ライフサイエンスコーパス: leukemia cell

1 to kill chemotherapy-resistant acute myeloid leukemia cells.

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

3 rring imatinib resistance in chronic myeloid leukemia cells.

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

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

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

7 ranulation tests of humanized rat basophilic leukemia cells.

8 roliferative activity against MLL-rearranged leukemia cells.

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

10 essing human primary melanoma and hairy cell leukemia cells.

11 roma-mediated chemoresistance in BM-resident leukemia cells.

12 osis of CD133 expressing acute lymphoblastic leukemia cells.

13 ive disease upon adoptive transfer than TCL1 leukemia cells.

14 ukemic activity against bortezomib-resistant leukemia cells.

15 rlie repression of tumor suppressor genes in leukemia cells.

16 re protected against rechallenge with viable leukemia cells.

17 AKT, and impaired engraftment of ROR1 x TCL1 leukemia cells.

18 -gamma and lacked cytolytic activity against leukemia cells.

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

20 ll-cell adhesion or cell death than did TCL1 leukemia cells.

21 signed to deliver synergistic drug ratios to leukemia cells.

22 fied by analysis of bortezomib-treated human leukemia cells.

23 ogenic growth of AE(+) mouse HSPCs and human leukemia cells.

24 ed to have specific cytotoxic effect against leukemia cells.

25 te HDAC1, -3, -4, and -5 in both myeloma and leukemia cells.

26 on and inhibits in vivo progression of human leukemia cells.

27 l-xL (BCL2L1) were examined in human myeloid leukemia cells.

28 ification to also remove contaminating TF-1a leukemia cells.

29 erapeutic efficacy in inducing maturation in leukemia cells.

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

31 agonist reported to decrease labile iron in leukemia cells.

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

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

34 oietic stem/progenitor and acute myelogenous leukemia cells.

35 myeloma cell lines and primary lymphoma and leukemia cells.

36 h increased CDC42 expression and activity in leukemia cells.

37 emotherapy-induced apoptosis in Jurkat human leukemia cells.

38 lly required gene between normal and myeloid leukemia cells.

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

40 he cytotoxic effect of cytidine analogues in leukemia cells.

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

42 In U937 leukemia cells, 2t was more potent than SAHA in inducing

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

44 ROR1 x TCL1 leukemia cells also had higher proportions of Ki-67-posi

45 ccupied many sites on the chromatin of human leukemia cells, although the presence of Sin3 was not as

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

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

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

49 s had higher levels of phospho-AKT than TCL1 leukemia cells and expressed high levels of human ROR1,

50 In leukemia cells and fibroblasts, Sin3b silencing led to M

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

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

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

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

55 Human leukemia cells and induced pluripotent stem cell neurons

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

57 e extremely potent activity of OSW-1 against leukemia cells and its unique mechanism of action sugges

58 for the cellular uptake of 5-azacytidine in leukemia cells and raise the possibility that hENT1 expr

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

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

61 -503, and show their profound effects in MLL leukemia cells and substantial survival benefit in mouse

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

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

64 ring structures that were endocytosed into T-leukemia cells and visualized therein.

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

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

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

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

69 tify a functional vulnerability of primitive leukemia cells, and suggest that clinical development of

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

71 Leukemia cells are protected from chemotherapy-induced a

72 Finally, we observed that CALM-AF10 leukemia cells are selectively sensitive to inhibition o

73 These adherent leukemia cells are sequestered in a quiescent state and

74 ges in NOTCH1 occupancy when T-lymphoblastic leukemia cells are toggled between the Notch-on and -off

75 These findings demonstrate that primitive leukemia cells are uniquely sensitive to agents that tar

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

77 , a protein kinase that drives glycolysis in leukemia cells, as a target for counteracting glucose-de

78 munotoxins, are delivered to the interior of leukemia cells based on antibody specificity for cell su

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

80 ed to significantly enhanced cytotoxicity in leukemia cells by inducing the apoptosis pathways, witho

81 odel; the chemotherapeutic effects of CPA on leukemia cells can be directly investigated in vitro in

82 oped a unique human primary hepatocyte (HPH)-leukemia cell coculture model; the chemotherapeutic effe

83 demand for a better understanding of stromal:leukemia cell communication.

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

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

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

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

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

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

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

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

92 ediated H3K79 methylation, thereby rendering leukemia cells dependent on Rnf20 to maintain their onco

93 c leukemia (APL), retinoic acid (RA) induces leukemia cell differentiation and transiently clears the

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

95 tion or stabilization of the induced myeloid leukemia cell differentiation protein (Mcl-1), leading t

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

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

98 of a folded protein (MCL-1, induced myeloid leukemia cell differentiation protein).

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

100 of the leukemia microenvironment to protect leukemia cells during ASNase treatment.

