ライフサイエンスコーパス: myeloid leukemia

1 nd in blast crisis transformation of chronic myeloid leukemia.

2 tion and is frequently dysregulated in acute myeloid leukemia.

3 e for the therapeutic targeting of METTL3 in myeloid leukemia.

4 rsor acute lymphoblastic leukemia, and acute myeloid leukemia.

5 ineages and a tendency to transform to acute myeloid leukemia.

6 ave been identified in Wilms tumor and acute myeloid leukemia.

7 make individual treatment decisions in acute myeloid leukemia.

8 a an in vivo RNAi screen in a model of acute myeloid leukemia.

9 failure, myelodysplastic syndrome, or acute myeloid leukemia.

10 MAC in patients with MDS or secondary acute myeloid leukemia.

11 ress to myelofibrosis and transform to acute myeloid leukemia.

12 s of patients receiving imatinib for chronic myeloid leukemia.

13 MLL-translocated molecular subtype of acute myeloid leukemia.

14 hese cancers, including extramedullary acute myeloid leukemia.

15 isis, similar to the course of human chronic myeloid leukemia.

16 rms of SON are markedly upregulated in acute myeloid leukemia.

17 N-Ras is a major contributor, such as acute myeloid leukemia.

18 omegaly, and a propensity to evolve to acute myeloid leukemia.

19 nd its inactivation is associated with acute myeloid leukemia.

20 hematological malignancies, including acute myeloid leukemia.

21 linically related diagnosis atypical chronic myeloid leukemia.

22 ivation in mice is sufficient to drive acute myeloid leukemia.

23 ich it may drive the transformation to acute myeloid leukemia.

24 fficient to promote the development of acute myeloid leukemia.

25 MAC in patients with MDS or secondary acute myeloid leukemia.

26 al effectors of tyrosine kinase oncogenes in myeloid leukemias.

27 iated with the occurrence of secondary acute myeloid leukemias.

28 w lead molecule targeting STAT5 signaling in myeloid leukemias.

29 9]); breast carcinoma (2.1 [1.8-2.4]); acute myeloid leukemia (1.9 [1.5-2.4]); and central nervous sy

30 rts, totaling 2888 BMT recipients with acute myeloid leukemia, acute lymphoblastic leukemia, or myelo

31 The review focuses on patients with acute myeloid leukemia, acute lymphocytic leukemia, multiple m

32 ancer, pancreatic cancer, lung cancer, acute myeloid leukemia, Alzheimer's disease, hemochromatosis,

33 FLT3-ITD(+) acute myeloid leukemia (AML) accounts for approximately 25% of

34 ear mortality after initial therapy of acute myeloid leukemia (AML) and (2) a novel, risk-stratifying

35 Patients with acute myeloid leukemia (AML) and a FLT3 mutation have poor out

36 majority of blasts from patients with acute myeloid leukemia (AML) and acute B-lymphoblastic leukemi

37 s, myelodysplastic syndrome (MDS), and acute myeloid leukemia (AML) and are associated with a DNA hyp

38 w nanomolar activity against models of acute myeloid leukemia (AML) and are at least 100-fold more se

39 t the molecular landscape of pediatric acute myeloid leukemia (AML) and characterize nearly 1,000 par

40 tions define the commonest subgroup of acute myeloid leukemia (AML) and frequently co-occur with FLT3

41 osomal translocations in some cases of acute myeloid leukemia (AML) and is associated with poor clini

42 The heterogeneous nature of acute myeloid leukemia (AML) and its poor prognosis necessitat

43 o xenobiotic nucleosides used to treat acute myeloid leukemia (AML) and other cancers remains a major

44 B signaling portends poor prognosis in acute myeloid leukemia (AML) and other cancers, but the functi

45 in of and a key therapeutic target for acute myeloid leukemia (AML) and other forms of cancer.(1-4) T

46 engraftment of primary patient-derived acute myeloid leukemia (AML) and other hematologic malignancie

