ライフサイエンスコーパス: leukemia cell

1 t SKIP re-expression enhances SK activity in leukemia cells.

2 IF1alpha/low MEIS1-expressing MLL-rearranged leukemia cells.

3 ion of MDM2 at concentrations <1 nM in human leukemia cells.

4 anticancer activity in breast, prostate, and leukemia cells.

5 olon-carcinoma cells and multidrug-resistant leukemia cells.

6 p) in doxorubicin-induced drug resistance of leukemia cells.

7 ial, and induced apoptosis of drug-resistant leukemia cells.

8 erlying stem cell-related characteristics in leukemia cells.

9 iation and inhibits proliferation of myeloid leukemia cells.

10 ular degranulation assays using rat basophil leukemia cells.

11 tress, suppresses differentiation of myeloid leukemia cells.

12 e at a subset of active enhancers in MLL-AF4 leukemia cells.

13 cetylase (HDAC)6 inhibition than JAK3 mutant leukemia cells.

14 emotherapy-induced apoptosis in Jurkat human leukemia cells.

15 to kill chemotherapy-resistant acute myeloid leukemia cells.

16 of human cancers and induced cell killing in leukemia cells.

17 onogenic cell growth effect on MLL-AF9 human leukemia cells.

18 agonist reported to decrease labile iron in leukemia cells.

19 and PUM2 levels in primary HSPCs and myeloid leukemia cells.

20 criptional profiles of THP-1 monocytic human leukemia cells.

21 oietic stem/progenitor and acute myelogenous leukemia cells.

22 myeloma cell lines and primary lymphoma and leukemia cells.

23 occupancy of USF2 at HOXA9 promoter in MLLr leukemia cells.

24 h increased CDC42 expression and activity in leukemia cells.

25 lly required gene between normal and myeloid leukemia cells.

26 of glioblastoma and B-cell acute lymphocytic leukemia cells.

27 he cytotoxic effect of cytidine analogues in leukemia cells.

28 athway in mouse fibroblasts as well as human leukemia cells.

29 onjugate was selective for targeted CCRF-CEM leukemia cells.

30 rring imatinib resistance in chronic myeloid leukemia cells.

31 h of mixed lineage leukemia (MLL)-rearranged leukemia cells.

32 g gammadelta T-cell killing capacity against leukemia cells.

33 pacity of MEIS1, and HOX-driven lymphoma and leukemia cells.

34 ranulation tests of humanized rat basophilic leukemia cells.

35 roliferative activity against MLL-rearranged leukemia cells.

36 ity of ST1326, particularly on acute myeloid leukemia cells.

37 lial cells, Jurkat cells, and rat basophilic leukemia cells.

38 Brd9&Jmjd6, Kat6a&Jmjd6, and Brpf1&Jmjd6 in leukemia cells.

39 efficacy AURKA and AURKB expression in K-562 leukemia cells.

40 patient-derived primary chronic lymphocytic leukemia cells.

41 recombinant enzymes and nuclear lysates from leukemia cells.

42 ion is highly sensitized in STAG2-mutant CMK leukemia cells.

43 ormal lymphocytes or standard- and high-risk leukemia cells.

44 effect that ultimately inhibits apoptosis in leukemia cells.

45 n looping at the MYC locus in BETi-resistant leukemia cells.

46 mes, resulting in less stromal protection of leukemia cells.

47 Quiescent and proliferating leukemia cells accumulate highly lethal DNA double-stran

48 growth factor (VEGF) secreted from suspended leukemia cells and adherent breast cancer cells.

