ライフサイエンスコーパス: leukemic

1 oach is that miR-26a can elicit in vivo anti-leukemic activities mediated by increased apoptosis.

2 gemcitabine and cabazitaxel, have broad anti-leukemic activity across subtypes and are more effective

3 how here that R-2HG also exerts a broad anti-leukemic activity in vitro and in vivo by inhibiting leu

4 ntly, only DAC potentiated HSPC-NK cell anti-leukemic activity in vivo.

5 The anti-leukemic agent asparaginase activates the integrated str

6 ncreases risk for liver toxicity by the anti-leukemic agent asparaginase, but the mechanism is unknow

7 Injected human leukemic and breast cancer cells exhibited cell-type spe

8 xpression profiles of in vivo chemoresistant leukemic and G0 models.

9 HDACi causes distinct chromatin responses in leukemic and host CD4(+) T cells, reprogramming host T c

10 whole-genome bisulfite sequencing of primary leukemic and non-leukemic cells in patients with or with

11 Both leukemic and nonleukemic cells exhibit higher BMP4 level

12 so exhibited improved capacity to graft both leukemic and solid tumor cells compared with NSI, NOG, a

13 In vivo treatment of leukemic animals with MLL-r FLT3mut leukemia reduced leu

14 ent to perturb HSC function by reprogramming leukemic-associated chromatin and gene transcription.

15 s in CLL patients are chronically exposed to leukemic B cells, which potentially impacts metabolic ho

16 ration, survival, and tissue infiltration of leukemic B cells.

17 iota-SATB2 signaling cascade is required for leukemic BCR-ABL(+) B-cell progenitor transformation and

18 ng was therefore not sufficient to eliminate leukemic behavior.

19 mbinant EGFL7 in vitro leads to increases in leukemic blast cell growth and levels of phosphorylated

20 unction that may result from infiltration of leukemic blast cells (LBCs) into lung parenchyma and int

21 ncy and gene expression patterns in purified leukemic blast cells.

22 related with Alox5 overexpression in MLL-AF9-leukemic blast cells; inhibition of the above signaling

23 Patients with 25% or more leukemic blasts after induction (early nonresponders) ha

24 By comparing LSCs to leukemic blasts and healthy HSPCs, we validate candidate

25 at CSF1R is not expressed on the majority of leukemic blasts but instead on a subpopulation of suppor

26 an autocrine mechanism supporting growth of leukemic blasts in patients with AML.

27 Several of these studies suggest that leukemic blasts occupy specific cellular and biochemical

28 cell death or differentiation and sensitized leukemic blasts toward genotoxic agents in vitro and in

29 stem cells, leukemic stem cells [LSCs], and leukemic blasts).

30 ity of decitabine in AML cell lines, primary leukemic blasts, and xenograft models.

31 maintenance of the undifferentiated state in leukemic blasts.

32 granules against KIR ligand-matched primary leukemic blasts.

33 od cells, characterized by overproduction of leukemic blasts.

34 which allows adequate protein production in leukemic blasts.

35 0 complex is exposed on the cell membrane of leukemic blasts.

36 otherapeutic agent Ara-C lowered bone marrow leukemic burden compared with DMSO or Ara-C alone, thus

37 in vitro and led to a 2-log reduction in the leukemic burden in patient-derived xenograft mice.

38 e Bcl-2 inhibitor, was effective in reducing leukemic burden in vitro and in vivo in patient-derived

39 tment of Cdx2 AML with azacitidine decreases leukemic burden.

40 IL2RA antibodies inhibited leukemic, but not normal, hematopoietic cells and synerg

41 Increased understanding of the leukemic cell biology and pathogenesis, and the ways the

42 protein responded with a greater decrease in leukemic cell count compared with those samples expressi

43 We finally show that selective leukemic cell death is achievable with a small molecule

44 r, which in turn regulates genes that induce leukemic cell death.

