ライフサイエンスコーパス: acute myeloid leukemia

1 myelofibrosis, myelodysplastic syndrome, or acute myeloid leukemia.

2 cant anti-tumor effects in various models of acute myeloid leukemia.

3 d in the United States for specific cases of acute myeloid leukemia.

4 ells and that the kinase TTK is important in acute myeloid leukemia.

5 e enriched for DNase Hypersensitive Sites in acute myeloid leukemia.

6 e microenvironment protected against CLL and acute myeloid leukemia.

7 pported CDK6 as a disease-specific target in acute myeloid leukemia.

8 (AraC) is the mainstay for the treatment of acute myeloid leukemia.

9 ase 3 (FLT3) involved in the pathogenesis of acute myeloid leukemia.

10 dmission among patients with newly diagnosed acute myeloid leukemia.

11 erapeutic option to target LSCs and to treat acute myeloid leukemia.

12 B cell lymphomas, it is highly expressed in acute myeloid leukemia.

13 nd increases survival in an in vivo model of acute myeloid leukemia.

14 unodeficiency, myelodysplastic syndrome, and acute myeloid leukemia.

15 m cells and their progenies in patients with acute myeloid leukemia.

16 bute to a wide spectrum of cancers including acute myeloid leukemia.

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

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

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

20 this crosstalk is linked to diseases such as acute myeloid leukemia.

21 s in mice transition from a healthy state to acute myeloid leukemia.

22 lineages and a high risk of developing into acute myeloid leukemia.

23 ondary mast cell leukemia (32%) or secondary acute myeloid leukemia (68%).

24 In a xenograft model of acute myeloid leukemia, a single injection of 10 million

25 Patients with acute myeloid leukemia (AML) and a FLT3 internal tandem

26 leoporin 98 (NUP98) are recurrently found in acute myeloid leukemia (AML) and are associated with poo

27 d in many hematologic malignancies including acute myeloid leukemia (AML) and blastic plasmacytoid de

28 The acute myeloid leukemia (AML) and chronic myeloid leukemi

29 f physically interacting RBPs upregulated in acute myeloid leukemia (AML) and crucial for maintaining

30 ation sequencing in cells from patients with acute myeloid leukemia (AML) and in normal bone marrow (

31 ansplantation to older adults with high-risk acute myeloid leukemia (AML) and myelodysplasia (MDS) bu

32 eic stem-cell transplantation (allo-SCT) for acute myeloid leukemia (AML) and myelodysplasia (MDS) re

33 Here we report a cohort of 86 acute myeloid leukemia (AML) and myelodysplastic syndrom

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

35 ion is associated with an aggressive form of acute myeloid leukemia (AML) and poor survival rate.

36 tients with Nucleophosmin1-mutated (NPM1mut) acute myeloid leukemia (AML) and represents a powerful t

37 get induction of cellular differentiation in acute myeloid leukemia (AML) and small cell lung cancer

38 The enzyme is overexpressed in acute myeloid leukemia (AML) and T-cell acute lymphoblas

39 Myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are diseases of abnormal he

40 lution of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) are driven by genomic event

41 the genomic and gene expression profiles of acute myeloid leukemia (AML) blasts purified from patien

42 , we address this question in the context of Acute Myeloid Leukemia (AML) by integrating whole genome

43 The R882H DNMT3A is a hotspot mutation in acute myeloid leukemia (AML) causing aberrant DNA methyl

44 lates two key metabolic enzymes required for acute myeloid leukemia (AML) cell growth.

45 motes the differentiation/apoptosis of human acute myeloid leukemia (AML) cell line cells and primary

46 Transcriptional changes in acute myeloid leukemia (AML) cell lines were distinct fr

47 was identified as an essential modulator for acute myeloid leukemia (AML) cell survival and prolifera

48 s study, we demonstrated that chemoresistant acute myeloid leukemia (AML) cells had a lower level of

49 Primary acute myeloid leukemia (AML) cells harvested from patien

50 IKZF2 depletion in acute myeloid leukemia (AML) cells reduced colony format

51 ormed pooled CRISPR-Cas9 knockout screens in acute myeloid leukemia (AML) cells treated with various

52 , we examined the influence of NOD2 in human acute myeloid leukemia (AML) cells, demonstrating that I

53 ochondrial genes necessary for the growth of acute myeloid leukemia (AML) cells, we identified the mi

54 on, we performed detailed genetic studies in acute myeloid leukemia (AML) cells.

