ライフサイエンスコーパス: myeloid leukemia

1 ges and a high risk of developing into acute myeloid leukemia.

2 fibrosis, myelodysplastic syndrome, or acute myeloid leukemia.

3 nti-tumor effects in various models of acute myeloid leukemia.

4 he United States for specific cases of acute myeloid leukemia.

5 nd that the kinase TTK is important in acute myeloid leukemia.

6 ched for DNase Hypersensitive Sites in acute myeloid leukemia.

7 oenvironment protected against CLL and acute myeloid leukemia.

8 eted or expressed at reduced levels in human myeloid leukemia.

9 d CDK6 as a disease-specific target in acute myeloid leukemia.

10 ) is the mainstay for the treatment of acute myeloid leukemia.

11 (FLT3) involved in the pathogenesis of acute myeloid leukemia.

12 on among patients with newly diagnosed acute myeloid leukemia.

13 tic option to target LSCs and to treat acute myeloid leukemia.

14 mann-Pick disease type C2); and secondary to myeloid leukemia.

15 rationale to therapeutically target IKZF2 in myeloid leukemia.

16 ment supported genesis of mixed early B cell/myeloid leukemia.

17 l lymphomas, it is highly expressed in acute myeloid leukemia.

18 reases survival in an in vivo model of acute myeloid leukemia.

19 epticemia) during remission, and 1 secondary myeloid leukemia.

20 rosstalk is linked to diseases such as acute myeloid leukemia.

21 ice transition from a healthy state to acute myeloid leukemia.

22 zyme in polyamine synthesis, is required for myeloid leukemia.

23 nthesis affects the MDR phenotype of chronic myeloid leukemias.

24 3a2 was seen across multiple mouse and human myeloid leukemias.

25 acute myeloid leukemia (AML, 1.19), chronic myeloid leukemia (1.54), and myelodysplastic syndrome (1

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

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

28 ) and to a lesser extent in atypical chronic myeloid leukemia (aCML) resulting in constitutive JAK-ST

29 eutrophilic leukemia (CNL), atypical chronic myeloid leukemia (aCML), and myelodysplastic/myeloprolif

30 c leukemia (CMML; n = 119), atypical chronic myeloid leukemia (aCML; n = 71), MDS/MPN with ring sider

31 ell lines, including acute lymphoblastic and myeloid leukemia (ALL/AML) and nonsmall cell lung cancer

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

33 in 98 (NUP98) are recurrently found in acute myeloid leukemia (AML) and are associated with poor prog

34 any hematologic malignancies including acute myeloid leukemia (AML) and blastic plasmacytoid dendriti

35 The acute myeloid leukemia (AML) and chronic myeloid leukemia (CML

36 ically interacting RBPs upregulated in acute myeloid leukemia (AML) and crucial for maintaining RNA s

37 sequencing in cells from patients with acute myeloid leukemia (AML) and in normal bone marrow (NBM) i

38 ntation to older adults with high-risk acute myeloid leukemia (AML) and myelodysplasia (MDS) but are

39 em-cell transplantation (allo-SCT) for acute myeloid leukemia (AML) and myelodysplasia (MDS) remain l

40 Here we report a cohort of 86 acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS

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

42 with Nucleophosmin1-mutated (NPM1mut) acute myeloid leukemia (AML) and represents a powerful tool to

43 duction of cellular differentiation in acute myeloid leukemia (AML) and small cell lung cancer (SCLC)

44 The enzyme is overexpressed in acute myeloid leukemia (AML) and T-cell acute lymphoblastic le

45 Myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are diseases of abnormal hematopo

46 of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) are driven by genomic events that

47 enomic and gene expression profiles of acute myeloid leukemia (AML) blasts purified from patients at

48 ddress this question in the context of Acute Myeloid Leukemia (AML) by integrating whole genome seque

49 R882H DNMT3A is a hotspot mutation in acute myeloid leukemia (AML) causing aberrant DNA methylation.

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

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

52 Transcriptional changes in acute myeloid leukemia (AML) cell lines were distinct from tho

53 entified as an essential modulator for acute myeloid leukemia (AML) cell survival and proliferation i