45 Leukemic cell dependence on Aldh3a2 was seen across mult

46 udies on the mechanisms/pathways involved in leukemic cell differentiation revealed that binding of S

47 Leukemic cell dissemination could be effectively blocked

48 tant to clarify the mechanisms of incomplete leukemic cell eradication by vemurafenib and to explore

49 , miR-26a was the most effective in reducing leukemic cell expansion.

50 a 1A (TCL1A) oncogene distinguishes the (pre)leukemic cell from regular postthymic T cells.

51 doxorubicin, as evidenced by suppression of leukemic cell growth and a significant reduction of the

52 ML lines and primary patient cells decreased leukemic cell growth and chemoresistance via downregulat

53 inhibition of PRMT1 significantly suppresses leukemic cell growth and survival.

54 trate that FOXP1 by itself supports HSPC and leukemic cell growth, thus mimicking PUM activities.

55 reover, we found that PUM1/2 sustain myeloid leukemic cell growth.

56 M1/2 and FOXP1 in regulating normal HSPC and leukemic cell growth.

57 as able to inhibit STAT5 phosphorylation and leukemic cell growth.

58 efforts to develop new models to study niche-leukemic cell interaction in human myeloid malignancies;

59 Using a leukemic cell line and diagnostic bone marrow cells from

60 rrow-derived macrophages (BMDMs) and a human leukemic cell line, U937 cells, dividing in hyperglycemi

61 note, cortactin is strongly overexpressed in leukemic cell lines and primary patient-derived leukemic

62 ed expression of GFI1 in several widely used leukemic cell lines inhibits their growth and decreases

63 lls and the effects of SKIP re-expression in leukemic cell lines.

64 oth in vitro and in a murine Hoxa9-dependent leukemic cell model.

65 AT mutations were not sufficient to initiate leukemic cell proliferation but rather only augmented si

66 oietic stem cells and summarizes its role on leukemic cell response to chemotherapy.

67 Furthermore, TAF1 is required for leukemic cell self-renewal and its reduction promotes th

68 pt ( P < 1.0E(-6)) and with lower diagnostic leukemic cell surface CD33 intensity ( P < 1.0E(-6)).

69 or IL-17RB led to significant suppression of leukemic cell survival and disease progression in vivo.

70 the retinoid X receptor to decrease BCR-ABL leukemic cell viability.

71 These studies form a basis for leukemic cell-targeted delivery of miR-29b as a promisin

72 ring CART19 manufacturing can lead to CAR19+ leukemic cells (CARB19) that are resistant to CART19 kil

73 metabolic disorders, were studied on ex-vivo leukemic cells activated in vitro by microenvironment st

74 The highly activated leukemic cells also revealed losses of negative-regulato

75 would contribute to reducing the survival of leukemic cells and also tackling their chemoresistance.

76 e, we used RNA-Seq-based analysis of patient leukemic cells and found that upregulation of the Tec fa

77 microenvironment to support the survival of leukemic cells and influence their response to therapeut

78 aft-membrane protein expressed by normal and leukemic cells and involved in cell signaling.

79 Finally, we observe that persistent residual leukemic cells are quiescent and can become responsive t

80 in a robust reduction of the progression of leukemic cells both in vitro and in vivo.

81 ox transcription factor CDX2 is expressed in leukemic cells but not during normal blood formation.

82 eased cell proliferation and self-renewal in leukemic cells by downregulating the Myc signature.

83 We induce chemoresistant and G0 leukemic cells by serum starvation or chemotherapy treat

84 Leukemic cells can remodel the niche into a permissive e

85 Transcriptional analysis of LSC and leukemic cells confirms similarity of the de novo leukem

86 d spontaneous apoptosis of Grasp55-deficient leukemic cells correlated with increased sensitivity of

87 -leukemic therapies, it has been elusive how leukemic cells could acquire the serious resistance agai

88 at, regardless of mutation status, high-risk leukemic cells could only be killed using RAS-inhibitor

89 es in leukemia and potentially other cancers.Leukemic cells depend on the nucleotide synthesis pathwa

90 However, the mechanisms that render leukemic cells drug resistant remain largely undefined.

91 ion, our study investigated how SHOC2 impact leukemic cells drug response.