49 PARI may restore differentiation ability of leukemia cells and antagonize their proliferation.

50 DNA-PK-deficient quiescent leukemia cells and BRCA/DNA-PK-deficient proliferating l

51 xenograft nude mice injected with human K562 leukemia cells and cell viability of primary leukemia ce

52 ial membrane potential of single lymphocytic leukemia cells and demonstrate that mitochondria hyperpo

53 vo using mice injected with human MLL-fusion leukemia cells and evaluated disease progression followi

54 at induce apoptosis and cell-cycle arrest in leukemia cells and finally demonstrate the efficacy of t

55 oughput drug screening on CEBPA/CSF3R mutant leukemia cells and identified sensitivity to inhibitors

56 against 21,321 pairs of drug targets in K562 leukemia cells and identified synthetic lethal drug targ

57 n unexpected role for MLL2 in MLL-rearranged leukemia cells and identify potential therapeutic target

58 h selective cytotoxicity toward human T-cell leukemia cells and indicate its potential use in cancer

59 Human leukemia cells and induced pluripotent stem cell neurons

60 cial effects of transplanted T cells against leukemia cells and infectious pathogens remained unaffec

61 es in intracellular accumulation of MTXPG in leukemia cells and its antileukemic effectsFUNDINGTHE Na

62 for example, distinguish between the target leukemia cells and other cancer cells within the matrix

63 eration and induced differentiation in acute leukemia cells and primary patient samples with MLL1 tra

64 ired expansion and colony-forming ability of leukemia cells and prolonged latency of leukemia develop

65 L1 is dynamically expressed in Cbfb-MYH11(+) leukemia cells and promotes their survival.

66 DNA replication in a subset of primary human leukemia cells and selectively targeted leukemia cells w

67 Here we show that interactions between leukemia cells and stromal cells (HS-5) upregulate CD20

68 -503, and show their profound effects in MLL leukemia cells and substantial survival benefit in mouse

69 Inhibiting DNM2 suppresses proliferation of leukemia cells and synergizes with CK2 inhibition.

70 ited the growth of acute and chronic myeloid leukemia cells and the phosphorylation and transcription

71 d the cytolytic activity of NK cells against leukemia cells and was also required for IL-15-mediated

72 cellular cytotoxicity against PRAME+HLA-A2+ leukemia cells and was therapeutically effective against

73 itory activity against T-cell prolymphocytic leukemia cells, and in vivo assays demonstrate durable p

74 nd mouse mast cells, as well as rat basophil leukemia cells, and in vivo in mice.

75 lity in quiescent and proliferating immature leukemia cells, and is thus a potential approach to erad

76 e show that PARI is overexpressed in myeloid leukemia cells, and its knockdown reduces leukemia cell

77 somes, which are subsequently endocytosed by leukemia cells, and protect leukemia cells from tyrosine

78 form higher-order oligomers in t(1;19) human leukemia cells, and that this property is required for o

79 In vitro, CD-160130 induced leukemia cell apoptosis, and could overcome bone marrow

80 reveals that the spatiotemporal dynamics of leukemia cells are critically dependent on syndecan sign

81 These data suggest that leukemia cells are dependent upon calcineurin for immune

82 Using BET inhibitor (BETi) resistant leukemia cells as a model system, we demonstrated herein

83 rs on the plasma membrane and delivered into leukemia cells as a potent antileukemic agent.

84 Here, we report TF-1 leukemia cells as a robust system useful for modeling th

85 ound IgE was measured by ELISA, rat basophil leukemia cell assay, and ex vivo using a basophil activa

86 NFAT-DsRed rat basophil leukemia cell attachment and retention during washing st

87 bility of BASIL to distinguish acute myeloid leukemia cells based on the phosphoproteome data.

88 dine deaminase, a dC-catabolizing enzyme, in leukemia cells both in cell culture and in mice reduced

89 -RARalpha in transforming myeloid cells into leukemia cells, but further uncover a topological framew

90 d heterocyclic activators of PP2A) that kill leukemia cells by allosterically assembling a specific h

91 l molecule that rapidly kills MLL-rearranged leukemia cells by targeting a metabolic vulnerability in

92 ished differentiation therapies, some mature leukemia cells can de-differentiate and reacquire clonog

93 des a basis for MSI2 increased dependency in leukemia cells compared to normal cells.

