ライフサイエンスコーパス: acute myelogenous leukemia

1 mary leukemic progenitors from patients with acute myelogenous leukemia.

2 ve significant activity in patients with MDS/acute myelogenous leukemia.

3 tipifarnib exhibits modest activity against acute myelogenous leukemia.

4 ransplantation into congenic WT mice, led to acute myelogenous leukemia.

5 ients with myelodysplastic syndrome (MDS) or acute myelogenous leukemia.

6 e agent in the treatment of certain forms of acute myelogenous leukemia.

7 d as the most frequent genetic alteration in acute myelogenous leukemia.

8 D816V, are seen in systemic mastocytosis and acute myelogenous leukemia.

9 received the therapeutic dose) and one with acute myelogenous leukemia.

10 iated with approximately 12% of the cases of acute myelogenous leukemia.

11 mutations contribute to the pathogenesis of acute myelogenous leukemia.

12 blast samples isolated from 10 patients with acute myelogenous leukemia.

13 cies, including myelodysplastic syndrome and acute myelogenous leukemia.

14 o be an effective chemotherapeutic agent for acute myelogenous leukemia.

15 a and a predisposition to myelodysplasia and acute myelogenous leukemia.

16 lative incidence of myelodysplastic syndrome/acute myelogenous leukemia.

17 ment-associated myelodysplastic syndrome and acute myelogenous leukemia.

18 nces of chronic cytopenias or progression to acute myelogenous leukemia.

19 ich is a principal defect in t(8;21)-related acute myelogenous leukemia.

20 ctly as MLL, acute lymphoblastic leukemia or acute myelogenous leukemia.

21 enzene is associated with hematotoxicity and acute myelogenous leukemia.

22 ultures of blood from a 5-year-old girl with acute myelogenous leukemia.

23 donor hematopoietic cell transplantation for acute myelogenous leukemia.

24 posing to myelodysplastic syndrome (MDS) and acute myelogenous leukemia.

25 tner in chromosome translocations that cause acute myelogenous leukemia.

26 sis balance and result in the development of acute myelogenous leukemia.

27 at 9u may be a potent candidate for treating acute myelogenous leukemia.

28 produces similar survival for patients with acute myelogenous leukemia.

29 in similar survival times for patients with acute myelogenous leukemia.

30 ity to transform to myelodysplastic syndrome/acute myelogenous leukemia.

31 gene are implicated in leukemias, especially acute myelogenous leukemia.

32 r deletions in myelodysplastic syndromes and acute myelogenous leukemias.

33 her HoxA7 or HoxA9 is characteristic of many acute myelogenous leukemias.

34 ed from conventional acute lymphoblastic and acute myelogenous leukemias.

35 The acute myelogenous leukemia-1 (AML1)-ETO fusion protein i

36 s with both acute lymphoblastic leukemia and acute myelogenous leukemia achieve remission with upfron

37 ated bone marrow or peripheral blood HCT for acute myelogenous leukemia, acute lymphoblastic leukemia

38 We report a patient with relapsed acute myelogenous leukemia after allogeneic stem cell tr

39 CT) were previously avoided in patients with acute myelogenous leukemia aged more than 55 years becau

40 related myelodysplastic syndrome (t-MDS) and acute myelogenous leukemia (AML) after autologous stem-c

41 hown to mediate antileukemic effects against acute myelogenous leukemia (AML) after mismatched transp

42 e the level of 27 C&Ckines in serum from 176 acute myelogenous leukemia (AML) and 114 myelodysplastic

43 D2 protein levels were robustly expressed in acute myelogenous leukemia (AML) and acute lymphoblastic

44 found in approximately 30% of patients with acute myelogenous leukemia (AML) and are associated with

45 city phosphatase, is overexpressed in 50% of acute myelogenous leukemia (AML) and associated with poo

46 otoxic T lymphocytes (CTLs) in patients with acute myelogenous leukemia (AML) and chronic myelogenous

47 P) has potent in vivo anticancer activity in acute myelogenous leukemia (AML) and endemic Burkitt lym

48 rized by platelet defects, predisposition to acute myelogenous leukemia (AML) and germ-line heterozyg

49 (miRNA) expression is frequently observed in acute myelogenous leukemia (AML) and has been implicated

50 he Flt3 gene (Flt3/ITD) has been reported in acute myelogenous leukemia (AML) and may be associated w

51 ancies, especially in patients with relapsed acute myelogenous leukemia (AML) and multiple myeloma.