92 ow that JAM-C expression defines a subset of leukemic cells endowed with leukemia-initiating cell act

93 tion by the agonist antibody, these relapsed leukemic cells enter into a differentiation process of k

94 tantially reduces chemoresistance in primary leukemic cells ex vivo and in vivo.

95 Patients' leukemic cells exposed ex vivo to BRAF inhibitors are sp

96 Moreover, the IL-17B-IL-17RB axis protected leukemic cells from chemotherapeutic agent-induced apopt

97 que targetable antigens that can distinguish leukemic cells from normal myeloid cells or myeloid prog

98 interleukin-2 (IL-2)-activated NK cells and leukemic cells from patients with acute myeloid leukemia

99 in A (all trans retinoic acid, ATRA) treated leukemic cells had increased apoptosis, decreased cells

100 In leukemic cells however, SHOC2 upregulation has been prev

101 istics related to stemness and quiescence of leukemic cells in acute myeloid leukemia (AML) patients.

102 ts glycosylated ligands expressed on myeloid-leukemic cells in flow, the FMCR assay was used to analy

103 lfite sequencing of primary leukemic and non-leukemic cells in patients with or without DNMT3A(R882)

104 nd effector function in response to CD200(+) leukemic cells in vitro.

105 CMML and JMML disease-initiating and mature leukemic cells in vivo, allowing creation of genetically

106 diagnosis revealed that SAMHD1 expression in leukemic cells inversely correlates with clinical respon

107 expansion than CAR T cells and killed CD19+ leukemic cells more effectively in long-term cultures.

108 patterns of intravascular distribution with leukemic cells moving faster than breast cancer cells.

109 imorphism on NK cell-mediated destruction of leukemic cells or on the course of leukemia is largely u

110 ophagy, we show that knockdown of Grasp55 in leukemic cells reduces spleen and bone marrow tumor burd

111 leukemia (CLL) results from accumulation of leukemic cells that are subject to iterative re-activati

112 Leukemic cells that still emerged in this system activat

113 ring TNFalpha and DUSP1 mRNAs and sensitizes leukemic cells to chemotherapy.

114 High levels of FTO sensitize leukemic cells to R-2HG, whereas hyperactivation of MYC

115 lls in donor grafts, recognize and eliminate leukemic cells via graft-versus-leukemia (GVL) reactivit

116 Strikingly, leukemic cells with Alox5 overexpression showed a signif

117 row niche is required to regenerate HSCs and leukemic cells with functional ability to rearrange the

118 esults suggest that increasing GFI1 level in leukemic cells with low GFI1 expression level could be a

119 mpairs growth and induces differentiation of leukemic cells without impacting normal hematopoietic ce

120 d by donor T cells reactive with antigens on leukemic cells(4).

121 Leukemic cells, but not their normal myeloid counterpart

122 AF15 disruption induced an inflamed state in leukemic cells, including increased expression of lympho

123 of our experimental systems, we show that in leukemic cells, MBNL1 regulates alternative splicing (pr

124 ression data generated from JAM-C-expressing leukemic cells, we defined a single cell core gene expre

125 matin accessibility and RNA-seq data in K562 leukemic cells, we identify the cell surface marker CD24

126 study post-transcriptional regulation in G0 leukemic cells, we systematically analyzed their transcr

127 imately relapse with loss of CD19 antigen on leukemic cells, which has been established as a novel me

128 ion of CDK8, and induces cell death in human leukemic cells.

129 -ABL1+ CD150+ lineage-negative Sca-1+ c-Kit+ leukemic cells.

130 ic, epigenetic and transcriptional states in leukemic cells.

131 , including human liver cancer and chronic B leukemic cells.

132 presence of CCR-specific stimuli or cognate leukemic cells.