54 y, we demonstrated that chemoresistant acute myeloid leukemia (AML) cells had a lower level of mitoch

55 Primary acute myeloid leukemia (AML) cells harvested from patients wit

56 IKZF2 depletion in acute myeloid leukemia (AML) cells reduced colony formation, i

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

58 xamined the influence of NOD2 in human acute myeloid leukemia (AML) cells, demonstrating that IFN-gam

59 rial genes necessary for the growth of acute myeloid leukemia (AML) cells, we identified the mitochon

60 performed detailed genetic studies in acute myeloid leukemia (AML) cells.

61 essary for the growth and viability of acute myeloid leukemia (AML) cells.

62 in the proliferation of AE-expressing acute myeloid leukemia (AML) cells.

63 y patients most suitable for intensive acute myeloid leukemia (AML) chemotherapy.

64 Our understanding of the genetics of acute myeloid leukemia (AML) development from myelodysplastic

65 epitranscriptome that are required for acute myeloid leukemia (AML) development.

66 Acute Myeloid Leukemia (AML) develops due to the acquisition o

67 Acute myeloid leukemia (AML) disrupts the generation of normal

68 eading cause of death in patients with acute myeloid leukemia (AML) entering HCT with poor-risk featu

69 We show that human acute myeloid leukemia (AML) expresses CD83 and that myeloid l

70 aluated 430 samples from patients with acute myeloid leukemia (AML) for germline and somatic mutation

71 Patients with acute myeloid leukemia (AML) harboring FLT3 internal tandem du

72 erapeutic targets for the treatment of acute myeloid leukemia (AML) harboring MLL translocations.

73 Treatment of relapsed or refractory acute myeloid leukemia (AML) has presented challenges for hema

74 proximately 8% to 19% of patients with acute myeloid leukemia (AML) have isocitrate dehydrogenase-2 (

75 Patients with acute myeloid leukemia (AML) in remission remain at risk for r

76 we investigated the function of p62 in acute myeloid leukemia (AML) in vitro and in murine in vivo mo

77 rent objectives regarding treatment of acute myeloid leukemia (AML) include achieving complete remiss

78 s for 34 patients with newly diagnosed acute myeloid leukemia (AML) ineligible for standard therapy w

79 Acute myeloid leukemia (AML) is a cancer derived from the myel

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

81 Acute myeloid leukemia (AML) is a heterogeneous clonal disorde

82 Acute myeloid leukemia (AML) is a heterogeneous disease caused

83 Acute myeloid leukemia (AML) is a heterogeneous disease that r

84 Acute myeloid leukemia (AML) is a heterogeneous disease with r

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

86 Acute myeloid leukemia (AML) is a highly heterogeneous disease

87 Acute myeloid leukemia (AML) is a systemic, heterogeneous hema

88 Acute myeloid leukemia (AML) is an age-related disease that is

89 Acute myeloid leukemia (AML) is an aggressive clonal disorder

90 Acute Myeloid Leukemia (AML) is an aggressive hematological ma

91 Acute myeloid leukemia (AML) is an attractive system for inves

92 TP53 mutation in acute myeloid leukemia (AML) is associated with poor prognosis

93 Acute myeloid leukemia (AML) is characterised by a series of g

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

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

96 Acute myeloid leukemia (AML) is often characterized by the pre

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

98 sful clinical remission to therapy for acute myeloid leukemia (AML) is required for long-term surviva

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

100 Acute myeloid leukemia (AML) is the most common diagnosed leuk

101 ment courses for younger patients with acute myeloid leukemia (AML) is uncertain.