55 as necessary for the growth and viability of acute myeloid leukemia (AML) cells.

56 l role in the proliferation of AE-expressing acute myeloid leukemia (AML) cells.

57 dentify patients most suitable for intensive acute myeloid leukemia (AML) chemotherapy.

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

59 Our understanding of the genetics of acute myeloid leukemia (AML) development from myelodyspl

60 f the epitranscriptome that are required for acute myeloid leukemia (AML) development.

61 Acute Myeloid Leukemia (AML) develops due to the acquisi

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

63 Acute myeloid leukemia (AML) disrupts the generation of

64 the leading cause of death in patients with acute myeloid leukemia (AML) entering HCT with poor-risk

65 We show that human acute myeloid leukemia (AML) expresses CD83 and that mye

66 al evaluated 430 samples from patients with acute myeloid leukemia (AML) for germline and somatic mu

67 Patients with acute myeloid leukemia (AML) harboring FLT3 internal tan

68 ing therapeutic targets for the treatment of acute myeloid leukemia (AML) harboring MLL translocation

69 Treatment of relapsed or refractory acute myeloid leukemia (AML) has presented challenges fo

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

71 Approximately 8% to 19% of patients with acute myeloid leukemia (AML) have isocitrate dehydrogena

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

73 Patients with acute myeloid leukemia (AML) in remission remain at risk

74 t have been implicated in the development of acute myeloid leukemia (AML) in the bone marrow microenv

75 Here, we investigated the function of p62 in acute myeloid leukemia (AML) in vitro and in murine in v

76 Current objectives regarding treatment of acute myeloid leukemia (AML) include achieving complete

77 results for 34 patients with newly diagnosed acute myeloid leukemia (AML) ineligible for standard the

78 Acute myeloid leukemia (AML) is a cancer derived from th

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

80 Acute myeloid leukemia (AML) is a heterogeneous clonal d

81 Acute myeloid leukemia (AML) is a heterogeneous disease

82 Acute myeloid leukemia (AML) is a heterogeneous disease

83 Acute myeloid leukemia (AML) is a heterogeneous disease

84 Acute myeloid leukemia (AML) is a high-risk disease with

85 Acute myeloid leukemia (AML) is a highly heterogeneous d

86 Acute myeloid leukemia (AML) is a systemic, heterogeneou

87 Acute myeloid leukemia (AML) is an age-related disease t

88 Acute myeloid leukemia (AML) is an aggressive clonal dis

89 Acute Myeloid Leukemia (AML) is an aggressive hematologi

90 Acute myeloid leukemia (AML) is an attractive system for

91 TP53 mutation in acute myeloid leukemia (AML) is associated with poor pro

92 Acute myeloid leukemia (AML) is characterised by a serie

93 A principal challenge in treating acute myeloid leukemia (AML) is chemotherapy refractory

94 The most frequent subtype of acute myeloid leukemia (AML) is defined by mutations in

95 A hallmark of acute myeloid leukemia (AML) is epigenetic dysregulation

96 Childhood acute myeloid leukemia (AML) is frequently characterized

97 Acute myeloid leukemia (AML) is often characterized by t

98 althy people as they age, but progression to acute myeloid leukemia (AML) is rare.

99 Successful clinical remission to therapy for acute myeloid leukemia (AML) is required for long-term s

100 The canonical view of acute myeloid leukemia (AML) is that it results from a c

101 Acute myeloid leukemia (AML) is the most common diagnose

102 treatment courses for younger patients with acute myeloid leukemia (AML) is uncertain.

103 Epigenetic reprogramming in Acute Myeloid Leukemia (AML) leads to the aberrant activ

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

105 Using acute myeloid leukemia (AML) mouse models, we show AML b

106 e previously shown that the highly prevalent acute myeloid leukemia (AML) mutation, Arg882His, in DNM

107 rmal hematopoietic progenitors expressing an acute myeloid leukemia (AML) oncogene MLL-AF9, we reveal

108 pproval for the treatment of therapy-related acute myeloid leukemia (AML) or AML with myelodysplasia-

109 However, their specific roles in acute myeloid leukemia (AML) pathogenesis remain unknown

110 viral miRNA with decreased survival in adult acute myeloid leukemia (AML) patients (P = 0.00013).