52 PURPOSE Acute myelogenous leukemia (AML) and myelodysplastic syn

53 ping to 5q31, a region frequently deleted in acute myelogenous leukemia (AML) and myelodysplastic syn

54 poietic stem cell transplantation (HSCT) for acute myelogenous leukemia (AML) and myelodysplastic syn

55 In acute myelogenous leukemia (AML) and other MDS subtypes,

56 cells are important for the pathogenesis of acute myelogenous leukemia (AML) and represent a reservo

57 One of them developed acute myelogenous leukemia (AML) and the other 2 develop

58 Patients with acute myelogenous leukemia (AML) and those undergoing bo

59 clinical responses in relapsed or refractory acute myelogenous leukemia (AML) are limited and transie

60 Outcomes for older adults with acute myelogenous leukemia (AML) are poor due to both di

61 Previous studies indicate that human acute myelogenous leukemia (AML) arises from a rare popu

62 One patient developed acute myelogenous leukemia (AML) at 6 years of age.

63 from a well-defined cohort of patients with acute myelogenous leukemia (AML) at diagnosis and relaps

64 is in a variety of Bcr/abl- cells, including acute myelogenous leukemia (AML) blasts and cell lines a

65 Similarly, primary acute myelogenous leukemia (AML) blasts exposed to ara-C

66 FLT3 receptor tyrosine kinase are common in acute myelogenous leukemia (AML) but are rare in adult a

67 ulation of folate receptor (FR) type-beta in acute myelogenous leukemia (AML) by all-trans retinoic a

68 scription factor family member, is linked to acute myelogenous leukemia (AML) by chromosomal events a

69 nd cellular responses to cytarabine in human acute myelogenous leukemia (AML) cell lines and clinical

70 n a polyphenylurea pharmacophore on cultured acute myelogenous leukemia (AML) cell lines and primary

71 ated expression of IGF1R and IR isoform A in acute myelogenous leukemia (AML) cell lines as well as i

72 nsequently, AEG-1 markedly protected HCC and acute myelogenous leukemia (AML) cells from retinoid- an

73 ent of strategies to eradicate primary human acute myelogenous leukemia (AML) cells is a major challe

74 factors that stimulate the proliferation of acute myelogenous leukemia (AML) cells transduce their s

75 Interaction between the integrin VLA-4 on acute myelogenous leukemia (AML) cells with stromal fibr

76 bute to cytogenetic instability in secondary acute myelogenous leukemia (AML) cells, we analyzed leuk

77 (FLT3) signaling are aberrantly activated in acute myelogenous leukemia (AML) cells.

78 )]-1-(p-t-butylphenyl) methane (DIM #34), in acute myelogenous leukemia (AML) cells.

79 aggressive, apoptosis-resistant phenotype on acute myelogenous leukemia (AML) cells.

80 tat and panobinostat) were examined in human acute myelogenous leukemia (AML) cells.

81 ility to protect naive mice against a lethal acute myelogenous leukemia (AML) challenge.

82 ic signaling cues in the microenvironment of acute myelogenous leukemia (AML) contribute to disease p

83 Acute myelogenous leukemia (AML) currently kills the maj

84 Acute myelogenous leukemia (AML) frequently relapses aft

85 Acquired, balanced translocations in acute myelogenous leukemia (AML) generally involve trans

86 The chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusi

87 Pediatric acute myelogenous leukemia (AML) has a poor prognosis, a

88 monoclonal antibody used in the treatment of acute myelogenous leukemia (AML) has been linked to the

89 he outcome for children and adolescents with acute myelogenous leukemia (AML) has substantially impro

90 dysplastic syndrome (MDS) that progresses to acute myelogenous leukemia (AML) in association with ove

91 log 2 (Trib2) is a pseudokinase that induces acute myelogenous leukemia (AML) in mice and is highly e

92 phase (CML-BC), in the rapid induction of an acute myelogenous leukemia (AML) in mice.