47 re of healthy donors and patients with acute myeloid leukemia (AML) and survived exposure to daunorub

48 ely considered a promising therapy for acute myeloid leukemia (AML) based on its ability to drive dif

49 CD33 is variably expressed on acute myeloid leukemia (AML) blasts and is targeted by gemtuzu

50 demonstrated antileukemic activity in acute myeloid leukemia (AML) but has yet to be critically eval

51 FLT3(ITD)) mutation is common in adult acute myeloid leukemia (AML) but rare in early childhood AML.

52 It causes acute myeloid leukemia (AML) by dysregulating the expression o

53 Acute myeloid leukemia (AML) can display de novo or acquired r

54 Most patients with acute myeloid leukemia (AML) can only be cured when allogeneic

55 isolated from plasma of patients with acute myeloid leukemia (AML) carry leukemia-associated antigen

56 e essentiality dataset across 14 human acute myeloid leukemia (AML) cell lines.

57 etic stem/progenitor cells (HSPCs) and acute myeloid leukemia (AML) cells carrying t(11q23), t(15;17)

58 Acute myeloid leukemia (AML) cells exhibit a high level of spo

59 Acute myeloid leukemia (AML) cells have increased mitochondria

60 Acute myeloid leukemia (AML) cells produce angiogenic factors,

61 otein are expressed more abundantly in acute myeloid leukemia (AML) cells than in healthy HSPCs or ot

62 al resistance against chemotherapy for acute myeloid leukemia (AML) cells.

63 Adults with acute myeloid leukemia (AML) commonly require support in the i

64 e increased in blasts of patients with acute myeloid leukemia (AML) compared with normal bone marrow

65 Acute myeloid leukemia (AML) continues to be a challenging dis

66 herapies, most patients diagnosed with acute myeloid leukemia (AML) die of their disease.

67 and decreased incidence of relapse for acute myeloid leukemia (AML) following allogeneic hematopoieti

68 an established diagnostic standard in acute myeloid leukemia (AML) for risk stratification.

69 cells evoke the expansion of MDSCs in acute myeloid leukemia (AML) has not been well described.

70 py to standard first-line treatment of acute myeloid leukemia (AML) has not yet been established.

71 Purpose Elderly patients with acute myeloid leukemia (AML) have a poor prognosis, and innova

72 norubicin during induction therapy for acute myeloid leukemia (AML) have been shown to improve remiss

73 Previous studies in childhood acute myeloid leukemia (AML) have shown a negative correlation

74 In this study, using acute myeloid leukemia (AML) human cell lines and a custom CRI

75 anscriptional and chromatin changes in acute myeloid leukemia (AML) human promyelocytic cells.

76 In addition, MLL-FP driven acute myeloid leukemia (AML) in mice is often used as a genera

77 lastic leukemia (AMKL) is a subtype of acute myeloid leukemia (AML) in which cells morphologically re

78 Acute myeloid leukemia (AML) is a deadly hematologic malignanc

79 Acute myeloid leukemia (AML) is a disease associated with epig

80 Acute myeloid leukemia (AML) is a genetically heterogeneous he

81 Acute Myeloid Leukemia (AML) is a hematologic malignancy with

82 Acute myeloid leukemia (AML) is a heterogeneous disease with c

83 Acute myeloid leukemia (AML) is a major unmet medical need.

84 Acute myeloid leukemia (AML) is an aggressive malignancy where

85 The front-line treatment for adult acute myeloid leukemia (AML) is anthracycline-based combinatio

86 found that transformation of HSC/P to acute myeloid leukemia (AML) is associated with increased CDC4

87 Acute myeloid leukemia (AML) is characterized by an impaired d

88 Acute myeloid leukemia (AML) is characterized by the accumulat

89 Its involvement in acute myeloid leukemia (AML) is diverse, with patients frequen

90 Childhood acute myeloid leukemia (AML) is frequently characterized by ch

91 Acute myeloid leukemia (AML) is induced by the cooperative act

92 The overall survival of patients with acute myeloid leukemia (AML) is poor and identification of new

93 Acute myeloid leukemia (AML) is sustained by a subpopulation o

94 Acute myeloid leukemia (AML) is the most common type of acute

95 association between tobacco smoke and acute myeloid leukemia (AML) is well established in adults but

