ライフサイエンスコーパス: acute myeloid leukemia

1 cell lineages and a tendency to transform to acute myeloid leukemia.

2 precursor acute lymphoblastic leukemia, and acute myeloid leukemia.

3 C with MAC in patients with MDS or secondary acute myeloid leukemia.

4 ions have been identified in Wilms tumor and acute myeloid leukemia.

5 ed to make individual treatment decisions in acute myeloid leukemia.

6 ion via an in vivo RNAi screen in a model of acute myeloid leukemia.

7 marrow failure, myelodysplastic syndrome, or acute myeloid leukemia.

8 o progress to myelofibrosis and transform to acute myeloid leukemia.

9 in the MLL-translocated molecular subtype of acute myeloid leukemia.

10 s of these cancers, including extramedullary acute myeloid leukemia.

11 isoforms of SON are markedly upregulated in acute myeloid leukemia.

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

13 splenomegaly, and a propensity to evolve to acute myeloid leukemia.

14 the myelodysplastic syndrome developing into acute myeloid leukemia.

15 esis and its inactivation is associated with acute myeloid leukemia.

16 h-risk hematological malignancies, including acute myeloid leukemia.

17 inactivation in mice is sufficient to drive acute myeloid leukemia.

18 rom which it may drive the transformation to acute myeloid leukemia.

19 is sufficient to promote the development of acute myeloid leukemia.

20 lar to MAC in patients with MDS or secondary acute myeloid leukemia.

21 rentiation and is frequently dysregulated in acute myeloid leukemia.

22 associated with the occurrence of secondary acute myeloid leukemias.

23 2.1-3.9]); breast carcinoma (2.1 [1.8-2.4]); acute myeloid leukemia (1.9 [1.5-2.4]); and central nerv

24 21 datasets related to three human diseases, acute myeloid leukemia (9 datasets), type II diabetes (5

25 2 cohorts, totaling 2888 BMT recipients with acute myeloid leukemia, acute lymphoblastic leukemia, or

26 The review focuses on patients with acute myeloid leukemia, acute lymphocytic leukemia, mult

27 tate cancer, pancreatic cancer, lung cancer, acute myeloid leukemia, Alzheimer's disease, hemochromat

28 FLT3-ITD(+) acute myeloid leukemia (AML) accounts for approximately

29 on 1-year mortality after initial therapy of acute myeloid leukemia (AML) and (2) a novel, risk-strat

30 Patients with acute myeloid leukemia (AML) and a FLT3 mutation have po

31 on the majority of blasts from patients with acute myeloid leukemia (AML) and acute B-lymphoblastic l

32 poiesis, myelodysplastic syndrome (MDS), and acute myeloid leukemia (AML) and are associated with a D

33 ess low nanomolar activity against models of acute myeloid leukemia (AML) and are at least 100-fold m

34 present the molecular landscape of pediatric acute myeloid leukemia (AML) and characterize nearly 1,0

35 -like tyrosine kinase 3 (FLT3) are common in acute myeloid leukemia (AML) and drive leukemic cell gro

36 1 mutations define the commonest subgroup of acute myeloid leukemia (AML) and frequently co-occur wit

37 chromosomal translocations in some cases of acute myeloid leukemia (AML) and is associated with poor

38 The heterogeneous nature of acute myeloid leukemia (AML) and its poor prognosis nece

39 a heterodimeric protein highly expressed in acute myeloid leukemia (AML) and largely dispensable for

40 ance to xenobiotic nucleosides used to treat acute myeloid leukemia (AML) and other cancers remains a

41 -kappaB signaling portends poor prognosis in acute myeloid leukemia (AML) and other cancers, but the

42 l origin of and a key therapeutic target for acute myeloid leukemia (AML) and other forms of cancer.(

43 erior engraftment of primary patient-derived acute myeloid leukemia (AML) and other hematologic malig

44 pertoire of healthy donors and patients with acute myeloid leukemia (AML) and survived exposure to da

45 Communication between acute myeloid leukemia (AML) and the bone marrow microen

46 Acute myeloid leukemia (AML) arises through multistep cl

47 is widely considered a promising therapy for acute myeloid leukemia (AML) based on its ability to dri