94 Abl, and display lower cytotoxicity against leukemia cells compared to those of the individual const

95 (ALL), and resistance to glucocorticoids in leukemia cells confers poor prognosis.

96 [(18)F]CFA accumulation in leukemia cells correlated with dCK expression and was ab

97 The amount of genomic information about leukemia cells currently far exceeds our overall underst

98 Stromal coculture did not prevent leukemia cell cycle activity, but a specific sensitivity

99 l study indicated that Az treatment promotes leukemia cell death by activating caspase-dependent apop

100 sed NADPH levels, resulting in ROS-dependent leukemia cell death characterized by the release of mito

101 wed that the active hybrid molecules promote leukemia cell death through a caspase-dependent apoptoti

102 nent MYC degradation concomitant with robust leukemia cell death.

103 The unresponsive MLL-rearranged leukemia cells did not undergo mitochondrial membrane de

104 kinase (JNK), increased induction of myeloid leukemia cell differentiation protein (Mcl-1) expression

105 cell lymphoma 2 (Bcl-2) and induced myeloid leukemia cell differentiation protein (Mcl-1), two major

106 specific expression of human induced myeloid leukemia cell differentiation protein Mcl-1 (CD68.hMcl-1

107 mation because B-lineage acute lymphoblastic leukemia cells display a pronounced block in differentia

108 ent incorporation of decitabine into myeloid leukemia cell DNA that correlated with extent of DNA hyp

109 ved that depletion of calcineurin B (CnB) in leukemia cells dramatically prolongs survival in immune-

110 surface expression of HLA-DR, -DQ and -DP on leukemia cells, due to downregulation of the HLA class I

111 fficiency of pseudodiploid mouse lymphocytic leukemia cells during normal proliferation and polyploid

112 or killing by chemotherapy of mouse or human leukemia cells, either in vitro or in vivo.

113 oxidation induced by vitamin C treatment in leukemia cells enhances their sensitivity to PARP inhibi

114 e of VEGF produced by ALL cells in mediating leukemia-cell entry into the CNS and leptomeningeal infi

115 molecular mechanisms and pathways mediating leukemia-cell entry into the CNS need to be understood t

116 In this study, we analyzed leukemia-cell entry into the CNS using a primograft ALL

117 study reveals a novel strategy for selective leukemia cell eradication based on a specific difference

118 Leukemia cells exhibit a dysregulated developmental prog

119 nts targeting CD22 or CD20 on B lymphoma and leukemia cells exhibit clinical efficacy for treating th

120 bservations in mice, patient-derived myeloid leukemia cells exhibit KRAS/RAC1/ROS/NLRP3/IL-1beta axis

121 that FLT3/internal tandem duplication (ITD) leukemia cells exhibit mechanisms of intrinsic signaling

122 We found that leukemia cells exhibited mechanical differences compared

123 lipidome, and genetic interactions of human leukemia cells exposed to palmitate.

124 In addition, unresponsive MLL-rearranged leukemia cells expressed increased levels of MEIS1, an i

125 Gene expression analyses of leukemia cells extracted from the BM identified Cn-depen

126 Destabilization of target programs shifts leukemia cell fate out of self-renewal into differentiat

127 inding, degranulation assays of rat basophil leukemia cells for in vitro efficacy, and mouse models o

128 ined the prednisolone sensitivity of primary leukemia cells from 444 patients newly diagnosed with AL

129 quencing of 103 leukemia-associated genes in leukemia cells from 841 treatment-naive patients with ch

130 Primary leukemia cells from high-risk patients overexpressed Not

131 leukemia cells and cell viability of primary leukemia cells from human patients, but shows minimal to

132 following affinity enrichment of circulating leukemia cells from peripheral blood.

133 ncluding chemotherapy, facilitated escape of leukemia cells from targeted third-generation ABCB1 inhi

134 y endocytosed by leukemia cells, and protect leukemia cells from tyrosine kinase inhibitors (TKIs).