96 Postremission therapy in patients with acute myeloid leukemia (AML) may consist of continuing chemoth

97 tor (CAR) T cells in preclinical human acute myeloid leukemia (AML) models at the cost of severe hema

98 to decitabine therapy in patients with acute myeloid leukemia (AML) or myelodysplastic syndromes (MDS

99 Acute myeloid leukemia (AML) originates from hematopoietic ste

100 Transcriptional analysis of human acute myeloid leukemia (AML) patient samples revealed that ZNF

101 (EVI-1) occurs in approximately 10% of acute myeloid leukemia (AML) patients and is associated with a

102 us clonal diversity in the majority of acute myeloid leukemia (AML) patients with activating FLT3 int

103 eted therapy is commonly used to treat acute myeloid leukemia (AML) patients, particularly in refract

104 utations occur in approximately 25% of acute myeloid leukemia (AML) patients.

105 evalent genetic abnormalities found in acute myeloid leukemia (AML) patients.

106 and identify predictive biomarkers in acute myeloid leukemia (AML) patients.

107 which is expressed in the majority of acute myeloid leukemia (AML) patients.

108 S-like tyrosine kinase 3 (FLT3)-mutant acute myeloid leukemia (AML) portends a poor prognosis, and in

109 s was associated with a higher risk of acute myeloid leukemia (AML) progression, which did not transl

110 f preleukemia stem cells could prevent acute myeloid leukemia (AML) relapse.

111 , the prospects for many patients with acute myeloid leukemia (AML) remain dismal.

112 MLL-rearranged acute myeloid leukemia (AML) remains a fatal disease with a hi

113 Effective therapy of acute myeloid leukemia (AML) remains an unmet need.

114 ession profiling analysis of 542 human acute myeloid leukemia (AML) samples and identified 55% with u

115 prove the engraftment of nonengrafting acute myeloid leukemia (AML) samples.

116 enetic and epigenetic abnormalities to acute myeloid leukemia (AML) should assist integrated design o

117 , cells from both primary and cultured acute myeloid leukemia (AML) sources take up functional mitoch

118 echanisms offer therapeutic targets in acute myeloid leukemia (AML) that are of great current interes

119 ished a mouse xenograft model of human acute myeloid leukemia (AML) that enabled chemotherapy-induced

120 osine kinase 3 (FLT3) is a hallmark of acute myeloid leukemia (AML) that harbors the FLT3-internal ta

121 Administration marketing approval for acute myeloid leukemia (AML) treatment: targeted therapies for

122 EG20) in relapsed/refractory/poor-risk acute myeloid leukemia (AML) was evaluated in 43 patients in a

123 e patients with relapsed or refractory acute myeloid leukemia (AML) were enrolled between January 201

124 Purpose Children with acute myeloid leukemia (AML) whose disease is refractory to st

125 BTSA1 potently suppressed human acute myeloid leukemia (AML) xenografts and increased host sur

126 Patients with SCN are predisposed to acute myeloid leukemia (AML), and progression from SCN to AML

127 0A8 and S100A9 are highly expressed in acute myeloid leukemia (AML), and S100A8 expression has been l

128 expression datasets from patients with acute myeloid leukemia (AML), breast cancer and lung cancer, g

129 FLT3-mutated acute myeloid leukemia (AML), despite not being recognized as

130 ions in DNMT3A are highly recurrent in acute myeloid leukemia (AML), DNMT3A mutations are almost neve

131 enesis of myeloid neoplasms, including acute myeloid leukemia (AML), has been greatly advanced by gen

132 nfirm that the Hh pathway is active in acute myeloid leukemia (AML), however, this activity is largel

133 -ALL and T-ALL, respectively), but not acute myeloid leukemia (AML), in mouse models of these tumors.