111 alysis of bone marrow cells derived from six acute myeloid leukemia (AML) patients and treated with t

112 d that leukemia stem cells (LSCs) in de novo acute myeloid leukemia (AML) patients are selectively re

113 tational hotspot, R222G, in DHX15 in ~ 6% of acute myeloid leukemia (AML) patients that carry the fus

114 We tested MASQ in a pilot study in acute myeloid leukemia (AML) patients who entered comple

115 19 it is estimated that more than 21,000 new acute myeloid leukemia (AML) patients will be diagnosed

116 ine kinase (FLT3), are frequently mutated in acute myeloid leukemia (AML) patients, and these mutatio

117 1 (NCAM1; CD56) is expressed in up to 20% of acute myeloid leukemia (AML) patients.

118 ary leukemia blast cells isolated from human acute myeloid leukemia (AML) patients.

119 ase 3alpha (DNMT3A) and poor prognoses among acute myeloid leukemia (AML) patients.

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

121 architecture and mutational histories of 123 acute myeloid leukemia (AML) patients.

122 stemness and quiescence of leukemic cells in acute myeloid leukemia (AML) patients.

123 apies, the clinical outcome of patients with acute myeloid leukemia (AML) remains suboptimal, prompti

124 conditioning regimen for older patients with acute myeloid leukemia (AML) remains unclear.

125 Acute myeloid leukemia (AML) represents the most common

126 Older patients with acute myeloid leukemia (AML) respond poorly to standard

127 Aberrant activation of mTOR signaling in acute myeloid leukemia (AML) results in a survival advan

128 e hematopoiesis as well as fully transformed acute myeloid leukemia (AML) results in changes in trans

129 Standard chemotherapy for acute myeloid leukemia (AML) targets proliferative cells

130 is a pathologically relevant event in human acute myeloid leukemia (AML) that contributes to impaire

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

132 of p53, MDM2, is frequently overexpressed in acute myeloid leukemia (AML) that retains wild-type TP53

133 found that HOTTIP is aberrantly activated in acute myeloid leukemia (AML) to alter HOXA-driven topolo

134 BC transfusion-independence in patients with acute myeloid leukemia (AML) treated with the isocitrate

135 The acute myeloid leukemia (AML) treatment landscape has cha

136 apply our method to an ultra-deep sequenced acute myeloid leukemia (AML) tumor and identify known ca

137 ssion therapy of young patients with de novo acute myeloid leukemia (AML) was decided combining cytog

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

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

140 are associated with a favorable prognosis in acute myeloid leukemia (AML) when an internal tandem dup

141 atment options are limited for patients with acute myeloid leukemia (AML) who cannot tolerate intensi

142 therapeutic challenge in older patients with acute myeloid leukemia (AML) who have obtained a complet

143 cause of treatment failure for patients with acute myeloid leukemia (AML) who undergo allogeneic stem

144 rt the development of a mouse model of human acute myeloid leukemia (AML) with autologous immune syst

145 em cell transplantation (HCT), patients with acute myeloid leukemia (AML) with internal tandem duplic

146 Acute myeloid leukemia (AML) with inv(3)/t(3;3)(q21q26)

147 Acute myeloid leukemia (AML) with mixed lineage leukemia

148 High CD33 expression in acute myeloid leukemia (AML) with mutated NPM1 provides

149 NP23-NHD13 double transgenic mice developed acute myeloid leukemia (AML) within three months, charac

150 n implicated in myelodysplastic syndrome and acute myeloid leukemia (AML) yet the precise biological

151 h-risk disease(3,4), rapid transformation to acute myeloid leukemia (AML)(5), resistance to conventio

152 In patients with acute myeloid leukemia (AML), 10% to 30% with the normal

153 In acute myeloid leukemia (AML), acquired genetic aberratio

154 However, in acute myeloid leukemia (AML), ALKBH5 was reported to be

155 te alteration during leukemogenesis of human acute myeloid leukemia (AML), and ALKBH5 is required for

156 in-1 (NPM1) are most frequent alterations in acute myeloid leukemia (AML), and are often coincidental

157 ion datasets related to Alzheimer's disease, acute myeloid leukemia (AML), and influenza.