48 CD33 is variably expressed on acute myeloid leukemia (AML) blasts and is targeted by g

49 A) is highly and differentially expressed in acute myeloid leukemia (AML) blasts compared with normal

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

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

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

53 roles in the development and progression of acute myeloid leukemia (AML) by regulating eukaryotic tr

54 Acute myeloid leukemia (AML) can display de novo or acqu

55 Most patients with acute myeloid leukemia (AML) can only be cured when allo

56 (EVs) isolated from plasma of patients with acute myeloid leukemia (AML) carry leukemia-associated a

57 plication (ITD), which mediate resistance to acute myeloid leukemia (AML) cell death, are poorly unde

58 a gene essentiality dataset across 14 human acute myeloid leukemia (AML) cell lines.

59 We show that acute myeloid leukemia (AML) cells are prone to fructose

60 atopoietic stem/progenitor cells (HSPCs) and acute myeloid leukemia (AML) cells carrying t(11q23), t(

61 Acute myeloid leukemia (AML) cells exhibit a high level

62 Acute myeloid leukemia (AML) cells have increased mitoch

63 Acute myeloid leukemia (AML) cells produce angiogenic fa

64 and protein are expressed more abundantly in acute myeloid leukemia (AML) cells than in healthy HSPCs

65 rks a fraction of human blast crisis CML and acute myeloid leukemia (AML) cells with similar biologic

66 ological resistance against chemotherapy for acute myeloid leukemia (AML) cells.

67 r induction of apoptosis in MDS cells and in acute myeloid leukemia (AML) cells.

68 Adults with acute myeloid leukemia (AML) commonly require support in

69 ein are increased in blasts of patients with acute myeloid leukemia (AML) compared with normal bone m

70 Acute myeloid leukemia (AML) comprises a heterogeneous g

71 While acute myeloid leukemia (AML) comprises many disparate ge

72 Acute myeloid leukemia (AML) continues to be a challengi

73 able therapies, most patients diagnosed with acute myeloid leukemia (AML) die of their disease.

74 ation and decreased incidence of relapse for acute myeloid leukemia (AML) following allogeneic hemato

75 ing is an established diagnostic standard in acute myeloid leukemia (AML) for risk stratification.

76 disease (EMD) at diagnosis in patients with acute myeloid leukemia (AML) has been recognized for dec

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

78 therapy to standard first-line treatment of acute myeloid leukemia (AML) has not yet been establishe

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

80 ne daunorubicin during induction therapy for acute myeloid leukemia (AML) have been shown to improve

81 Patients with acute myeloid leukemia (AML) have increased myeloid cell

82 Previous studies in childhood acute myeloid leukemia (AML) have shown a negative corre

83 In this study, using acute myeloid leukemia (AML) human cell lines and a cust

84 to transcriptional and chromatin changes in acute myeloid leukemia (AML) human promyelocytic cells.

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

86 karyoblastic leukemia (AMKL) is a subtype of acute myeloid leukemia (AML) in which cells morphologica

87 Although the majority of patients with acute myeloid leukemia (AML) initially respond to chemot

88 Acute myeloid leukemia (AML) is a deadly hematologic mal

89 Acute myeloid leukemia (AML) is a disease associated wit

90 Acute Myeloid Leukemia (AML) is a fatal hematological ca

91 Acute myeloid leukemia (AML) is a genetically heterogene

92 Acute Myeloid Leukemia (AML) is a hematologic malignancy

93 Acute myeloid leukemia (AML) is a heterogeneous disease

94 Acute myeloid leukemia (AML) is a major unmet medical ne

95 Acute myeloid leukemia (AML) is an aggressive malignancy

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

97 We found that transformation of HSC/P to acute myeloid leukemia (AML) is associated with increase

98 iatric acute lymphoblastic leukemia (ALL) or acute myeloid leukemia (AML) is associated with worse ev