134 sis of myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), myeloproliferative neoplasm (MPN

135 -075 efficiently triggers apoptosis in acute myeloid leukemia (AML), non-Hodgkin lymphoma, and multip

136 ny hematologic malignancies, including acute myeloid leukemia (AML), suggesting that combinations of

137 myelodysplastic syndrome (MDS) and/or acute myeloid leukemia (AML), suggesting that DDX41 acts as a

138 ce and poor prognosis in patients with acute myeloid leukemia (AML), T-cell acute lymphoblastic leuke

139 In acute myeloid leukemia (AML), the high rate of relapse may in

140 Acute myeloid leukemia (AML), the most common adult acute leuk

141 In acute myeloid leukemia (AML), therapy resistance frequently oc

142 nalyzing data from 1,540 patients with acute myeloid leukemia (AML), we explore how large knowledge b

143 To identify potential CAR targets in acute myeloid leukemia (AML), we probed the AML surfaceome for

144 he most frequent autosomal monosomy in acute myeloid leukemia (AML), where it associates with poor cl

145 This is especially true in acute myeloid leukemia (AML), which exhibits striking heteroge

146 ation found in 20-30% of patients with acute myeloid leukemia (AML), which makes FLT3 an attractive t

147 hese mutations has not been studied in acute myeloid leukemia (AML).

148 opoiesis and a tendency to evolve into acute myeloid leukemia (AML).

149 erexpressed in 25-30% of patients with acute myeloid leukemia (AML).

150 sted extensively to limited benefit in acute myeloid leukemia (AML).

151 LSCs) is the ultimate goal of treating acute myeloid leukemia (AML).

152 in approximately 12% of patients with acute myeloid leukemia (AML).

153 ation for the treatment of FLT3-mutant acute myeloid leukemia (AML).

154 an emerging understanding of a role in acute myeloid leukemia (AML).

155 to myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML).

156 U.1 is often impaired in patients with acute myeloid leukemia (AML).

157 n human cancer and frequently occur in acute myeloid leukemia (AML).

158 val in three mouse models of resistant acute myeloid leukemia (AML).

159 onjugate, is a re-emerging therapy for acute myeloid leukemia (AML).

160 f-life health care among patients with acute myeloid leukemia (AML).

161 ferentiation of leukemia stem cells in acute myeloid leukemia (AML).

162 chemotherapy in younger patients with acute myeloid leukemia (AML).

163 nomic status (SES) affects survival in acute myeloid leukemia (AML).

164 nt blasts are key oncogenic drivers in acute myeloid leukemia (AML).

165 as myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML).

166 and salvage chemotherapy regimens for acute myeloid leukemia (AML).

167 of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML).

168 t in a murine xenograft model of human acute myeloid leukemia (AML).

169 by cytopenias and clonal evolution to acute myeloid leukemia (AML).

170 ancers, including approximately 12% of acute myeloid leukemia (AML).

171 nse are the main prognostic factors in acute myeloid leukemia (AML).

172 ly elevated in many cancers, including acute myeloid leukemia (AML).

173 chromosomal abnormalities observed in acute myeloid leukemia (AML).

174 eukemia stem cells (LSCs) in secondary acute myeloid leukemia (AML).

175 acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).

176 s of myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML).

177 therapeutic approach for patients with acute myeloid leukemia (AML).

178 ve in preclinical models of refractory acute myeloid leukemia (AML).

179 ogenesis when mutated in patients with acute myeloid leukemia (AML).

180 nd its inactivation is associated with acute myeloid leukemia (AML).

181 se, plays a critical oncogenic role in acute myeloid leukemia (AML).

182 owth and survival signals in high risk acute myeloid leukemia (AML).

183 n of human chronic myeloid diseases to acute myeloid leukemia (AML).