158 energetics crucial for glucose metabolism in acute myeloid leukemia (AML), and its inhibition delays

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

160 valent in Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML), and the most common mutati

161 These may include induction chemotherapy for acute myeloid leukemia (AML), as well as autologous hema

162 ntative examples, we present our results for acute myeloid leukemia (AML), breast cancer and prostate

163 ntly mutated genes in cytogenetically normal acute myeloid leukemia (AML), but little is known about

164 ion of oxidative phosphorylation (OxPHOS) in acute myeloid leukemia (AML), but not in normal cells.

165 In acute myeloid leukemia (AML), chemorefractory relapses r

166 significant efforts to improve therapies for acute myeloid leukemia (AML), clinical outcomes remain p

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

168 In fit patients with newly diagnosed acute myeloid leukemia (AML), immediate treatment start

169 t in a variety of cancers, including glioma, acute myeloid leukemia (AML), melanoma, and cholangiocar

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

171 usion genes like CBFB-MYH11 are prevalent in acute myeloid leukemia (AML), often necessary for leukem

172 Antigen-directed immunotherapies for acute myeloid leukemia (AML), such as chimeric antigen r

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

174 To identify new therapeutic targets in acute myeloid leukemia (AML), we performed small-molecul

175 ontext for Ezh2 loss during the evolution of acute myeloid leukemia (AML), where we observed stage-sp

176 inhibitor venetoclax has an emerging role in acute myeloid leukemia (AML), with promising response ra

177 idoxal phosphate (PLP) from vitamin B6-as an acute myeloid leukemia (AML)-selective dependency.

178 commonly both over-expressed and mutated in acute myeloid leukemia (AML).

179 l (HSC) quiescence, and a poor prognosis for acute myeloid leukemia (AML).

180 secondary myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML).

181 chemotherapy resistance and poor outcome in acute myeloid leukemia (AML).

182 igh expression predicts treatment failure in acute myeloid leukemia (AML).

183 hylase FTO, which is commonly deregulated in acute myeloid leukemia (AML).

184 er therapeutic paradigm for the treatment of acute myeloid leukemia (AML).

185 st responses observed in relapsed/refractory acute myeloid leukemia (AML).

186 cells and leukemic cells from patients with acute myeloid leukemia (AML).

187 arded as interchangeable in the treatment of acute myeloid leukemia (AML).

188 Ds) are prognostic driver mutations found in acute myeloid leukemia (AML).

189 t chromosomal translocations associated with acute myeloid leukemia (AML).

190 ship to infectious outcomes in patients with acute myeloid leukemia (AML).

191 cRNA in patients with NPM1-mutated (NPM1mut) acute myeloid leukemia (AML).

192 the most frequent chromosome aberrations in acute myeloid leukemia (AML).

193 ong independent adverse prognostic marker in acute myeloid leukemia (AML).

194 , we investigated the role of PRMT5 in human acute myeloid leukemia (AML).

195 he efficacy of kinase inhibitors in FLT3-ITD acute myeloid leukemia (AML).

196 tRUNX1) is associated with poorer outcome in acute myeloid leukemia (AML).

197 eukemia stem cells (LSCs) from patients with acute myeloid leukemia (AML).

198 ell disorders with risk of transformation to acute myeloid leukemia (AML).

199 ell acute lymphoblastic leukemia (B-ALL) and acute myeloid leukemia (AML).

200 (NPM1) is the most commonly mutated gene in acute myeloid leukemia (AML).

201 bine (AraC) is the mainstay chemotherapy for acute myeloid leukemia (AML).

202 typically hierarchical malignancies, such as acute myeloid leukemia (AML).

203 entified as a new target in the treatment of acute myeloid leukemia (AML).

204 pecific focus on infection, in patients with acute myeloid leukemia (AML).