135 llectively, these results characterize human leukemia cell functional heterogeneity and suggest that

136 introduce the P95H mutation to SRSF2 in K562 leukemia cells, generating an isogenic model so that spl

137 H1 gene, has emerged as a major regulator of leukemia cell growth and metabolism.

138 6 18S rRNA 2'-O-methylation is essential for leukemia cell growth and survival.

139 M-808 effectively inhibits leukemia cell growth at low nanomolar concentrations and

140 ession and induced apoptosis, thus affecting leukemia cell growth.

141 tyltransferase (HAT) MOF to be important for leukemia cell growth.

142 igatus when mice were heavily engrafted with leukemia cells, had severe chemotherapy-induced neutrope

143 After receiving higher numbers of TCL1 leukemia cells, half of p110deltaD910A/D910A mice sponta

144 forensic DNA markers to demonstrate that the leukemia cells have a clonal origin and appear to be tra

145 We present results for leukemia cells (HL60) as a model circulatory cell as wel

146 n regulatory domains in murine acute myeloid leukemia cells identifies six known drug targets and 19

147 landscape is essential for sustaining proper leukemia cell identity and that loss of a single factor

148 roma inhibited B-lymphoid differentiation of leukemia cells, illuminating a mechanism of age-specific

149 iating potential of MLL-AF9(+) acute myeloid leukemia cells in a dose-dependent manner in vitro and i

150 t with UC-961 inhibited engraftment of ROR1+ leukemia cells in immune-competent ROR1-transgenic mice.

151 B cell lines and primary chronic lymphocytic leukemia cells in sera depleted of single complement com

152 When driven by MLL-AF9, leukemia cells in the adult microenvironment sustained a

153 nds reduced the viability of chronic myeloid leukemia cells in the micromolar range.

154 xic effects in human MDSL, HL-60, and MV4-11 leukemia cells in vitro.

155 itro, and primed CD56bright cells controlled leukemia cells in vivo in a murine xenograft model.

156 angina drug is able to effectively eliminate leukemia cells in vivo, and is a novel therapeutic strat

157 e and dasatinib also impaired engraftment of leukemia cells in vivo.

158 ortical thymocyte stage and that a subset of leukemia cells inappropriately reexpress stem cell genes

159 Of note, SKIP re-expression in leukemia cells increased ceramide levels 2-fold, inactiv

160 ducing CEP72 expression in human neurons and leukemia cells increased their sensitivity to vincristin

161 micking T-cell receptor activation in Jurkat leukemia cells induced sequential activation of downstre

162 ive polyglutamylated metabolites (MTXPGs) in leukemia cells influence its antileukemic effects.METHOD

163 reactive oxygen species in HL-60 and Jurkat leukemia cells, inhibit cell growth, induce apoptosis an

164 We found that actively proliferating leukemia cells inhibited normal hematopoietic stem and p

165 esented whereas direct T cell recognition of leukemia cells intensifies exhaustion.

166 e in adult humans, we examined the adipocyte-leukemia cell interactions to determine if they are esse

167 ed inhibitors (GW809897X and GW806742X) in a leukemia cell line as a potential novel therapy for ALL

168 4me3 domains in the K562 chronic myelogenous leukemia cell line as well as the MCF-7 breast cancer ce

169 arcinoma cell line HepG2 over both the human leukemia cell line CEM and the normal hematopoietic CFU-

170 death in eosinophils and the human mast cell leukemia cell line HMC-1.2.

171 MDA-MB-231, lung cancer cell line PC-9, and leukemia cell line K-562 using both live-cell and in-sit

172 to RNA-seq data of the human chronic myeloid leukemia cell line K562 in response to shRNA knockdown o

173 ntial genes in the human chronic myelogenous leukemia cell line K562.

174 strates >100-fold selectivity over the HL-60 leukemia cell line lacking MLL fusion.