102 Epigenetic reprogramming in Acute Myeloid Leukemia (AML) leads to the aberrant activation

103 Using acute myeloid leukemia (AML) mouse models, we show AML blasts

104 iously shown that the highly prevalent acute myeloid leukemia (AML) mutation, Arg882His, in DNMT3A di

105 ematopoietic progenitors expressing an acute myeloid leukemia (AML) oncogene MLL-AF9, we reveal that

106 l for the treatment of therapy-related acute myeloid leukemia (AML) or AML with myelodysplasia-relate

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

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

109 of bone marrow cells derived from six acute myeloid leukemia (AML) patients and treated with the nuc

110 leukemia stem cells (LSCs) in de novo acute myeloid leukemia (AML) patients are selectively reliant

111 We tested MASQ in a pilot study in acute myeloid leukemia (AML) patients who entered complete rem

112 is estimated that more than 21,000 new acute myeloid leukemia (AML) patients will be diagnosed in the

113 M1; CD56) is expressed in up to 20% of acute myeloid leukemia (AML) patients.

114 ukemia blast cells isolated from human acute myeloid leukemia (AML) patients.

115 lpha (DNMT3A) and poor prognoses among acute myeloid leukemia (AML) patients.

116 ecture and mutational histories of 123 acute myeloid leukemia (AML) patients.

117 ss and quiescence of leukemic cells in acute myeloid leukemia (AML) patients.

118 the clinical outcome of patients with acute myeloid leukemia (AML) remains suboptimal, prompting the

119 ioning regimen for older patients with acute myeloid leukemia (AML) remains unclear.

120 Acute myeloid leukemia (AML) represents the most common acute

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

122 errant activation of mTOR signaling in acute myeloid leukemia (AML) results in a survival advantage t

123 Standard chemotherapy for acute myeloid leukemia (AML) targets proliferative cells and e

124 pathologically relevant event in human acute myeloid leukemia (AML) that contributes to impaired diff

125 , MDM2, is frequently overexpressed in acute myeloid leukemia (AML) that retains wild-type TP53 allel

126 that HOTTIP is aberrantly activated in acute myeloid leukemia (AML) to alter HOXA-driven topologicall

127 nsfusion-independence in patients with acute myeloid leukemia (AML) treated with the isocitrate dehyd

128 The acute myeloid leukemia (AML) treatment landscape has changed s

129 our method to an ultra-deep sequenced acute myeloid leukemia (AML) tumor and identify known cancer g

130 therapy of young patients with de novo acute myeloid leukemia (AML) was decided combining cytogenetic

131 sociated with a favorable prognosis in acute myeloid leukemia (AML) when an internal tandem duplicati

132 eutic challenge in older patients with acute myeloid leukemia (AML) who have obtained a complete remi

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

134 development of a mouse model of human acute myeloid leukemia (AML) with autologous immune system for

135 l transplantation (HCT), patients with acute myeloid leukemia (AML) with internal tandem duplication

136 Acute myeloid leukemia (AML) with inv(3)/t(3;3)(q21q26) is a d

137 Acute myeloid leukemia (AML) with mixed lineage leukemia 1 (ML

138 High CD33 expression in acute myeloid leukemia (AML) with mutated NPM1 provides a rati

139 NHD13 double transgenic mice developed acute myeloid leukemia (AML) within three months, characterize

140 icated in myelodysplastic syndrome and acute myeloid leukemia (AML) yet the precise biological impact

141 disease(3,4), rapid transformation to acute myeloid leukemia (AML)(5), resistance to conventional th

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

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

144 eration during leukemogenesis of human acute myeloid leukemia (AML), and ALKBH5 is required for maint

145 tasets related to Alzheimer's disease, acute myeloid leukemia (AML), and influenza.

146 tics crucial for glucose metabolism in acute myeloid leukemia (AML), and its inhibition delays leukem

147 in Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML), and the most common mutation is

148 may include induction chemotherapy for acute myeloid leukemia (AML), as well as autologous hematopoie

149 e examples, we present our results for acute myeloid leukemia (AML), breast cancer and prostate cance

150 utated genes in cytogenetically normal acute myeloid leukemia (AML), but little is known about how th

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

152 In acute myeloid leukemia (AML), chemorefractory relapses result

153 icant efforts to improve therapies for acute myeloid leukemia (AML), clinical outcomes remain poor.

