiated state of the LSCs in a concentration dependent manner.

285 The PL emission of the LSCs is centered at about 700 nm with 99.4+/-0.4 % PLQY

286 Treatment of the LSCs with DAPT and SAHM1 reduced the proliferation rate

287 overall levels of amino acids contribute to LSC energy metabolism, our current findings suggest that

288 tion, tightly coupling miR-126 expression to LSC function.

289 , reducing production of ATP, and leading to LSC death.

290 issecting the molecular machinery underlying LSC self-renewal.

291 acterized by the confluence of understanding LSCs and the ability to target them, is shifting from "i

292 nstrated that RANKL specifically upregulates LSC proliferation through activation of Cyclin D1.

293 c characterization of functionally validated LSCs, blasts, and healthy HSPCs, representing a valuable

294 AHR signaling manifestations in HSCs versus LSCs.

295 components of anti-tumour immunity(5), which LSCs must escape to induce cancer.

296 We review the ways in which LSCs take advantage of normal HSC properties to promote

297 AML cells with LSC properties can be isolated by their lack of expressi

298 Compared with LSCs prepared with classic CsPbI(3) NCs, the stability o

299 Distinct transcriptional profiles within LSCs of Mll-AF9/NRAS(G12V) murine AML were identified us

300 ved from WT mice treated with pIL6 ((IL6) WT LSCs) had significantly less proliferation and no tumori