205 RA) in treatment-naive elderly patients with acute myeloid leukemia (AML).

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

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

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

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

210 cell (LSC) pool determine aggressiveness of acute myeloid leukemia (AML).

211 s highly associated with a poor prognosis in acute myeloid leukemia (AML).

212 cell gene expression and promotes relapse in acute myeloid leukemia (AML).

213 loci in mouse resulted in the development of acute myeloid leukemia (AML).

214 rement for Runx1 in a mouse model of inv(16) acute myeloid leukemia (AML).

215 enced by hypermethylation of its promoter in acute myeloid leukemia (AML).

216 promised by adaptive or innate resistance in acute myeloid leukemia (AML).

217 pproved for treatment of IDH1-mutant (mIDH1) acute myeloid leukemia (AML).

218 atopoiesis and are frequently deregulated in acute myeloid leukemia (AML).

219 new therapy for older or unfit patients with acute myeloid leukemia (AML).

220 among the most common initiating events for acute myeloid leukemia (AML).

221 RUNX1 is mutated in ~10% of adult acute myeloid leukemia (AML).

222 ial bulk RNA-seq data from a murine model of acute myeloid leukemia (AML).

223 would define distinctive vulnerabilities in acute myeloid leukemia (AML).

224 gimens are needed for children with relapsed acute myeloid leukemia (AML).

225 astic syndromes (MDS) frequently progress to acute myeloid leukemia (AML); however, the cells leading

226 syndrome (MDS) was most common, followed by acute myeloid leukemia (AML); they accounted for 75% of

227 , lung (1.17), and cervix (1.52), as well as acute myeloid leukemia (AML, 1.19), chronic myeloid leuk

228 sent the most common genetic lesion in adult acute myeloid leukemia (AML; about one third of cases),

229 led pancytopenia with peripheral blasts, and acute myeloid leukemia (AML; French-American-British M2,

230 Secondary acute myeloid leukemias (AMLs) evolving from an antecede

231 In up to 15% of acute myeloid leukemias (AMLs), a recurring chromosomal

232 amilial myelodysplastic syndromes (MDSs) and acute myeloid leukemias (AMLs).

233 1), which is mutated in approximately 30% of acute myeloid leukemias (AMLs).

234 risk of childhood leukemia, particularly for acute myeloid leukemia, among children under 6 y of age,

235 SD-36 inhibits the growth of a subset of acute myeloid leukemia and anaplastic large-cell lymphom

236 Application of our methods to primary acute myeloid leukemia and breast cancer tumors quantifi

237 ized as a low toxicity therapeutic for human acute myeloid leukemia and confirm the LMI approach as a

238 Notably, two individuals developed cancer, acute myeloid leukemia and Hodgkin lymphoma, in childhoo

239 ine and etoposide in pediatric patients with acute myeloid leukemia and may reduce rates of cardiomyo

240 ted as a promising therapeutic treatment for acute myeloid leukemia and multiple solid tumors.

241 Together with corroborative findings in acute myeloid leukemia and myelodysplastic syndrome pati

242 e nucleotide polymorphism array results from acute myeloid leukemia and prostate cancer datasets avai

243 hildren receiving intensive chemotherapy for acute myeloid leukemia and relapsed acute lymphoblastic

244 roved drug for myelodysplastic syndromes and acute myeloid leukemia, and is under investigation for d

245 ic malignancies (lymphoma, multiple myeloma, acute myeloid leukemia, and myelodysplastic syndrome).

246 urs frequently in various cancers, including acute myeloid leukemia, and our results suggest that the

247 k neuroblastoma, embryonal rhabdomyosarcoma, acute myeloid leukemia, and relapsed acute lymphoblastic

248 Children, adolescents, and young adults with acute myeloid leukemia are at high risk of life-threaten

249 ly diagnosed de novo, relapsed, or secondary acute myeloid leukemia being treated at 115 US and Canad

250 We analyzed 152 cells from three acute myeloid leukemia cell lines, resulting in a total

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

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

253 nstrated the ability of BASIL to distinguish acute myeloid leukemia cells based on the phosphoproteom

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

255 and are also common in clonal hematopoiesis, acute myeloid leukemia, chronic lymphocytic leukemia, an