93 We studied LSCs in mouse models of acute myelogenous leukemia (AML) induced either by coexp

94 Anthracyclines used in the treatment of acute myelogenous leukemia (AML) inhibit the activity of

95 As the pathophysiology of acute myelogenous leukemia (AML) involves a block of mye

96 Acute myelogenous leukemia (AML) is a heterogeneous dise

97 Acute myelogenous leukemia (AML) is a heterogeneous dise

98 Acute Myelogenous Leukemia (AML) is an aggressive cancer

99 Acute myelogenous leukemia (AML) is an aggressive diseas

100 The microenviroment of acute myelogenous leukemia (AML) is suppressive for immu

101 Acute myelogenous leukemia (AML) is the most common leuk

102 Human acute myelogenous leukemia (AML) is thought to arise fro

103 Acute myelogenous leukemia (AML) is typically a disease

104 lop and implement therapeutic approaches for acute myelogenous leukemia (AML) originated primarily fr

105 ising target for therapeutic intervention in acute myelogenous leukemia (AML) owing particularly to i

106 Using acute myelogenous leukemia (AML) patient-derived xenogra

107 kinase are detected in approximately 30% of acute myelogenous leukemia (AML) patients and affect dow

108 titutively activated in approximately 30% of acute myelogenous leukemia (AML) patients and appears to

109 In blasts from acute myelogenous leukemia (AML) patients, 2 classes of

110 tly, IDH1 mutations were identified in 8% of acute myelogenous leukemia (AML) patients.

111 ith autoimmune disorders and in NPM1-mutated acute myelogenous leukemia (AML) patients.

112 tive state in primary specimens derived from acute myelogenous leukemia (AML) patients.

113 and 8 were also screened against M9-ENL1 and acute myelogenous leukemia (AML) primary cell lines and

114 Patients with relapsed or refractory acute myelogenous leukemia (AML) received gemcitabine fo

115 The survival of most patients with acute myelogenous leukemia (AML) remains poor, and novel

116 es to leukemogenesis in T cells, its role in acute myelogenous leukemia (AML) remains unclear.

117 els and next-generation sequencing to assess acute myelogenous leukemia (AML) response to induction c

118 n in a series of 260 newly diagnosed primary acute myelogenous leukemia (AML) samples.

119 ethality was observed in four of six primary acute myelogenous leukemia (AML) specimens.

120 However, the interactions and influence of acute myelogenous leukemia (AML) stem cells with the mic

121 of a regimen that selectively targets human acute myelogenous leukemia (AML) stem cells.

122 ll lung cancer, one prostate cancer, and one acute myelogenous leukemia (AML) subtype M4.

123 Acute myelogenous leukemia (AML) subtypes that result fr

124 1A in a panel of cell lines representing all acute myelogenous leukemia (AML) subtypes using selectiv

125 DNA-binding protein 2 (SSBP2) is a candidate acute myelogenous leukemia (AML) suppressor gene located

126 , Gal-9 presented by cell lines, and primary acute myelogenous leukemia (AML) targets that endogenous

127 onmelanoma skin cancers, and 68 cases of MDS/acute myelogenous leukemia (AML) were observed at a medi

128 osed to further accrual after three cases of acute myelogenous leukemia (AML) were reported of a tota

129 dysplastic syndrome (MDS) transforms into an acute myelogenous leukemia (AML) with associated increas

130 expression of the MLL-AF9 fusion results in acute myelogenous leukemia (AML) with different behavior

131 o hematopoietic progenitor cells and induces acute myelogenous leukemia (AML) with long latency in bo