99 Acute myeloid leukemia (AML) is characterized by an impa

100 Acute myeloid leukemia (AML) is characterized by the acc

101 Acute myeloid leukemia (AML) is characterized by the pro

102 Its involvement in acute myeloid leukemia (AML) is diverse, with patients f

103 Childhood acute myeloid leukemia (AML) is frequently characterized

104 Acute myeloid leukemia (AML) is induced by the cooperati

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

106 Acute myeloid leukemia (AML) is sustained by a subpopula

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

108 The association between tobacco smoke and acute myeloid leukemia (AML) is well established in adul

109 Postremission therapy in patients with acute myeloid leukemia (AML) may consist of continuing c

110 receptor (CAR) T cells in preclinical human acute myeloid leukemia (AML) models at the cost of sever

111 terogeneous in treatment-naive primary human acute myeloid leukemia (AML) myeloblasts, and this heter

112 onses to decitabine therapy in patients with acute myeloid leukemia (AML) or myelodysplastic syndrome

113 Acute myeloid leukemia (AML) originates from hematopoiet

114 Transcriptional analysis of human acute myeloid leukemia (AML) patient samples revealed th

115 ed with shorter remission in newly diagnosed acute myeloid leukemia (AML) patient samples, indicating

116 ite 1 (EVI-1) occurs in approximately 10% of acute myeloid leukemia (AML) patients and is associated

117 emendous clonal diversity in the majority of acute myeloid leukemia (AML) patients with activating FL

118 n targeted therapy is commonly used to treat acute myeloid leukemia (AML) patients, particularly in r

119 MT3A mutations occur in approximately 25% of acute myeloid leukemia (AML) patients.

120 ost prevalent genetic abnormalities found in acute myeloid leukemia (AML) patients.

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

122 CD33, which is expressed in the majority of acute myeloid leukemia (AML) patients.

123 FMS-like tyrosine kinase 3 (FLT3)-mutant acute myeloid leukemia (AML) portends a poor prognosis,

124 The diagnosis and risk stratification of acute myeloid leukemia (AML) primarily rely on morpholog

125 of ESAs was associated with a higher risk of acute myeloid leukemia (AML) progression, which did not

126 hway of preleukemia stem cells could prevent acute myeloid leukemia (AML) relapse.

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

128 MLL-rearranged acute myeloid leukemia (AML) remains a fatal disease wit

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

130 could prevent pneumonia in a mouse model of acute myeloid leukemia (AML) remission induction therapy

131 e expression profiling analysis of 542 human acute myeloid leukemia (AML) samples and identified 55%

132 to improve the engraftment of nonengrafting acute myeloid leukemia (AML) samples.

133 s of genetic and epigenetic abnormalities to acute myeloid leukemia (AML) should assist integrated de

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

135 d in the Leucegene collection of 415 primary acute myeloid leukemia (AML) specimens, and describe for

136 ased mechanisms offer therapeutic targets in acute myeloid leukemia (AML) that are of great current i

137 established a mouse xenograft model of human acute myeloid leukemia (AML) that enabled chemotherapy-i

138 ke tyrosine kinase 3 (FLT3) is a hallmark of acute myeloid leukemia (AML) that harbors the FLT3-inter

139 bition has elicited encouraging responses in acute myeloid leukemia (AML) therapy.

140 d Drug Administration marketing approval for acute myeloid leukemia (AML) treatment: targeted therapi

141 (ADI-PEG20) in relapsed/refractory/poor-risk acute myeloid leukemia (AML) was evaluated in 43 patient

142 ty-five patients with relapsed or refractory acute myeloid leukemia (AML) were enrolled between Janua

143 Purpose Children with acute myeloid leukemia (AML) whose disease is refractory

144 scription factors (TFs) in a murine model of acute myeloid leukemia (AML) with genetically and phenot

145 Acute myeloid leukemia (AML) with t(8;21) or inv(16) hav

146 BTSA1 potently suppressed human acute myeloid leukemia (AML) xenografts and increased ho

147 s the most common fusion oncoprotein causing acute myeloid leukemia (AML), a disease with a 5-year su

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

149 r, S100A8 and S100A9 are highly expressed in acute myeloid leukemia (AML), and S100A8 expression has