175 activated murine CD8+ T-cell and lymphocytic leukemia cell line lineages.

176 onfirmed by a second in vivo model using the leukemia cell line NALM6.

177 Earlier work with the DT40 chicken B cell leukemia cell line showed that Syk was required to trans

178 MEG-01 is the human megakaryoblastic leukemia cell line that can be differentiated in vitro b

179 We performed CRISPR-Cas9 screens in a leukemia cell line to identify perturbations that enhanc

180 The HL-60 leukemia cell line was differentiated to a neutrophil-li

181 concentrations as low as 30 pM in the RS4;11 leukemia cell line, achieves an IC50 value of 51 pM in i

182 Cells of human promyelocytic leukemia cell line-60 were differentiated into neutrophi

183 TOP2A cleavage genome-wide in the human K562 leukemia cell line.

184 ve GCSF using the mouse M-NFS-60 myelogenous leukemia cell line.

185 JAK3(A572V) mutation-positive acute myeloid leukemia cell line.

186 bian lymphocytes and the Jurkat human T cell leukemia cell line.

187 properties against the MV4-11 acute myeloid leukemia cell line.

188 lular species in real time from a suspension leukemia cell line.

189 urther evaluated using THP-1 human monocytic leukemia cell line.

190 ions on chemotherapy sensitivity in isogenic leukemia cell lines and in murine leukemia generated fro

191 these findings in T cell acute lymphoblastic leukemia cell lines and patient samples and show that on

192 activation effectively promotes apoptosis in leukemia cell lines and patient samples while sparing he

193 ivity of the novel CPT1a inhibitor ST1326 on leukemia cell lines and primary cells obtained from pati

194 liferation, survival, and chemoresistance in leukemia cell lines and primary samples.

195 tivities against a broad panel of cancer and leukemia cell lines and some antiviral activity against

196 ukemia (AML) expresses CD83 and that myeloid leukemia cell lines are readily killed by CD83 CAR T cel

197 fects in vitro against a panel of cancer and leukemia cell lines as well as antiviral effects against

198 , we documented that ST1326 inhibited FAO in leukemia cell lines associated with a dose- and time-dep

199 hibits cell growth in the MV4;11 and MOLM-13 leukemia cell lines carrying MLL fusion with IC(50) valu

200 terized a panel of ABT-199-resistant myeloid leukemia cell lines derived through chronic exposure to

201 ons than control cells, and SKIP-transfected leukemia cell lines exhibited increased SK activity.

202 nd selectively inhibits cell growth in human leukemia cell lines harboring MLL translocations and is

203 ectively inhibits cell growth in human acute leukemia cell lines harboring the rearranged mixed linea

204 xpression restrained growth of murine B-cell leukemia cell lines in vitro and in vivo, independently

205 rthermore, METTL3 depletion in human myeloid leukemia cell lines induces cell differentiation and apo

206 ar export receptor CRM1 were observed in the leukemia cell lines LOUCY and MEGAL.

207 used CRISPR-Cas9 to generate isogenic human leukemia cell lines of the most common TP53 missense mut

208 own of ZNF521 reduced proliferation in human leukemia cell lines possessing MLL-AF9 translocations.

209 is in a subset (7/11, 64%) of MLL-rearranged leukemia cell lines within a few hours of treatment.

210 Tested in leukemia cell lines, 35 and 39 induced apoptosis and/or

211 city was first demonstrated in vitro against leukemia cell lines, and NK cells might play a crucial r

212 Cbz-B3A slows cellular growth of some human leukemia cell lines, but is not cytotoxic.

213 cluding multiple myeloma (MM), lymphoma, and leukemia cell lines, ER stress leads to caspase-mediated

214 y low cytotoxicity as a single agent against leukemia cell lines, it augmented the apoptosis inductio

215 active in normal human bone marrow, multiple leukemia cell lines, MCF-7 cells, and subjects after GM-

216 analyzed 152 cells from three acute myeloid leukemia cell lines, resulting in a total of 2558 identi

217 alyses, and siRNA-mediated gene silencing in leukemia cell lines, we show that AICAr-mediated differe

218 r activity was demonstrated in acute myeloid leukemia cell lines, where significant impairment of pro

219 so low nanomolar IC(50) values in a panel of leukemia cell lines.