133 impedes the in vitro expansion of murine pre-leukemic cells.

134 effective in delivering miRNA molecules into leukemic cells.

135 in the microenvironment of hematopoietic and leukemic cells.

136 ss that is suppressed in treatment-resistant leukemic cells.

137 enter underwent gene expression profiling of leukemic cells.

138 d synergize with a cytidine analogue against leukemic cells.

139 /f)Mx1-CreCbfb(+/56M) and Mx1-CreCbfb(+/56M) leukemic cells.

140 results in a drastic reduction of Ara-CTP in leukemic cells.

141 acrophages may provide a protective niche to leukemic cells.

142 includes the PAFc, MLL1, HOXA9 and STAT5 in leukemic cells.

143 kemic cell lines and primary patient-derived leukemic cells.

144 to the cytoplasm of target myeloid cells and leukemic cells.

145 bearing animals by accelerating apoptosis of leukemic cells.

146 splacement of MLL chimeras from chromatin in leukemic cells.

147 during CLL progression and suggest that the leukemic clone can generate an autoactivation loop throu

148 f the microenvironment in maintenance of the leukemic clone, as well as in treatment resistance.

149 nalysis of RANK/RANKL loop activation in the leukemic clone, given recent reports on its role in CLL

150 ture and increase proliferating potential of leukemic clone.

151 herapy options are limited for patients with leukemic clones bearing multiple BCR-ABL1 mutations.

152 and sometimes divergent interval changes in leukemic clones within a single cycle of therapy, highli

153 ribute to the development of chemo-resistant leukemic clones.

154 of the bone marrow where mechanisms of inter-leukemic communication and cell-to-cell interactions are

155 Inhibiting TIFA perturbed leukemic cytokine secretion and reduced the IC50 of chem

156 function, which facilitates MLL-AF9-mediated leukemic disease in mice.

157 reduced proliferation resulting in extended leukemic disease latency in vivo.

158 feration was enhanced and durable control of leukemic disease was maintained better in patient-derive

159 e rise to leukemia in vivo and reestablished leukemic DNA methylation/gene expression patterns, inclu

160 t they retained leukemic mutations but reset leukemic DNA methylation/gene expression patterns.

161 omic analysis of the non-leukemic single and leukemic double mutant progenitors, isolated from these

162 DNA-damage related modulation, several anti-leukemic drugs has been tested and we did confirm that t

163 Anti-leukemic effect of BET/BRD4 (BETP) protein inhibition ha

164 pleen and bone marrow tumor burden upon i.v. leukemic engraftment.

165 ing the emergence, selection, and subsequent leukemic evolution of these "leukemia-poised" clones rem

166 "niche-facilitated" bone marrow failure and leukemic evolution, their underlying molecular mechanism

167 e marrow failure and a strong propensity for leukemic evolution.

168 provide mechanistic insight into which Nup98 leukemic fusion proteins promote AML.

169 tion of Pol I transcription reduces both the leukemic granulocyte-macrophage progenitor and leukemia-

170 We found that Runx1 deletion inhibits mouse leukemic growth in vivo and that RUNX silencing in human

171 ific AHR agonist FICZ significantly impaired leukemic growth, promoted differentiation, and repressed

172 s of AML while tracking its development (pre-leukemic haematopoietic stem cells, leukemic stem cells

173 tem cell (SC) compartment in both normal and leukemic hematopoiesis has been challenging due to the i

174 cytosolic fumarate metabolism, in normal and leukemic hematopoiesis.

175 Non-leukemic hematopoietic cells with DNMT3A(R882H) displaye

176 mutations are present and expressed within a leukemic hematopoietic stem cell has engendered some con

177 sive chromatin signatures that distinguished leukemic, host, and normal CD4(+) T cells.

178 regions have reduced capacity to support non-leukemic HSCs, correlating with loss of normal hematopoi

179 Leukemic IL-17RB signaling regulates leukemic survival a

180 survival and self-renewal in CML cells with leukemic-initiating capacity that can be targeted with s

181 rleukin 15 plays a key role in activation of leukemic LGL.