150 In expression datasets from patients with acute myeloid leukemia (AML), breast cancer and lung can

151 en shown to induce response in patients with acute myeloid leukemia (AML), but these responses are al

152 m cell transplantations for the treatment of acute myeloid leukemia (AML), but they are not successfu

153 In acute myeloid leukemia (AML), chromatin accessibility un

154 FLT3-mutated acute myeloid leukemia (AML), despite not being recogniz

155 mutations in DNMT3A are highly recurrent in acute myeloid leukemia (AML), DNMT3A mutations are almos

156 pathogenesis of myeloid neoplasms, including acute myeloid leukemia (AML), has been greatly advanced

157 we confirm that the Hh pathway is active in acute myeloid leukemia (AML), however, this activity is

158 mia (B-ALL and T-ALL, respectively), but not acute myeloid leukemia (AML), in mouse models of these t

159 variety of cancers, but for some, including acute myeloid leukemia (AML), its role in immune evasion

160 In spite of high complete remission rates in Acute Myeloid Leukemia (AML), little progress has been m

161 diagnosis of myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), myeloproliferative neoplas

162 t ABBV-075 efficiently triggers apoptosis in acute myeloid leukemia (AML), non-Hodgkin lymphoma, and

163 in many hematologic malignancies, including acute myeloid leukemia (AML), suggesting that combinatio

164 onset myelodysplastic syndrome (MDS) and/or acute myeloid leukemia (AML), suggesting that DDX41 acts

165 sistance and poor prognosis in patients with acute myeloid leukemia (AML), T-cell acute lymphoblastic

166 In acute myeloid leukemia (AML), the high rate of relapse m

167 Acute myeloid leukemia (AML), the most common adult acut

168 In acute myeloid leukemia (AML), therapy resistance frequen

169 ures are widely used in children treated for acute myeloid leukemia (AML), there is little evidence o

170 by reanalyzing data from 1,540 patients with acute myeloid leukemia (AML), we explore how large knowl

171 To address the impact of cellular origin on acute myeloid leukemia (AML), we generated an inducible

172 To identify potential CAR targets in acute myeloid leukemia (AML), we probed the AML surfaceo

173 7 is the most frequent autosomal monosomy in acute myeloid leukemia (AML), where it associates with p

174 ose to study this question in the context of acute myeloid leukemia (AML), where, using in vitro and

175 This is especially true in acute myeloid leukemia (AML), which exhibits striking he

176 ng mutation found in 20-30% of patients with acute myeloid leukemia (AML), which makes FLT3 an attrac

177 een tested extensively to limited benefit in acute myeloid leukemia (AML).

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

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

180 inistration for the treatment of FLT3-mutant acute myeloid leukemia (AML).

181 re is an emerging understanding of a role in acute myeloid leukemia (AML).

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

183 ctor PU.1 is often impaired in patients with acute myeloid leukemia (AML).

184 mmon in human cancer and frequently occur in acute myeloid leukemia (AML).

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

186 survival in three mouse models of resistant acute myeloid leukemia (AML).

187 mmunoconjugate, is a re-emerging therapy for acute myeloid leukemia (AML).

188 end-of-life health care among patients with acute myeloid leukemia (AML).

189 he differentiation of leukemia stem cells in acute myeloid leukemia (AML).

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

191 cioeconomic status (SES) affects survival in acute myeloid leukemia (AML).

192 alignant blasts are key oncogenic drivers in acute myeloid leukemia (AML).

193 , such as myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML).

194 many cancers, including approximately 12% of acute myeloid leukemia (AML).

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

196 benefit in a murine xenograft model of human acute myeloid leukemia (AML).

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

198 response are the main prognostic factors in acute myeloid leukemia (AML).

199 n highly elevated in many cancers, including acute myeloid leukemia (AML).

200 equent chromosomal abnormalities observed in acute myeloid leukemia (AML).

201 tant leukemia stem cells (LSCs) in secondary acute myeloid leukemia (AML).

202 cers, including myeloid malignancies such as acute myeloid leukemia (AML).

203 We sought to identify new such targets in acute myeloid leukemia (AML).

204 yelodysplasia (MDS) and 30% of patients with acute myeloid leukemia (AML).