184 diagnosed patients ages 18 to 65 with acute myeloid leukemia (AML)/high-risk myelodysplastic syndrom

185 survival in adults <60 years old with acute myeloid leukemia (AML); however, at initial analysis, th

186 an increased early risk of developing acute myeloid leukemia (AML; hazard ratio, 1.79; 95% CI, 1.13

187 ML), but blast crisis CML (BC-CML) and acute myeloid leukemias (AML) are GVL resistant.

188 al trials investigating primary murine acute myeloid leukemias (AMLs) generated by retroviral inserti

189 of adults with newly diagnosed CD33(+) acute myeloid leukemia and for patients aged >/=2 years with C

190 blastic leukemia and lymphoma but also acute myeloid leukemia and multiple myeloma.

191 ed risk for relapse in recipients with acute myeloid leukemia and myelodysplastic syndrome (hazard ra

192 ltransferase 3A (DNMT3A) are common in acute myeloid leukemia and portend a poor prognosis; thus, new

193 bitors in a model of Kras(G12D) mutant acute myeloid leukemia and propose its use as a predictive bio

194 ic profile when compared with those of acute myeloid leukemia and T-acute lymphoblastic leukemia, as

195 iased agonists in malignancies such as acute myeloid leukemia and to avoid undesired side effects whe

196 n in Patients With Core Binding Factor Acute Myeloid Leukemia and Treating Patients with Childhood Ac

197 lt patients (age, 18 to 60 years) with acute myeloid leukemia, and addressed the question of whether

198 R140 and R172 are commonly observed in acute myeloid leukemia, and elevated 2HG is observed in cells

199 atures, high rate of transformation to acute myeloid leukemia, and historically poor survival.

200 Expression of Icsbp is decreased in chronic myeloid leukemia, and Icsbp(-/-) mice exhibit progressiv

201 are seen in myelodysplastic syndrome, acute myeloid leukemia, and in blast crisis transformation of

202 nal deregulation plays a major role in acute myeloid leukemia, and therefore identification of epigen

203 the role of clonal evolution in lymphoid and myeloid leukemia as a driver of tumor initiation, diseas

204 a, natural killer/T-cell lymphoma, and acute myeloid leukemia, as well as in solid tumors.

205 Children with myeloid leukemia associated with Down syndrome (ML-DS) h

206 In blast crisis chronic myeloid leukemia (BC CML), we show that increased JAK2 s

207 lation, whereas it decreases that of chronic myeloid leukemia BCR-ABL(+) K-562 cells.

208 Atypical chronic myeloid leukemia, BCR-ABL1 negative (aCML) is a rare mye

209 h Childhood Oncology Group (DCOG), and Acute Myeloid Leukemia-Berlin-Frankfurt-Munster (AML-BFM) stud

210 ogy designated AMG 330 targets CD33 on acute myeloid leukemia blast cells.

211 pro-apoptotic protein BAX to suppress acute myeloid leukemia both alone and together with venetoclax

212 y associated with a worse prognosis in acute myeloid leukemia, breast cancer, glioblastoma multiforme

213 gene is associated typically with aggressive myeloid leukemia, but is also detectable in breast carci

214 ens (n = 127 ALL in comparison with 38 acute myeloid leukemia cases in a comparison group) revealed p

215 rophage-specific expression of human induced myeloid leukemia cell differentiation protein Mcl-1 (CD6

216 ATS-DVR to RNA-seq data of the human chronic myeloid leukemia cell line K562 in response to shRNA kno

217 n characterized a panel of ABT-199-resistant myeloid leukemia cell lines derived through chronic expo

218 Furthermore, METTL3 depletion in human myeloid leukemia cell lines induces cell differentiation

219 nticancer activity was demonstrated in acute myeloid leukemia cell lines, where significant impairmen

220 driven antiproliferative activities in acute myeloid leukemia cell lines.

221 7f inhibited the growth of acute and chronic myeloid leukemia cells and the phosphorylation and trans

222 stone methyltransferase SETDB1 enables acute myeloid leukemia cells to evade sensing of retrotranspos

223 th PUM1 and PUM2 levels in primary HSPCs and myeloid leukemia cells.