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

155 variety of cancers, including glioma, acute myeloid leukemia (AML), melanoma, and cholangiocarcinoma

156 genes like CBFB-MYH11 are prevalent in acute myeloid leukemia (AML), often necessary for leukemogenes

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

158 To identify new therapeutic targets in acute myeloid leukemia (AML), we performed small-molecule and

159 for Ezh2 loss during the evolution of acute myeloid leukemia (AML), where we observed stage-specific

160 tor venetoclax has an emerging role in acute myeloid leukemia (AML), with promising response rates in

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

162 erapy for older or unfit patients with acute myeloid leukemia (AML).

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

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

165 lk RNA-seq data from a murine model of acute myeloid leukemia (AML).

166 define distinctive vulnerabilities in acute myeloid leukemia (AML).

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

168 nly both over-expressed and mutated in acute myeloid leukemia (AML).

169 ) quiescence, and a poor prognosis for acute myeloid leukemia (AML).

170 ary myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML).

171 therapy resistance and poor outcome in acute myeloid leukemia (AML).

172 pression predicts treatment failure in acute myeloid leukemia (AML).

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

174 rapeutic paradigm for the treatment of acute myeloid leukemia (AML).

175 ponses observed in relapsed/refractory acute myeloid leukemia (AML).

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

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

178 e prognostic driver mutations found in acute myeloid leukemia (AML).

179 mosomal translocations associated with acute myeloid leukemia (AML).

180 n patients with NPM1-mutated (NPM1mut) acute myeloid leukemia (AML).

181 dependent adverse prognostic marker in acute myeloid leukemia (AML).

182 nvestigated the role of PRMT5 in human acute myeloid leukemia (AML).

183 o infectious outcomes in patients with acute myeloid leukemia (AML).

184 icacy of kinase inhibitors in FLT3-ITD acute myeloid leukemia (AML).

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

186 a stem cells (LSCs) from patients with acute myeloid leukemia (AML).

187 sorders with risk of transformation to acute myeloid leukemia (AML).

188 ute lymphoblastic leukemia (B-ALL) and acute myeloid leukemia (AML).

189 ost frequent chromosome aberrations in acute myeloid leukemia (AML).

190 treatment-naive elderly patients with acute myeloid leukemia (AML).

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

192 ly associated with a poor prognosis in acute myeloid leukemia (AML).

193 ene expression and promotes relapse in acute myeloid leukemia (AML).

194 n mouse resulted in the development of acute myeloid leukemia (AML).

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

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

197 ed by adaptive or innate resistance in acute myeloid leukemia (AML).

198 d for treatment of IDH1-mutant (mIDH1) acute myeloid leukemia (AML).

199 esis and are frequently deregulated in acute myeloid leukemia (AML).

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

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

202 (1.17), and cervix (1.52), as well as acute myeloid leukemia (AML, 1.19), chronic myeloid leukemia (

203 he most common genetic lesion in adult acute myeloid leukemia (AML; about one third of cases), and th

204 ncytopenia with peripheral blasts, and acute myeloid leukemia (AML; French-American-British M2, t[8;2

205 Secondary acute myeloid leukemias (AMLs) evolving from an antecedent mye

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

207 l myelodysplastic syndromes (MDSs) and acute myeloid leukemias (AMLs).

208 ich is mutated in approximately 30% of acute myeloid leukemias (AMLs).

209 f childhood leukemia, particularly for acute myeloid leukemia, among children under 6 y of age, and w

210 bl) is a driver oncogene that causes chronic myeloid leukemia and a subset of acute lymphoid leukemia

211 Application of our methods to primary acute myeloid leukemia and breast cancer tumors quantified the

212 The significant increase of myeloid leukemia and CLL incidences was strongly correla

213 aging Americans; however, the incidences of myeloid leukemia and CLL significantly outpaced that of

214 s a low toxicity therapeutic for human acute myeloid leukemia and confirm the LMI approach as a robus

215 s an essential element in the progression of myeloid leukemia and could be an attractive target for t