132 cute lymphocytic leukemia (ALL), 2 of 4 with acute myelogenous leukemia (AML), 1 with chronic lymphoc

133 tive immunotherapy could reduce lethality to acute myelogenous leukemia (AML), a novel technique was

134 Interestingly, patients with acute myelogenous leukemia (AML), acute lymphoblastic le

135 nts with chronic myelogenous leukemia (CML), acute myelogenous leukemia (AML), and acute lymphoblasti

136 tion for acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), and chronic myelogenou

137 iology and clinical outcome of patients with acute myelogenous leukemia (AML), and conventional karyo

138 ell disorders, as well as cases of seminoma, acute myelogenous leukemia (AML), and gastrointestinal s

139 rointestinal stromal tumor (GIST), seminoma, acute myelogenous leukemia (AML), and mastocytosis.

140 tified in approximately 30% of patients with acute myelogenous leukemia (AML), and recently in a smal

141 stinal stromal tumors (GISTs), some cases of acute myelogenous leukemia (AML), and systemic mastocyto

142 have been implicated in the pathogenesis of acute myelogenous leukemia (AML), but the functional sig

143 lastase, and familial platelet disorder with acute myelogenous leukemia (AML), caused by mutations in

144 pleted HLA-identical sibling transplants for acute myelogenous leukemia (AML), chronic myelogenous le

145 irls (P = .0001) and children diagnosed with acute myelogenous leukemia (AML), chronic myelogenous le

146 ng blast phase, myelodysplastic syndrome, or acute myelogenous leukemia (AML), impairs hematopoiesis

147 osine kinase commonly found in patients with acute myelogenous leukemia (AML), led to the down-regula

148 e (HAT) domain for transformation and causes acute myelogenous leukemia (AML), often preceded by a my

149 ising target for therapeutic intervention in acute myelogenous leukemia (AML), owing particularly to

150 Among 5394 cases with acute myelogenous leukemia (AML), the 2-year cumulative

151 successful use of cytotoxic chemotherapy in acute myelogenous leukemia (AML), the biological basis f

152 In acute myelogenous leukemia (AML), the FLT3 receptor tyro

153 cation (ITD) mutations and poor prognosis in acute myelogenous leukemia (AML), we conducted a phase 1

154 er our understanding of the genetic basis of acute myelogenous leukemia (AML), we determined the codi

155 yrosine kinase that is frequently mutated in acute myelogenous leukemia (AML), we developed resistant

156 The development of acute myelogenous leukemia (AML), which is characterized

157 inst Flt3, an additional important target in acute myelogenous leukemia (AML), with pharmacologically

158 te recovery after intensive chemotherapy for acute myelogenous leukemia (AML).

159 kemia-initiating cells (SL-ICs), are rare in acute myelogenous leukemia (AML).

160 equent in myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML).

161 The majority of patients (76%) had acute myelogenous leukemia (AML).

162 y trilineage dysplasia and susceptibility to acute myelogenous leukemia (AML).

163 sis, with an increased propensity to develop acute myelogenous leukemia (AML).

164 somal translocation products associated with acute myelogenous leukemia (AML).

165 rexpression are frequent molecular events in acute myelogenous leukemia (AML).

166 2) is a candidate tumor suppressor for human acute myelogenous leukemia (AML).

167 xpression is a negative prognostic factor in acute myelogenous leukemia (AML).

168 ell proliferation and survival advantages in acute myelogenous leukemia (AML).

169 me, B-cell acute lymphoblastic leukemia, and acute myelogenous leukemia (AML).

170 ival signaling in approximately one-third of acute myelogenous leukemia (AML).

171 transplantations for myelodysplasia (MDS) or acute myelogenous leukemia (AML).

172 ostulated to contribute to transformation to acute myelogenous leukemia (AML).

173 blasts of approximately 90% of patients with acute myelogenous leukemia (AML).

174 ound in significant numbers of patients with acute myelogenous leukemia (AML).

175 bed in several human malignancies, including acute myelogenous leukemia (AML).