224 ferentially required gene between normal and myeloid leukemia cells.

225 ploited to kill chemotherapy-resistant acute myeloid leukemia cells.

226 l hematologic malignancies including chronic myeloid leukemia (CML) and myelodysplastic syndromes (MD

227 em cells (LSCs) drive progression of chronic myeloid leukemia (CML) and tyrosine kinase inhibitor res

228 ate receptor-beta-positive (FRbeta+) chronic myeloid leukemia (CML) cells, resulting in more intracel

229 kinase inhibitor (TKI) treatment of chronic myeloid leukemia (CML) has limited efficacy against leuk

230 Chronic myeloid leukemia (CML) is a hematopoietic stem cell (HSC

231 Chronic myeloid leukemia (CML) is caused by the acquisition of t

232 Chronic myeloid leukemia (CML) is currently treated with tyrosin

233 the LSC population in chronic phase chronic myeloid leukemia (CML) patients at diagnosis and followi

234 vement of deep molecular response in chronic myeloid leukemia (CML) patients on tyrosine kinase inhib

235 of a population of highly quiescent chronic myeloid leukemia (CML) SCs that is enriched following th

236 re than 2,000 SCs from patients with chronic myeloid leukemia (CML) throughout the disease course, re

237 nhibitors has significantly affected chronic myeloid leukemia (CML) treatment, transforming the life

238 rial with ponatinib in patients with chronic myeloid leukemia (CML) was interrupted due to an importa

239 ely be discontinued in patients with chronic myeloid leukemia (CML) who have had undetectable minimal

240 Treatment of chronic myeloid leukemia (CML) with imatinib mesylate and other

241 ibitors (TKI) changed the outcome of chronic myeloid leukemia (CML), turning a life-threatening disea

242 hematopoietic malignancies including chronic myeloid leukemia (CML), where BCL6 expression was shown

243 rate proof of concept in the case of chronic myeloid leukemia (CML), wherein our model recapitulated

244 ve clonal hematopoiesis resembling a chronic myeloid leukemia (CML)-like disease manifesting in "lymp

245 oved the prognosis for patients with chronic myeloid leukemia (CML).

246 rotein kinase-induced mouse model of chronic myeloid leukemia (CML).

247 o evaluate 2G-TKI discontinuation in chronic myeloid leukemia (CML).

248 ls: melanoma, pancreatic cancer, and chronic myeloid leukemia (CML).

249 utionized treatment of patients with chronic myeloid leukemia (CML).

250 ; 95% CI, 1.13 to 2.82; P = .01) and chronic myeloid leukemia (CML; hazard ratio, 3.44; 95% CI, 1.87

251 d risk of myelodysplastic syndrome and acute myeloid leukemia, collectively termed therapy-related my

252 merge as patients with chronic phase chronic myeloid leukemia (CP-CML) are treated with tyrosine kina

253 These include new subtypes of acute myeloid leukemia defined by mutations in RUNX1 or BCR-AB

254 by microRNAs during granulopoiesis or acute myeloid leukemia development has not been studied.

255 ABL1 inhibitors for the treatment of chronic myeloid leukemia do not eliminate leukemic stem cells (L

256 a development in a mouse model of aggressive myeloid leukemia driven by loss of Cbl and Cbl-b Importa

257 tients enrolled in the PONATINIB for Chronic Myeloid Leukemia Evaluation and Ph(+)Acute Lymphoblastic

258 Mutations that affect myelodysplasia/myeloid leukemia factor (MLF) proteins are associated wi

259 on of the BCR-ABL1 fusion delineates chronic myeloid leukemia from classic BCR-ABL1(-) MPNs, which ar

260 e 3A (DNMT3A) is frequently mutated in acute myeloid leukemia genomes.

261 loss-of-function mutations as found in acute myeloid leukemias highlight the importance of this trans

262 sformation to myelodysplastic syndrome/acute myeloid leukemia in patients with SDS.