216 d etoposide in pediatric patients with acute myeloid leukemia and may reduce rates of cardiomyopathy

217 ogether with corroborative findings in acute myeloid leukemia and myelodysplastic syndrome patient sa

218 eotide polymorphism array results from acute myeloid leukemia and prostate cancer datasets available

219 n receiving intensive chemotherapy for acute myeloid leukemia and relapsed acute lymphoblastic leukem

220 al heterogeneity is a common feature of many myeloid leukemias and a significant reason for treatment

221 hich is linked to the increased incidence of myeloid leukemias and production of myeloid-derived supp

222 ignancies (lymphoma, multiple myeloma, acute myeloid leukemia, and myelodysplastic syndrome).

223 equently in various cancers, including acute myeloid leukemia, and our results suggest that the effec

224 oblastoma, embryonal rhabdomyosarcoma, acute myeloid leukemia, and relapsed acute lymphoblastic leuke

225 en, adolescents, and young adults with acute myeloid leukemia are at high risk of life-threatening in

226 een using Msi2-reporter blast crisis chronic myeloid leukemia (bcCML) and identify several adhesion m

227 eloid leukemia (AML) expresses CD83 and that myeloid leukemia cell lines are readily killed by CD83 C

228 We analyzed 152 cells from three acute myeloid leukemia cell lines, resulting in a total of 255

229 ed the ability of BASIL to distinguish acute myeloid leukemia cells based on the phosphoproteome data

230 th our observations in mice, patient-derived myeloid leukemia cells exhibit KRAS/RAC1/ROS/NLRP3/IL-1b

231 Ro treatment in mouse and human myeloid leukemia cells results in an increase in differe

232 s, approximately 100, 1,000, and 10,000 U937 myeloid leukemia cells were processed, and a one-tenth o

233 We show that PARI is overexpressed in myeloid leukemia cells, and its knockdown reduces leukem

234 ved in differentiation of NB4 and HL60 human myeloid leukemia cells, suggesting that O-GlcNAcylation

235 e also common in clonal hematopoiesis, acute myeloid leukemia, chronic lymphocytic leukemia, and a va

236 otherapeutic used primarily to treat chronic myeloid leukemia (CML) and gastrointestinal stromal tumo

237 tivity and specificity in live human chronic myeloid leukemia (CML) cell lines.

238 ve been established for treatment of chronic myeloid leukemia (CML) in adults treated with tyrosine k

239 The acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) incidences remained constant prio

240 Chronic myeloid leukemia (CML) is a stem cell disease of the bon

241 A major obstacle to curing chronic myeloid leukemia (CML) is the intrinsic resistance of CM

242 Chronic myeloid leukemia (CML) is the model cancer, demonstratin

243 Patients with chronic myeloid leukemia (CML) often have comorbidities, at an i

244 Chronic myeloid leukemia (CML) originates in a hematopoietic ste

245 In chronic myeloid leukemia (CML) patients, tyrosine kinase inhibit

246 AMD1 was highly upregulated as chronic myeloid leukemia (CML) progressed from the chronic phase

247 riptome profiling in treatment-naive chronic myeloid leukemia (CML) stem/progenitor cells and identif

248 t clinical findings in patients with chronic myeloid leukemia (CML) suggest that the risk of molecula

249 that loss of K3 in a mouse model of chronic myeloid leukemia (CML) triggers the release of LSCs from

250 Chronic myeloid leukemia (CML), caused by constitutively active

251 d durable responses in patients with chronic myeloid leukemia (CML), issues of drug resistance and re

252 ase progression in a murine model of chronic myeloid leukemia (CML)-like myeloproliferative neoplasia

253 se inhibitor (TKI)-free remission in chronic myeloid leukemia (CML).

254 tween normal and cancerous states in chronic myeloid leukemia (CML).