182 enitor cell numbers, reduced regeneration of leukemic long-term hematopoietic stem cells in secondary

183 The B-ALL cell line was stained against a leukemic marker (terminal deoxynucleotidyl transferase,

184 beta-catenin was detected in all leukemic MCL samples and its level of expression rapidly

185 ogether, atypical 3q26 recapitulate the main leukemic mechanism of inv(3)/t(3;3) AML, namely EVI1 ove

186 Weekly administration of PF-06747143 to leukemic mice significantly reduced leukemia development

187 get inhibition in a pharmacodynamic study in leukemic mice.

188 arious cell types shown to contribute to the leukemic microenvironment as well as treatment resistanc

189 In contrast, using an Myc-dependent leukemic model addicted to autophagy, we show that knock

190 rearrangements and found that they retained leukemic mutations but reset leukemic DNA methylation/ge

191 opoietic stem cells attributable to acquired leukemic mutations in genes such as DNMT3A or TET2.

192 racterized by replacement of the thymus with leukemic myeloblasts.

193 s and could be targeted in LSCs to normalize leukemic myeloid cell production.

194 ch were also negative for Mac1 and Gr1) from leukemic NHD13/NP23 mice demonstrated that DN thymocytes

195 l hematopoietic stem cells (HSCs) within the leukemic niche are poorly understood, especially in the

196 l "niches." Effective dissection of critical leukemic niche components using single-cell approaches h

197 In pre-leukemic NMPs Cebpa and Gata2 mutations synergize by inc

198 ecular subtypes, conventional MCL (cMCL) and leukemic non-nodal MCL (nnMCL), that differ in their cli

199 we mutagenized a selected region within the leukemic oncogene BCR-ABL1 Using bulk competitions with

200 FTO enhances leukemic oncogene-mediated cell transformation and leuke

201 s transcription of a subset of SE-associated leukemic oncogenes, including MYC.

202 SCs in patients with AML may be derived from leukemic or apparently normal progenitors.

203 g the oral microbiome network in a cohort of leukemic patients.

204 in patients with circulating tumor burden in leukemic phase disease.

205 AML-iPSCs lacked leukemic potential, but when differentiated into hematop

206 vely identify specific clones with increased leukemic potential.

207 Furthermore, Ncam1 was highly expressed in leukemic progenitor cells in a murine leukemia model, an

208 AML patient blasts, and isolated AML patient leukemic progenitor/stem cells, with negligible effects

209 Primary human and murine BCR-ABL(+) leukemic progenitors have increased activation of Cdc42

210 or IgG1 control-treated animals showed that leukemic progenitors were also targeted by PF-06747143.

211 iating mutations can generate neomorphic pre-leukemic progenitors, defining the lineage identity of t

212 trate the PAFc regulates Prmt5 to facilitate leukemic progression and is a potential therapeutic targ

213 herapeutic reduction of ROS may thus prevent leukemic progression and relapse in myeloid malignancies

214 in a MLL-AF9 mouse model of leukemia delayed leukemic progression in vivo.

215 tly inhibits the initiation and reverses the leukemic progression of both B cell and T cell acute lym

216 iscuss features of CH that are predictive of leukemic progression, and explore the role of hematopoie

217 inically silent clonal hematopoiesis (CH) to leukemic progression.

218 1 in MLL-AF9 leukemia: PAR-1 inhibited rapid leukemic proliferation when there were a large number of

219 cal regulator to define +19-enhancer and the leukemic prone promoter IV interaction for TAL1 activati

220 or patients with an anticipated high risk of leukemic relapse, because multiple studies strongly indi

221 (NK) cell alloreactivity in HCT can control leukemic relapse, but capturing alloreactivity in HLA-ma

222 patients with AAP who subsequently developed leukemic relapse, but neither AAP nor the asparaginase t

223 e inability to separate and study normal and leukemic SCs at the single-cell level.