263 Children with acute myeloid leukemia, infant acute lymphoblastic leukemia, h

264 ers, including secondary glioblastoma, acute myeloid leukemia, intrahepatic cholangiocarcinoma, and c

265 sed in these cells and frequently mutated in myeloid leukemias, may be a key contributor to this plas

266 -MYC, BCL2 and PTEN mRNAs in the human acute myeloid leukemia MOLM-13 cell line.

267 d inhibition of tumor growth in MV4-11 acute myeloid leukemia mouse xenografts without having a negat

268 ns included cancer of unknown primary, acute myeloid leukemia/myelofibrosis and Waldenstrom macroglob

269 d in primary FLT3-ITD normal karyotype acute myeloid leukemia (NK-AML) compared with wild-type FLT3 N

270 Patients with myeloid leukemia of Down syndrome (ML-DS) have favorable

271 omparing MAC with RIC in patients with acute myeloid leukemia or myelodysplastic syndromes.

272 standard of care for fit patients with acute myeloid leukemia or myelodysplastic syndromes.

273 h high pCRKL and pSTAT5 signaling in chronic myeloid leukemia patient blood samples.

274 ASXL2, which is frequently mutated in acute myeloid leukemia patients bearing the RUNX1-RUNX1T1 (AML

275 ith age and disease risk index-matched acute myeloid leukemia patients receiving fludarabine-melphala

276 nalysis, we compared the outcome of 13 acute myeloid leukemia patients receiving this conditioning re

277 ion is highly elevated particularly in acute myeloid leukemia patients with C-terminal CEBPA mutation

278 ic marker in cytogenetically high-risk acute myeloid leukemia patients.

279 plasms, myelodysplastic syndromes, and acute myeloid leukemia, reside in a highly complex and dynamic

280 t BRD9-binding chemotypes in models of acute myeloid leukemia resolves bromodomain polypharmacology i

281 Patients with secondary acute myeloid leukemia (sAML) arising from myelodysplastic syn

282 Enriched in secondary acute myeloid leukemia (sAML; in comparison to high-risk MDS),

283 wo specific cellular antiapoptotic proteins, myeloid leukemia sequence 1 (Mcl-1) and heat shock prote

284 ivation in mice is sufficient to drive acute myeloid leukemia.Significance: This study defines a tumo

285 fashion to generate rapid lethal lymphoid or myeloid leukemias similar to their human counterparts.

286 odgkin lymphoma, non-Hodgkin lymphoma, acute myeloid leukemia, soft-tissue sarcoma, and central nervo

287 ntify SYNCRIP as a new RBP that controls the myeloid leukemia stem cell program.

288 Evidence of human acute myeloid leukemia stem cells (AML LSCs) was first reporte

289 in hematopoietic stem cells (HSCs) and acute myeloid leukemia stem cells (LSCs) compared with their d

290 a consistent finding in patients with acute myeloid leukemia subtype M4 with eosinophilia, which gen

291 ibitors overcame resistance of primary acute myeloid leukemia to birinapant.

292 ouse model of DNMT3A(R882H)/NRAS(G12D) acute myeloid leukemia to define a cascade of chromatin change

293 ffness regulates proliferation of some acute myeloid leukemia types, including MLL-AF9(+) MOLM-14 cel

294 ogy group clinical trials in pediatric acute myeloid leukemia underestimates AE rates.

295 ailed picture of the BM vasculature in acute myeloid leukemia using intravital two-photon microscopy.

296 a, and blast cells, and a diagnosis of acute myeloid leukemia was made.

297 In the C1498 mouse model of myeloid leukemia, we showed that leukemia was eradicated

298 patients aged >/=2 years with CD33(+) acute myeloid leukemia who have experienced a relapse or who h

299 One patient with acute myeloid leukemia who received allogeneic hematopoietic s

300 a and Treating Patients with Childhood Acute Myeloid Leukemia with Interleukin-2 trials (age, 1-60 ye