176 porin Nup98 gene is frequently rearranged in acute myelogenous leukemia (AML).

177 the most frequently mutated gene in cases of acute myelogenous leukemia (AML).

178 apoptosis of leukemic cell lines and primary acute myelogenous leukemia (AML).

179 nt cytogenetic abnormalities associated with acute myelogenous leukemia (AML).

180 ypes of acute lymphocytic leukemia (ALL) and acute myelogenous leukemia (AML).

181 ated fusion protein, have been identified in acute myelogenous leukemia (AML).

182 s, was conducted in 53 children with de novo acute myelogenous leukemia (AML).

183 cogenesis in multiple human tumors including acute myelogenous leukemia (AML).

184 tment of myelodysplastic syndromes (MDS) and acute myelogenous leukemia (AML).

185 d extend long-term survival of patients with acute myelogenous leukemia (AML).

186 overall survival (OS) for older adults with acute myelogenous leukemia (AML).

187 ell transplantation (alloSCT) in adults with acute myelogenous leukemia (AML).

188 ivity in elderly adults with newly diagnosed acute myelogenous leukemia (AML).

189 , HLA-B, would titrate NK reactivity against acute myelogenous leukemia (AML).

190 expressed in subsets of pediatric and adult acute myelogenous leukemia (AML).

191 wing induction chemotherapy for treatment of acute myelogenous leukemia (AML).

192 in patients with less-than-favorable risk of acute myelogenous leukemia (AML).

193 led, including 31 patients with nonremission acute myelogenous leukemia (AML).

194 d donors from 1409 unrelated transplants for acute myelogenous leukemia (AML; n = 1086) and acute lym

195 enced by CpG island hypermethylation in most acute myelogenous leukemias (AML), and this epigenetic p

196 A total of 50 patients were treated (44 with acute myelogenous leukemia [AML]/myelodysplasia [MDS], 5

197 Acute myelogenous leukemias (AMLs) and endothelial cells

198 been detected in about 30% of patients with acute myelogenous leukemia and a small number of patient

199 Here, we identify two patients with acute myelogenous leukemia and B-cell acute lymphoblasti

200 ccelerating bone metastatic cancers, such as acute myelogenous leukemia and breast cancer.

201 G-CSF on the outcomes of allogeneic HCT for acute myelogenous leukemia and chronic myelogenous leuke

202 h MDS, increasing the time to progression to acute myelogenous leukemia and improving overall respons

203 t(7;11)(p15;p15) translocation, observed in acute myelogenous leukemia and myelodysplastic syndrome,

204 deoxycytidine) is increasingly used to treat acute myelogenous leukemia and myelodysplastic syndrome,

205 ports of inactivating mutations of DNMT3A in acute myelogenous leukemia and myelodysplastic syndrome,

206 afe and effective new therapeutic agents for acute myelogenous leukemia and possibly other FLT3-expre

207 s for transplantation were treatment-related acute myelogenous leukemia and primary refractory Hodgki

208 ng bone marrow failure and high incidence of acute myelogenous leukemia and solid tumors.

209 recent efforts to disrupt FLT3 signaling in acute myelogenous leukemia and to identify potential the

210 the sole caregiver for her husband, who has acute myelogenous leukemia and was undergoing allogeneic

211 to chemotherapy in patients with refractory acute myelogenous leukemia (and other hematologic malign

212 an increased risk of leukemia, specifically acute myelogenous leukemia, and benzene poisoning.

213 osis, GISTs, mast cell leukemia, subtypes of acute myelogenous leukemia, and testicular cancer.

214 s developed treatment-related myelodysplasia/acute myelogenous leukemia, and three patients died whil

215 de (LPS) could lead to DCs with in vivo anti-acute myelogenous leukemia (anti-AML) activity.

216 a oncogenic KIT in systemic mastocytosis and acute myelogenous leukemia are poorly understood.