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

102 Transplanted Nalm-6 or Molm-13 human leukemia cells engrafted at a threefold higher rate in a

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

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

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

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

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

108 Leukemia cells exhibit a dysregulated developmental prog

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

110 BV8 shRNA expressing leukemia cells exhibit reduced STAT3 activity and tumor

111 ietic stem cells or non-LIC fractions within leukemia cells, exhibited constitutive NF-kappaB activit

112 Accordingly, synergisms were only seen in leukemia cells expressing wild-type CD44 and CD49d.

113 ified miR-150 as the most abundant, but with leukemia cell expression levels that varied among patien

114 High-level leukemia cell expression of micro-RNA 155 (miR-155) is a

115 We sampled leukemia cells from 18 patients at two time points.

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

117 y inhibitor obatoclax mesylate in diagnostic leukemia cells from 54 infants with ALL/bilineal acute l

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

119 with increased lysine acetylation in primary leukemia cells from human patients, providing mechanisti

120 ll as diverse human cancer cells and primary leukemia cells from human patients.

121 , also demonstrates activity against primary leukemia cells from individuals with JMML.

122 on in diverse human cancer cells and primary leukemia cells from patients.

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

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

125 onment, in which accessory cells can promote leukemia cell growth and/or survival.

126 ify glutaminolysis as a critical pathway for leukemia cell growth downstream of NOTCH1 and a key dete

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

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

129 with activation of RAS that was required for leukemia cells growth in vitro and in vivo.

130 scriptome analyses revealed that ROR1 x TCL1 leukemia cells had higher expression of subnetworks impl

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

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

133 as well as in some solid tumors and myeloid leukemia cells, heme oxygenase-1 (HO-1), the anti-oxidan

134 slocation and superoxide production in human leukemia cells (HL-60) and COS-7 cells.

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

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

137 evels of RANKL were found to be expressed on leukemia cells in 53 of 78 (68%) investigated patients.

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

139 MLL-AF4 controlled antitumor program to kill leukemia cells in an oncogene dose- and cell type-depend

140 pathways could eliminate acute lymphoblastic leukemia cells in animal models.

141 is peptide can be confirmed on primary human leukemia cells in culture and in vivo, and is identical

142 or an important role for factors secreted by leukemia cells in damaging and suppressing normal hemato

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

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

145 uced the stromal-mediated drug resistance in leukemia cells in vitro and in vivo.

146 leukemia and primary human acute myelogenous leukemia cells in vitro.

147 egrin Beta 3 (Itgb3) is essential for murine leukemia cells in vivo and for human leukemia cells in x

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

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

150 even aggressive, treatment-refractory acute leukemia cells in vivo.

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

152 murine leukemia cells in vivo and for human leukemia cells in xenotransplantation studies.

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

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

155 ular cytotoxicity activation, which affected leukemia cells independent of CD44/CD49d tail mutations.

156 t Polycomb inhibition, in RUNX1-translocated leukemia cells induced terminal differentiation.

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

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

159 Knocking down BV8 in human myeloid leukemia cells inhibits STAT3 activity and expression of

160 rmation in several cell types, we found that leukemia cells instead rely on Brg1 to support their onc

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

162 cell leukemia, we find that infiltration of leukemia cells into the bone marrow rewires the tumor mi

163 ciprocal NF-kappaB activation in BM-MSCs and leukemia cells is essential for promoting chemoresistanc

164 4me3 domains in the K562 chronic myelogenous leukemia cell line as well as the MCF-7 breast cancer ce

165 as as well as in ML2, a human myelomonocytic leukemia cell line bearing the t(6;11)(q27;q23) transloc

166 lines (Beas-2B and A549) and Jurkat cells, a leukemia cell line derived from T lymphocytes.

167 ls as well as the human MLL-AF6-positive ML2 leukemia cell line displayed specific sensitivity to EPZ

168 cancer, we selected the multidrug-resistant leukemia cell line HL-60[R] by exposing it to ATRA, foll

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

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

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

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

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

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

175 ifferentiation of the human megakaryoblastic leukemia cell line UT7-MPL.

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

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

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

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

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

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

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

183 e than 2000 of these predictions in the K562 leukemia cell line.

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

185 the most abundant nucleoside transporter in leukemia cell lines and in AML patient samples.

186 In addition, IRAIN was downregulated both in leukemia cell lines and in blood obtained from high-risk

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

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

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

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

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

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

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

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

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

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

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

198 olaparib and veliparib sensitize the myeloid leukemia cell lines ML-1 and K562, the ovarian cancer li

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

200 Studies using human FLT3/ITD mutant leukemia cell lines revealed the half maximal inhibitory

201 T1 activity and blocks cell proliferation in leukemia cell lines with different genetic lesions.

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

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

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

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

206 and is expressed in a number of human B cell leukemia cell lines, primary human chronic myeloid leuke

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

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

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

210 in lung cancer and breast cancer as well as leukemia cell lines.