256 also conduct a retrospective analysis on an acute myeloid leukemia cohort, demonstrating the potenti

257 Using The Cancer Genome Atlas acute myeloid leukemia data set, we found an inverse cor

258 pound with emerging therapeutic potential in acute myeloid leukemia, debilitating fibroses, and obesi

259 y reveals that leukemia stem cells (LSCs) in acute myeloid leukemia downregulate natural killer cell-

260 ceptor is an important therapeutic target in acute myeloid leukemia due to high incidence of mutation

261 patients with de novo or relapsed/refractory acute myeloid leukemia during the study period, with inv

262 Several acute myeloid leukemia genetic sub-types converge on hig

263 emotherapy-treated mice and had no effect on acute myeloid leukemia growth in vivo.

264 s to model the initiation and development of acute myeloid leukemia, identifying transcriptomic pertu

265 Emerging acute myeloid leukemia impaired mesenchymal osteogenic d

266 ng independent predictor of infection during acute myeloid leukemia induction chemotherapy (IC) among

267 munications have now firmly established that acute myeloid leukemia is a highly dynamic oligoclonal d

268 Acute myeloid leukemia is characterized by the accumulat

269 HOXA9, implicated in acute myeloid leukemia, is one of them.

270 d acute GVHD without impairing GVL against 2 acute myeloid leukemia lines (MLL-AF9-eGFP and C1498-luc

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

272 and 2.6 nM in esophageal cancer KYSE520 and acute myeloid leukemia MV4;11 cells, respectively, and i

273 MA) have become the backbone of nonintensive acute myeloid leukemia/myelodysplastic syndrome (AML/MDS

274 , and prospectively phenotyped children with acute myeloid leukemia (n=41).

275 yzed DNA methylation data from IDH1/2 mutant acute myeloid leukemia, oligodendroglioma, astrocytoma,

276 dels derived from patients with either MLL-r acute myeloid leukemia or MLL-r acute lymphoblastic leuk

277 Data from 2222 patients with acute myeloid leukemia or myelodysplastic syndrome were

278 opoietic stressors in the evolution of CH to acute myeloid leukemia or myelodysplastic syndrome.

279 is study, we conducted a reanalysis of 2,213 acute myeloid leukemia patients compared to 548 healthy

280 cell transplantation in multiple myeloma and acute myeloid leukemia patients indicate that cf-mRNA le

281 al blood mononuclear cells were sampled from acute myeloid leukemia patients longitudinally and singl

282 overall response of newly diagnosed elderly acute myeloid leukemia patients to a venetoclax and azac

283 through AraC suggests that TLS inhibition in acute myeloid leukemia patients would increase the effec

284 ate with poor survival of Cytarabine-treated acute myeloid leukemia patients, qualifying AK1 as a pat

285 children, adolescents, and young adults with acute myeloid leukemia, prophylaxis with caspofungin com

286 therapy in patients with relapsed/refractory acute myeloid leukemia (R/R AML).

287 s were classified as CMV(+/-) The respective acute myeloid leukemia recipients were followed for dise

288 mprove our therapeutic armamentarium against acute myeloid leukemia relapse.

289 In t(8;21)+ acute myeloid leukemia, RUNX1 is fused to nearly the ent

290 set from the German Study Alliance Leukemia-Acute Myeloid Leukemia (SAL-AML) registry.

291 odysplastic syndrome (sMDS) and/or secondary acute myeloid leukemia (sAML) in 30-40%.

292 The boundary between MDS and secondary acute myeloid leukemia (sAML) is arbitrarily defined and

293 alysis of clinical outcomes in patients with acute myeloid leukemia showed no evidence of GOF for TP5

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

295 Late cardiotoxicity after pediatric acute myeloid leukemia therapy causes substantial morbid

296 ldren and adolescents receiving treatment of acute myeloid leukemia, to those undergoing allogeneic H

297 ollow-up among 1,022 pediatric patients with acute myeloid leukemia treated in the Children's Oncolog

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

299 both acute promyelocytic leukemia (APL) and acute myeloid leukemia, we arrived at an integrative sco

300 (MM), chronic lymphocytic leukemia (CLL) and acute myeloid leukemia, we compare the performance of pu