217 identified as chromosomal translocations in acute myelogenous leukemia, are transcriptional corepres

218 ed Apo-2L/TRAIL-induced apoptosis of primary acute myelogenous leukemia blast samples isolated from 1

219 -60, K562, and Jurkat) as well as in primary acute myelogenous leukemia blasts in relation to differe

220 i, Jurkat, Karpas, K562, U266 cells, primary acute myelogenous leukemia blasts, but not in normal CD3

221 leukemic blasts isolated from patients with acute myelogenous leukemia but was relatively sparing of

222 as, secondary glioblastomas, and a subset of acute myelogenous leukemias but have not been detected i

223 prove the clinical outcome for patients with acute myelogenous leukemia by reducing the incidence of

224 ranslocation that characterizes a subtype of acute myelogenous leukemia cases results in the formatio

225 treatment of primary and relapsed CML and/or acute myelogenous leukemia caused by FLT3 mutations.

226 Human acute myelogenous leukemia cells (HL-60 cells) can be in

227 he generation of the effects of As(2)O(3) on acute myelogenous leukemia cells and raise the potential

228 , and of colony formation of eIF4E-dependent acute myelogenous leukemia cells derived from human pati

229 on of TF-1 erythroleukemia and primary human acute myelogenous leukemia cells in vitro.

230 is for the differential sensitivity of human acute myelogenous leukemia cells to retinoids.

231 nstrate that Id genes are expressed in human acute myelogenous leukemia cells, and that knock down of

232 tiation of hematopoietic stem/progenitor and acute myelogenous leukemia cells.

233 ellular signal-regulated kinase signaling in acute myelogenous leukemia cells.

234 is essential for development and survival of acute myelogenous leukemia cells.

235 atients with acute lymphoblastic leukemia or acute myelogenous leukemia compared with normal bone mar

236 MDS1/EVI1 and EVI1, previously implicated in acute myelogenous leukemia, contribute to the pathophysi

237 se 1 (IDH1), frequently found in gliomas and acute myelogenous leukemia, creates a neoenzyme that pro

238 3) treatment in HL-60 cells, a cell model of acute myelogenous leukemia, decreased miR181b expression

239 ciated with chronic myelogenous leukemia and acute myelogenous leukemia, displays a complex pattern o

240 ot hypermethylated in any of the 40 cases of acute myelogenous leukemia examined.

241 t seven patients developed myelodysplasia or acute myelogenous leukemia, four of those being the rare

242 al platelet disorder with predisposition for acute myelogenous leukemia (FPD/AML).

243 egulated gene in knock-in mice expressing an acute myelogenous leukemia fusion protein, AML1-ETO, as

244 hat ectopic overexpression of hsp70 in human acute myelogenous leukemia HL-60 cells (HL-60/hsp70) and

245 leukemia Jurkat, B lymphoblast SKW 6.4, and acute myelogenous leukemia HL-60 cells.

246 onstitutive expression of c-Kit are found in acute myelogenous leukemia, human mast cell disease, and

247 data on patients with autoimmune diseases or acute myelogenous leukemia illustrate the potential use

248 n increased risk of development of secondary acute myelogenous leukemia involving the mixed-lineage l

249 Acute myelogenous leukemia is a hematological disorder w

250 sed by Rhizomucor pusillus in a patient with acute myelogenous leukemia is described.

251 Acute myelogenous leukemia is propagated by a subpopulat

252 riety of human tumor cell lines and clinical acute myelogenous leukemia isolates, which express abund

253 ffects in lymphohematopoietic cell lines and acute myelogenous leukemia isolates.

254 at had erythroid hyperplasia in bone marrow, acute myelogenous leukemia M1, M2, and chronic myelogeno

255 tified in approximately 30% of patients with acute myelogenous leukemia, making it one of the most co

256 row samples from 15 myelodysplastic syndrome/acute myelogenous leukemia (MDS/AML) patients undergoing

257 phase-specific nucleoside analogues in human acute myelogenous leukemia ML-1 cells, we found that DNA

258 r, GI stromal tumors (GISTs), breast cancer, acute myelogenous leukemia, multiple endocrine neoplasia

259 ified as the cause of some familial cases of acute myelogenous leukemia/myelodysplastic syndrome and

260 Transformation to acute myelogenous leukemia occurred as the first event i

261 f primary blasts isolated from patients with acute myelogenous leukemia or acute lymphocytic leukemia

262 c marker in various types of cancer, such as acute myelogenous leukemia or breast carcinoma.