255 conduct a retrospective analysis on an acute myeloid leukemia cohort, demonstrating the potential to

256 Using The Cancer Genome Atlas acute myeloid leukemia data set, we found an inverse correlati

257 with emerging therapeutic potential in acute myeloid leukemia, debilitating fibroses, and obesity-rel

258 als that leukemia stem cells (LSCs) in acute myeloid leukemia downregulate natural killer cell-activa

259 is an important therapeutic target in acute myeloid leukemia due to high incidence of mutations asso

260 ts with de novo or relapsed/refractory acute myeloid leukemia during the study period, with invasive

261 ploy a proteomics-based approach to identify myeloid leukemia factor 2 (MLF2) as a luminal component

262 Several acute myeloid leukemia genetic sub-types converge on high expr

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

264 odel the initiation and development of acute myeloid leukemia, identifying transcriptomic perturbatio

265 Emerging acute myeloid leukemia impaired mesenchymal osteogenic differe

266 Myeloid leukemia in Down syndrome (ML-DS) clonally evolv

267 an arrest proliferation, and, in the case of myeloid leukemia, induce differentiation of cancer cells

268 ependent predictor of infection during acute myeloid leukemia induction chemotherapy (IC) among clini

269 tions have now firmly established that acute myeloid leukemia is a highly dynamic oligoclonal disease

270 Acute myeloid leukemia is characterized by the accumulation of

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

272 e GVHD without impairing GVL against 2 acute myeloid leukemia lines (MLL-AF9-eGFP and C1498-luciferas

273 .6 nM in esophageal cancer KYSE520 and acute myeloid leukemia MV4;11 cells, respectively, and is capa

274 ve become the backbone of nonintensive acute myeloid leukemia/myelodysplastic syndrome (AML/MDS) trea

275 erived from patients with either MLL-r acute myeloid leukemia or MLL-r acute lymphoblastic leukemia (

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

277 ic stressors in the evolution of CH to acute myeloid leukemia or myelodysplastic syndrome.

278 ransplantation in multiple myeloma and acute myeloid leukemia patients indicate that cf-mRNA levels r

279 od mononuclear cells were sampled from acute myeloid leukemia patients longitudinally and single-cell

280 ll response of newly diagnosed elderly acute myeloid leukemia patients to a venetoclax and azacitidin

281 h AraC suggests that TLS inhibition in acute myeloid leukemia patients would increase the effectivene

282 th poor survival of Cytarabine-treated acute myeloid leukemia patients, qualifying AK1 as a patient s

283 However, in blast crisis chronic myeloid leukemia progenitors, loss of EZH2 expression an

284 en, adolescents, and young adults with acute myeloid leukemia, prophylaxis with caspofungin compared

285 y in patients with relapsed/refractory acute myeloid leukemia (R/R AML).

286 classified as CMV(+/-) The respective acute myeloid leukemia recipients were followed for disease re

287 our therapeutic armamentarium against acute myeloid leukemia relapse.

288 In t(8;21)+ acute myeloid leukemia, RUNX1 is fused to nearly the entire ET

289 rom the German Study Alliance Leukemia-Acute Myeloid Leukemia (SAL-AML) registry.

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

291 The boundary between MDS and secondary acute myeloid leukemia (sAML) is arbitrarily defined and has b

292 ssion of differentiation markers in clinical myeloid leukemia samples, suggesting that targeting PARI

293 of clinical outcomes in patients with acute myeloid leukemia showed no evidence of GOF for TP53 miss

294 n of m(6)A demethylase ALKBH5 in maintaining myeloid leukemia stem cells.

295 Late cardiotoxicity after pediatric acute myeloid leukemia therapy causes substantial morbidity an

296 and adolescents receiving treatment of acute myeloid leukemia, to those undergoing allogeneic HSCT pr

297 up among 1,022 pediatric patients with acute myeloid leukemia treated in the Children's Oncology Grou

298 acute promyelocytic leukemia (APL) and acute myeloid leukemia, we arrived at an integrative score in

299 chronic lymphocytic leukemia (CLL) and acute myeloid leukemia, we compare the performance of public s

300 nt mice, transduced HSPCs give rise to human myeloid leukemia, whereas untransduced HSPCs give rise t