205 both acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).

206 ;21 is found in 40% of the FAB M2 subtype of acute myeloid leukemia (AML).

207 ncer, but only limited data are available in acute myeloid leukemia (AML).

208 agnosis of myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML).

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

210 y active in preclinical models of refractory acute myeloid leukemia (AML).

211 leukemogenesis when mutated in patients with acute myeloid leukemia (AML).

212 esis and its inactivation is associated with acute myeloid leukemia (AML).

213 ethylase, plays a critical oncogenic role in acute myeloid leukemia (AML).

214 cal growth and survival signals in high risk acute myeloid leukemia (AML).

215 rmation of human chronic myeloid diseases to acute myeloid leukemia (AML).

216 e of these mutations has not been studied in acute myeloid leukemia (AML).

217 hematopoiesis and a tendency to evolve into acute myeloid leukemia (AML).

218 is overexpressed in 25-30% of patients with acute myeloid leukemia (AML).

219 newly diagnosed patients ages 18 to 65 with acute myeloid leukemia (AML)/high-risk myelodysplastic s

220 verall survival in adults <60 years old with acute myeloid leukemia (AML); however, at initial analys

221 d with an increased early risk of developing acute myeloid leukemia (AML; hazard ratio, 1.79; 95% CI,

222 ated SIRs of specific SPCs were observed for acute myeloid leukemia (AML; SIR = 4.9) in Germany and f

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

224 clinical trials investigating primary murine acute myeloid leukemias (AMLs) generated by retroviral i

225 s occurred in 4 patients with extramedullary acute myeloid leukemia and 1 patient with the myelodyspl

226 In those days, acute myeloid leukemia and acute lymphoblastic leukemia

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

228 al killer cell alloreactions that eradicated acute myeloid leukemia and improved survival.

229 lymphoblastic leukemia and lymphoma but also acute myeloid leukemia and multiple myeloma.

230 ecreased risk for relapse in recipients with acute myeloid leukemia and myelodysplastic syndrome (haz

231 erived NK cell system in patients with adult acute myeloid leukemia and pediatric B-cell precursor ac

232 methyltransferase 3A (DNMT3A) are common in acute myeloid leukemia and portend a poor prognosis; thu

233 K inhibitors in a model of Kras(G12D) mutant acute myeloid leukemia and propose its use as a predicti

234 riptomic profile when compared with those of acute myeloid leukemia and T-acute lymphoblastic leukemi

235 d H2 biased agonists in malignancies such as acute myeloid leukemia and to avoid undesired side effec

236 duction in Patients With Core Binding Factor Acute Myeloid Leukemia and Treating Patients with Childh

237 R = 1.00; 95% CI: 0.93, 1.07), but increased acute myeloid leukemia and/or myelodysplastic syndrome d

238 ng adult patients (age, 18 to 60 years) with acute myeloid leukemia, and addressed the question of wh

239 H2 at R140 and R172 are commonly observed in acute myeloid leukemia, and elevated 2HG is observed in

240 tic features, high rate of transformation to acute myeloid leukemia, and historically poor survival.

241 ations are seen in myelodysplastic syndrome, acute myeloid leukemia, and in blast crisis transformati

242 riptional deregulation plays a major role in acute myeloid leukemia, and therefore identification of

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

244 , Dutch Childhood Oncology Group (DCOG), and Acute Myeloid Leukemia-Berlin-Frankfurt-Munster (AML-BFM

245 -oncology designated AMG 330 targets CD33 on acute myeloid leukemia blast cells.

246 of the pro-apoptotic protein BAX to suppress acute myeloid leukemia both alone and together with vene

247 icantly associated with a worse prognosis in acute myeloid leukemia, breast cancer, glioblastoma mult

248 specimens (n = 127 ALL in comparison with 38 acute myeloid leukemia cases in a comparison group) reve

249 nced anticancer activity was demonstrated in acute myeloid leukemia cell lines, where significant imp

250 cMyc-driven antiproliferative activities in acute myeloid leukemia cell lines.