263 ghteen patients with relapsed and refractory acute myelogenous leukemia or chronic myelomonocytic leu

264 s 56 years (range, 18-69 years), and 95% had acute myelogenous leukemia or high-risk myelodysplastic

265 in the human hippocampus after treatment for acute myelogenous leukemia or medulloblastoma.

266 Among 10 elderly patients with acute myelogenous leukemia or myelodysplastic syndrome,

267 ise the diagnostic and response criteria for acute myelogenous leukemia originally published in 1990,

268 ial platelet syndrome with predisposition to acute myelogenous leukemia, Paris-Trousseau, Wiskott-Ald

269 lines as well as in the majority of primary acute myelogenous leukemia patient samples.

270 heart, lungs, and spleen is described in an acute myelogenous leukemia patient.

271 tyrosine kinase FLT3 are frequently found in acute myelogenous leukemia patients and confer poor clin

272 2 and acinus are overexpressed in some human acute myelogenous leukemia patients and correlate with e

273 is issue, we analyzed outcomes of 2223 adult acute myelogenous leukemia patients who underwent alloge

274 ononuclear cells derived from bone marrow of acute myelogenous leukemia patients, and this correlated

275 lines and primary leukemic progenitors from acute myelogenous leukemia patients.

276 The acute myelogenous leukemia-related fusion protein AML1ET

277 liferative neoplasms (MDS/MPN), or secondary acute myelogenous leukemia (sAML) and may point toward g

278 nt mice given injections of primary FLT3/ITD acute myelogenous leukemia samples or myeloid cell lines

279 s in both leukemic cell lines and in primary acute myelogenous leukemia samples that was not abrogate

280 of neoplastic cell lines as well as clinical acute myelogenous leukemia specimens.

281 t is therefore unlikely that benzene-induced acute myelogenous leukemia stems from events invoked for

282 astic syndrome (t-MDS) and treatment-related acute myelogenous leukemia (t-AML) after treatment with

283 Therapy-related acute myelogenous leukemia (t-AML) is an important late

284 Etoposide-induced treatment-related acute myelogenous leukemia (t-AML) is characterized by r

285 herapy-related myelodysplastic syndromes and acute myelogenous leukemia (t-MDS/AML) comprise an incre

286 Therapy-related myelodysplasia or acute myelogenous leukemia (t-MDS/AML) is a lethal compl

287 l syndrome of radiation-associated secondary acute myelogenous leukemia that had AML1 translocations.

288 tional corepressors originally identified in acute myelogenous leukemia that have recently been linke

289 NO80C) could act as prognostic biomarkers of acute myelogenous leukemia though influencing cancer-rel

290 reatment-related myelodysplastic syndrome or acute myelogenous leukemia (tMDS/AML).

291 sion correlates with sensitivity of clinical acute myelogenous leukemia to chemotherapy, whereas low

292 Finally, in patients with acute myelogenous leukemia treated with hematopoietic st

293 on correlated with response in patients with acute myelogenous leukemia treated with low doses (5-20

294 relatively young or have a normal karyotype, acute myelogenous leukemia-type chemotherapy or transpla

295 rouped into biologic or targeted, therapies, acute myelogenous leukemia-type chemotherapy, and alloge

296 A 37-yr-old female with recently diagnosed acute myelogenous leukemia was admitted to the ICU with

297 Myelodysplasia or acute myelogenous leukemia was reported in five patients

298 In human acute myelogenous leukemia we showed that all preleukemi

299 ger apoptosis of CSC derived from chronic or acute myelogenous leukemias when administered at supraph

300 ion is a common theme in many types of human acute myelogenous leukemia, which is characterized by a