211 16.1 nM) and inhibits the growth of multiple leukemia cell lines.

212 n the growth of several MLL1-fusion-mediated leukemia cell lines.

213 response and the comparison of lymphoblastic leukemia cell lines.

214 nhibitors in both mouse and human BCR-ABL(+) leukemia cell lines.

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

216 ntiproliferative activities in acute myeloid leukemia cell lines.

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

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

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

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

221 dministered vaccine consisting of irradiated leukemia cells loaded with the natural killer T (NKT)-ce

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

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

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

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

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

227 gamma-GT) protects human acute promyelocytic leukemia cells (NB4) from Dar, but not from DMAC, sugges

228 encing coupled with the screening of primary leukemia cells obtained from patients with CNL or atypic

229 The binding of leukemia cells onto pre-activated ECs exerted a mechanic

230 ncing of E2A activity by AML1-ETO in t(8;21) leukemia cells or by ETO-2 in normal hematopoietic cells

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

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

233 ppaB signaling expanded LIC frequency within leukemia cell populations.

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

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

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

237 regulation of ACC2 and consequently impedes leukemia cell proliferation.

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

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

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

241 1 is a receptor for Wnt5a, which can promote leukemia-cell proliferation and survival, and can be tar

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

243 IgE-specific immunoblotting and rat basophil leukemia cell (RBL-SX38) mediator release assay.

244 ation of Hsp70 protein in HL60 promyelocytic leukemia cells recovering from acute thermal stress.

245 e witnessing a renaissance of the concept of leukemia cell redistribution in modern CLL therapy.

246 Leukemia cells rely on two nucleotide biosynthetic pathw

247 gh endogenous expression of these enzymes in leukemia cells remains negligible.

248 high levels of Bcl-2 in chronic lymphocytic leukemia cells, repressing B-cell receptor-induced Ca(2+

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

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

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

252 rimethoxy derivatives in chronic lymphocytic leukemia cells revealed that co-treatment of 1alpha,25-d

253 f p53, resulting in selective elimination of leukemia cells, revealing Csnk1a1 as a potential therape

254 beta-catenin signaling, which is involved in leukemia cell self-renewal.

255 e expression, we discovered that ATL patient leukemia cells shifted expression toward the noncanonica

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

257 In leukemia cells, SPARC expression was mediated by the SP1

258 important for the continued proliferation of leukemia cells, suggesting that MYB may be a therapeutic

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

260 A better description of the leukemia cell surface proteome (surfaceome) is a prerequ

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

262 Consistently, human adult T cell leukemia cells that acquire elevated APC(Cdc20) activity

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

264 e established role of the leptin receptor in leukemia cells, the data suggest an important role of CT

265 Finally, because leukemia cells themselves induce EC activation, we postu

266 ated ECs induce the adhesion of a sub-set of leukemia cells through the cell adhesion molecule E-sele

267 Conditional deletion of alpha4 sensitized leukemia cell to nilotinib.

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

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

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

271 sistance mechanisms alter the sensitivity of leukemia cells to immune system effector cells.

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

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

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

275 ling of BM-MSCs revealed that coculture with leukemia cells upregulated the transcription of genes as

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

277 imally perturbed cell cycle in human myeloid leukemia cells using centrifugal elutriation combined wi

278 nstrated strong and selective effects in MLL leukemia cells, validating specific mechanism of action.

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

280 of differentiated HL-60 human promyelocytic leukemia cells was blocked by PPTN with a concentration

281 acterizing their binding with HL-60 and KG-1 leukemia cells, we are able to induce the mechanical cha

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

283 downstream mediators of Csnk1a1 critical for leukemia cells, we performed an in vivo pooled shRNA scr

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

285 se lenalidomide (5 mg per day) and found the leukemia cells were also induced to express p21 in vivo.

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

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

288 Using HL60 model human myeloid leukemia cells, where all-trans retinoic acid (RA) induc

289 PU.1 is highly expressed in leukemia cells, whereas RUNX1 is frequently inactivated

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

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

292 ell lines and in primary chronic lymphocytic leukemia cells, while being up to 6 orders less cytotoxi

293 ant growth in T-ALL and further suggest that leukemia cells will deploy multiple mechanisms to develo

294 activity against primary chronic lymphocytic leukemia cells with a therapeutic window 31- and 107-fol

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

296 eatment of primary human chronic lymphocytic leukemia cells with Lenalidomide results in reduced RhoH

297 in cell lines or primary chronic lymphocytic leukemia cells with the exception of CD19 and CD38.

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

299 proliferation arrest and differentiation of leukemia cells, with a minimal impact on growth of sever

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