220 ntiproliferative activities in acute myeloid leukemia cell lines.

221 encies in inhibition of cell growth in acute leukemia cell lines.

222 presses cell growth by inducing apoptosis in leukemia cell lines.

223 uman blood mononuclear cells and a subset of leukemia cell lines.

224 of a TET2-dependent gene signature in human leukemia cell lines.

225 treatment with an EZH2 inhibitor in several leukemia cell lines.

226 the growth of both murine and human MLL-AF9 leukemia cell lines.

227 ly induced cell death in chronic myelogenous leukemia cell lines.

228 y potential on the proliferation of specific leukemia cell lines.

229 ly inhibit the clonogenic potential of acute leukemia cell lines.

230 survival and proliferation in multiple human leukemia cell lines.

231 e novel prodrug also induced T cell mediated leukemia cell lysis.

232 We show that MLL-AF9 leukemia cells maintain cell polarity in the context of

233 nd mouse, the identified KLF4-DPYSL2 axis in leukemia cells may serve as a potential therapeutic targ

234 rs autophagy as a salvage pathway supporting leukemia cell metabolism.

235 Furthermore, in a leukemia cell model system, we found a correlation betwe

236 s and cell lines including solid cancers and leukemia cell models to explore its potential therapeuti

237 lls and was not abrogated by the presence of leukemia cells or cytotoxic agents.

238 on of the two methods on human promyelocytic leukemia cells, our results surprisingly reveal that adh

239 from the leukemia microenvironment leads to leukemia cell persistence, development of resistance, an

240 compared with sensitive ALL cells, resistant leukemia cells possess a fundamentally rewired central m

241 TET2 suppresses leukemia cell proliferation and colony formation in a ma

242 id leukemia cells, and its knockdown reduces leukemia cell proliferation in vitro and in vivo in xeno

243 Leukemia cell proliferation requires up-regulation and r

244 Ectopic expression of Hoxa9 rescued impaired leukemia cell proliferation upon USF2 loss.

245 geting wild-type MLL degradation impedes MLL leukemia cell proliferation, and it downregulates a spec

246 regulation of ACC2 and consequently impedes leukemia cell proliferation.

247 hibited cellular PRMT1 activity, and blocked leukemia cell proliferation.

248 toward 32D cells or HSCs, nor did it augment leukemia cell proliferation.

249 regulated HOXA9 expression and impaired MLLr leukemia cell proliferation.

250 activity in vitro and in vivo by inhibiting leukemia cell proliferation/viability and by promoting c

251 1 is a receptor for Wnt5a, which can promote leukemia-cell proliferation and survival, and can be tar

252 e, in part, to difficulty in eliminating the leukemia cells protected by stromal microenvironment.

253 of immune evasion can involve abrogation of leukemia cell recognition due to loss of HLA genes, immu

254 Leukemia cells rely on two nucleotide biosynthetic pathw

255 naling pathways, most notably JAK/STAT, that leukemia cells require for proliferation.

256 Inhibition of Hsp72 in acute lymphoblastic leukemia cells resulted in increased multipolar spindle

257 activator NLRP3 in glucocorticoid-resistant leukemia cells, resulting from significantly lower somat

258 Ro treatment in mouse and human myeloid leukemia cells results in an increase in differentiation

259 hardly induced degranulation of rat basophil leukemia cells sensitized with Art v 1-specific mouse or

260 Hopx(-/-) MN1-overexpressed leukemia cells showed higher proliferation rate and down

261 nterestingly, isolated nuclei from high-risk leukemia cells showed increased viscosity than their cou

262 )P2 depletion in primary chronic lymphocytic leukemia cells significantly impaired their migration ca

263 ifferentiation of NB4 and HL60 human myeloid leukemia cells, suggesting that O-GlcNAcylation is invol

264 cytokine production in response to CD200(+) leukemia cells, supporting clinical translation.