224 ted by beta-catenin/Hoxa9/Prmt1 in governing leukemic self-renewal.

225 ed in LSK-derived MLL-CSCs and helps sustain leukemic self-renewal.

226 Transcriptomic analysis of the non-leukemic single and leukemic double mutant progenitors,

227 nation of stem cells at both preleukemic and leukemic stages.

228 eatures (collectively) consistent with a pre-leukemic state.

229 ombination with WNT974 significantly reduced leukemic stem and progenitor cell numbers, reduced regen

230 scripts in hematopoietic and patient-derived leukemic stem and progenitor cells, and reduced progress

231 ncer, neuronal, and normal hematopoietic and leukemic stem and progenitor cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

262 ddC also targeted leukemic stem cells in secondary AML xenotransplantation

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

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

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

266 The de novo AML, with CD123(+) leukemic stem or initiating cells (LSC), resembles NPM1c

267 nistically, KLF4 repressed the Dyrk2 gene in leukemic stem/progenitor cells; thus, loss of KLF4 resul

268 and RAS-mutations are mutually exclusive in leukemic sub-clones, causing dichotomy in therapeutic ta

269 aneous T-cell lymphoma (CTCL), including the leukemic subtype Sezary syndrome.

270 While the isoform aPKCzeta behaves as a leukemic suppressor, aPKClambda/iota is critically requi

271 Leukemic IL-17RB signaling regulates leukemic survival and chemoresistance.

272 erized inherited bone marrow failure and pre-leukemic syndrome.

273 introducing the human iNKT-TCR into a human leukemic T cell line carrying an NF-kappaB-driven fluore

274 JAK kinase inhibitors have depressed leukemic T cell line proliferation.

275 data modeling drug-resistance acquisition in leukemic T cells.

276 mice, while reactivation of HOTTIP restores leukemic TADs, transcription, and leukemogenesis in the

277 dely recognized as a novel strategy for anti-leukemic therapies, it has been elusive how leukemic cel

278 genetically normal AML that contributes to a leukemic transcriptome.

279 on in HSPCs is an inducible model of de novo leukemic transformation and can be used to optimize trea

280 constitutive Hh/Gli1 activation accelerated leukemic transformation and decreased overall survival.

281 referred option, even though their impact on leukemic transformation and survival has not been proved

282 ow microenvironment is sufficient to promote leukemic transformation and survival in both a cell auto

283 -intrinsic and -extrinsic mechanisms driving leukemic transformation at this level remain poorly unde

284 Hematopoietic stressors may contribute to leukemic transformation by increasing the mutation rate

285 ew known risk factors for the development of leukemic transformation in MPNs, recent progress made in

286 multi-hit state predicted risk of death and leukemic transformation independently of the Revised Int

287 ecent findings on the impact of autophagy on leukemic transformation of normal hematopoietic stem cel

288 ars), 63 (16%) of 383 patients experienced a leukemic transformation to secondary mast cell leukemia

289 ng of the molecular features associated with leukemic transformation, current treatment strategies, a

290 een linked to genetic damage associated with leukemic transformation, including etoposide-induced chr

291 To define mechanisms of leukemic transformation, we combined exome and targeted

292 ltifaceted activities of DNMT3A(R882mut) and leukemic transformation.

293 tem cells that drive disease progression and leukemic transformation.

294 geted to enhance old HSC fitness and prevent leukemic transformation.

295 rration of which is a dominant mechanism for leukemic transformation.

296 at certain niche alterations can even induce leukemic transformation.

297 ssociate with H3K4me3-enriched chromatin and leukemic transformation.

298 sets of genes that are tightly regulated in leukemic transformations and commonly mutated in other t

299 e effect of patient characteristics and anti-leukemic treatment on ciprofloxacin exposure, the area u

300 EDM1161V) identified in Sezary Syndrome, the leukemic variant of CTCL.

301 We detect leukemic variants in the blood and bone marrow samples o