251 the histone methyltransferase SETDB1 enables acute myeloid leukemia cells to evade sensing of retrotr

252 be exploited to kill chemotherapy-resistant acute myeloid leukemia cells.

253 e the accuracy of AE reporting for pediatric acute myeloid leukemia clinical trials and to test wheth

254 creased risk of myelodysplastic syndrome and acute myeloid leukemia, collectively termed therapy-rela

255 These include new subtypes of acute myeloid leukemia defined by mutations in RUNX1 or

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

257 roptosis, as having a key role in inhibiting acute myeloid leukemia development.

258 sferase 3A (DNMT3A) is frequently mutated in acute myeloid leukemia genomes.

259 s and loss-of-function mutations as found in acute myeloid leukemias highlight the importance of this

260 eveloped as targeted therapy for FLT3-ITD(+) acute myeloid leukemia; however, their use is complicate

261 n cultured tumor cells and cancer cells from acute myeloid leukemia human patients; and (iii) NiPT in

262 cy granulopoiesis accelerated progression to acute myeloid leukemia in Icsbp(-/-) mice.

263 e transformation to myelodysplastic syndrome/acute myeloid leukemia in patients with SDS.

264 individual developed a hematological cancer (acute myeloid leukemia) in childhood.

265 Children with acute myeloid leukemia, infant acute lymphoblastic leuke

266 f cancers, including secondary glioblastoma, acute myeloid leukemia, intrahepatic cholangiocarcinoma,

267 n of c-MYC, BCL2 and PTEN mRNAs in the human acute myeloid leukemia MOLM-13 cell line.

268 marked inhibition of tumor growth in MV4-11 acute myeloid leukemia mouse xenografts without having a

269 ciations included cancer of unknown primary, acute myeloid leukemia/myelofibrosis and Waldenstrom mac

270 levated in primary FLT3-ITD normal karyotype acute myeloid leukemia (NK-AML) compared with wild-type

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

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

273 MDS and acute myeloid leukemia patient samples harboring U2AF35(

274 aralog ASXL2, which is frequently mutated in acute myeloid leukemia patients bearing the RUNX1-RUNX1T

275 imen with age and disease risk index-matched acute myeloid leukemia patients receiving fludarabine-me

276 roup analysis, we compared the outcome of 13 acute myeloid leukemia patients receiving this condition

277 xpression is highly elevated particularly in acute myeloid leukemia patients with C-terminal CEBPA mu

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

279 r oncoprotein involved in the development of acute myeloid leukemia; previous work has shown it to in

280 ve neoplasms, myelodysplastic syndromes, and acute myeloid leukemia, reside in a highly complex and d

281 vergent BRD9-binding chemotypes in models of acute myeloid leukemia resolves bromodomain polypharmaco

282 Patients with secondary acute myeloid leukemia (sAML) arising from myelodysplast

283 Enriched in secondary acute myeloid leukemia (sAML; in comparison to high-risk

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

285 oid, Hodgkin lymphoma, non-Hodgkin lymphoma, acute myeloid leukemia, soft-tissue sarcoma, and central

286 % CI: 1.10, 1.99; n = 12); it was higher for acute myeloid leukemia (sRR = 2.07; 95% CI: 1.34, 3.20)

287 Evidence of human acute myeloid leukemia stem cells (AML LSCs) was first r

288 essed in hematopoietic stem cells (HSCs) and acute myeloid leukemia stem cells (LSCs) compared with t

289 16 is a consistent finding in patients with acute myeloid leukemia subtype M4 with eosinophilia, whi

290 es, the summary relative risk was higher for acute myeloid leukemia (summary relative risk (sRR) = 2.

291 38 inhibitors overcame resistance of primary acute myeloid leukemia to birinapant.

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

293 ix stiffness regulates proliferation of some acute myeloid leukemia types, including MLL-AF9(+) MOLM-

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

295 a detailed picture of the BM vasculature in acute myeloid leukemia using intravital two-photon micro

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

297 For acute myeloid leukemia, we identified a MEGS with five g

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

299 One patient with acute myeloid leukemia who received allogeneic hematopoi

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