265 a mechanism for the requirement of PRMT5 for leukemia cell survival and provides potential biomarkers

266 than sTRAIL and induced apoptosis in primary leukemia cells taken directly from BPL patients.

267 used to sort K562 human chronic myelogenous leukemia cells that have either been treated or untreate

268 patients harbor subpopulations of resistant leukemia cells that mediate disease recurrence.

269 an intrinsically unresponsive MLL-rearranged leukemia cell to CCI-006, indicating that this pathway p

270 und that stable knockdown of 6PGD sensitizes leukemia cells to antimalarial agent dihydroartemisinin

271 We show that exposure of leukemia cells to daunorubicin activated an integrated s

272 thyltransferase SETDB1 enables acute myeloid leukemia cells to evade sensing of retrotransposons by i

273 one acetylation and increased sensitivity of leukemia cells to histone deacetylase inhibitors.

274 an in vitro model of Nilotinib-resistant Ph+ leukemia cells to investigate whether low dose radiation

275 FTO inhibition sensitizes leukemia cells to T cell cytotoxicity and overcomes hypo

276 eterogeneity and insensitivity in individual leukemia cells treated with a multi-drug panel of FDA-ap

277 nalyze the gene expression profiles of HL-60 leukemia cells treated with a small molecule drug librar

278 iR-181a/b gene cluster in APL blasts and NB4 leukemia cells upon ATRA treatment as a key event in the

279 HLA expression on leukemia cells-upregulated in the post-HCT environment-s

280 t oxidase-derived ROS promotes the growth of leukemia cells via the glycolytic regulator PFKFB3.

281 f the type I PRMT inhibitor MS023 to inhibit leukemia cell viability parallels baseline FLT3 R972/973

282 , leading to synergistic inhibition of human leukemia cell viability.

283 the cell size of SNORD42A deletion carrying leukemia cells was decreased.

284 creased secretion of IL12 from CnB-deficient leukemia cells was sufficient to induce T-cell activatio

285 addition, in both the murine model and human leukemia cells, we found that Meis1 loss led to increase

286 ls expressing SERT and intact rat basophilic leukemia cells, we show that agents such as Na(+) and co

287 sing the DOT1L inhibitor EPZ-5676 in MLL-AF4 leukemia cells, we show that H3K79me2/3 is required for

288 itive cells, the unresponsive MLL-rearranged leukemia cells were characterized by a more glycolytic m

289 drug screen revealed that JAK3/Suz12 mutant leukemia cells were more sensitive to histone deacetylas

290 ximately 100, 1,000, and 10,000 U937 myeloid leukemia cells were processed, and a one-tenth of each s

291 ells and BRCA/DNA-PK-deficient proliferating leukemia cells were sensitive to PARP1 inhibitors that w

292 HL60 (leukemia cells) were also studied as a model circulatory

293 y inhibiting colony formation in THP-1 human leukemia cells, were assessed in mouse for their prelimi

294 (m(6)A) RNA modification in R-2HG-sensitive leukemia cells, which in turn decreases the stability of

295 uman leukemia cells and selectively targeted leukemia cells while sparing normal progenitor cells.

296 onstrated by quantifying all dNTPs in CEM-SS leukemia cells with and without hydroxyurea or auranofin

297 In Figure 3D, treatment of MLL-fusion leukemia cells with I-BET151 resulted in transcriptional

298 Treatment of CSF3R/CEBPA mutant leukemia cells with LSD1 inhibitors reactivates differen

299 ation and lethality by driving engagement of leukemia cells with their microenvironment and maintaini

300 ells, mouse and human T cells, primary human leukemia cells, yeast, Escherichia coli and Enterococcus