ライフサイエンスコーパス: myeloid leukaemia

1 y METTL3 in this way are necessary for acute myeloid leukaemia.

2 MSI2-BCAT1 axis drives cancer progression in myeloid leukaemia.

3 ue to the development of MDS-like disease or myeloid leukaemia.

4 sed paediatric patients with high-risk acute myeloid leukaemia.

5 ohort of treatment-naive patients with acute myeloid leukaemia.

6 n patients with relapsed or refractory acute myeloid leukaemia.

7 is required for disease maintenance in acute myeloid leukaemia.

8 n previously untreated patients with chronic myeloid leukaemia.

9 ars (95% CI 0.2-2.4) for patients with acute myeloid leukaemia.

10 ndrome and myelodysplastic syndrome or acute myeloid leukaemia.

11 c patients with relapsed or refractory acute myeloid leukaemia.

12 ing treatment method for patients with acute myeloid leukaemia.

13 iagnosed patients with chronic-phase chronic myeloid leukaemia.

14 ed BTK in patients with CD117-positive acute myeloid leukaemia.

15 h advanced myelodysplastic syndrome or acute myeloid leukaemia.

16 r patients with relapsed or refractory acute myeloid leukaemia.

17 y is not suitable with newly diagnosed acute myeloid leukaemia.

18 onse mechanisms underlies the development of myeloid leukaemia.

19 e patients with relapsed or refractory acute myeloid leukaemia.

20 n patients with relapsed or refractory acute myeloid leukaemia.

21 is dose is also safe for patients with acute myeloid leukaemia.

22 ents with myelodysplastic syndrome and acute myeloid leukaemia.

23 igh-risk myelodysplastic syndromes and acute myeloid leukaemia.

24 r myelodysplastic syndrome, or de-novo acute myeloid leukaemia.

25 dose was not reached in patients with acute myeloid leukaemia.

26 h IDH2-mutated, relapsed or refractory acute myeloid leukaemia.

27 erapy in cancer, and was developed for acute myeloid leukaemia.

28 ch protects mice from death related to acute myeloid leukaemia.

29 ne-induced differentiation blockade in acute myeloid leukaemia.

30 ogical disorder rapidly progressing to acute myeloid leukaemia.

31 on chemotherapy in adult patients with acute myeloid leukaemia.

32 novel pharmacotherapeutic approach to acute myeloid leukaemia.

33 cell disorder myelodysplastic syndromes and myeloid leukaemia.

34 therapeutic target in t(8;21)-positive acute myeloid leukaemia.

35 levated in several cancers including chronic myeloid leukaemia.

36 y in an eight-year-old boy treated for acute myeloid leukaemia.

37 rds, represent a major risk factor for acute myeloid leukaemia.

38 usly untreated patients with high-risk acute myeloid leukaemia.

39 usly untreated patients with high-risk acute myeloid leukaemia.

40 mia and three (8%) had therapy-related acute myeloid leukaemia.

41 em cells (LSCs) and the development of acute myeloid leukaemia.

42 nduction chemotherapy in patients with acute myeloid leukaemia.

43 dentified using NGS in patients with chronic myeloid leukaemia.

44 d induction treatment of patients with acute myeloid leukaemia.

45 e kinase inhibitors in patients with chronic myeloid leukaemia.

46 or older patients with newly diagnosed acute myeloid leukaemia.

47 CR5 (CCR5Delta32/Delta32) to treat his acute myeloid leukaemia.

48 n patients with relapsed or refractory acute myeloid leukaemia.

49 as a potential therapeutic target for acute myeloid leukaemia.

50 ncephalopathy, neutropenic sepsis, and acute myeloid leukaemia]).

51 0, and June 26, 2012, 29 patients with acute myeloid leukaemia (19 newly diagnosed, ten relapsed or r

52 mmunotherapy and one patient developed acute myeloid leukaemia 5 months after receiving radioimmunoth

53 and Sept 9, 2014, 41 patients, 36 with acute myeloid leukaemia, a median age of 70 years (IQR 60-75)

54 ra A kinase (AAK) expression occurs in acute myeloid leukaemia; AAK inhibition is a promising therape

55 of older treatment-naive patients with acute myeloid leukaemia achieved a composite complete response

56 idence of myelodysplastic syndrome and acute myeloid leukaemia across PARP inhibitor groups was 0.73%

57 ed myelodysplastic syndrome, secondary acute myeloid leukaemia after myelodysplastic syndrome, or de-

58 omplete remission <=6 months) FLT3-ITD acute myeloid leukaemia after standard therapy with or without

59 one owing to tumour flare and one from acute myeloid leukaemia after study discontinuation.

60 the Wnt pathway in the development of acute myeloid leukaemia (AML) and find that the beta-catenin p

61 marrow cancer cells from patients with acute myeloid leukaemia (AML) and induce the differentiation o

62 cluding acute lymphoblastic leukaemia, acute myeloid leukaemia (AML) and myelodysplastic syndrome (MD

63 ove outcome in patients with childhood acute myeloid leukaemia (AML) by applying risk-directed therap

64 tion of oncogenes, and specifically in acute myeloid leukaemia (AML) by mutation.

65 tivation of key SE-associated genes in acute myeloid leukaemia (AML) cells.

66 Most patients with acute myeloid leukaemia (AML) die from progressive disease aft

67 Approximately 20% of patients with acute myeloid leukaemia (AML) have a mutation in FMS-like-tyro

68 in chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) have been advanced paradigms for

69 Available treatments for acute myeloid leukaemia (AML) have limited durable activity an

70 s) and 95% CIs for the risk of ALL and acute myeloid leukaemia (AML) in children aged 0-14 years at d

71 Acute myeloid leukaemia (AML) is a heterogeneous clonal disord

72 Acute myeloid leukaemia (AML) is a heterogeneous disease chara

73 Paediatric acute myeloid leukaemia (AML) is a heterogeneous disease chara

74 Acute myeloid leukaemia (AML) is a life threatening cancer for

75 Acute myeloid leukaemia (AML) is a malignancy of haematopoieti

76 Acute myeloid leukaemia (AML) is caused by acquired somatic mu

77 Acute myeloid leukaemia (AML) is characterized by a block in m

78 Acute myeloid leukaemia (AML) is characterized by subpopulatio

79 Current therapy for acute myeloid leukaemia (AML) is suboptimal with a high incide

80 Patients with acute myeloid leukaemia (AML) often achieve remission after th

81 ) are detected in approximately 20% of acute myeloid leukaemia (AML) patients and are associated with

82 Responses of acute myeloid leukaemia (AML) patients to cytarabine (Ara-C)-b

83 sponse of leukocytes in bone marrow of acute myeloid leukaemia (AML) patients, and the complex immune

84 human myeloid leukaemia cell lines and acute myeloid leukaemia (AML) samples, and downregulated upon

85 a well-defined model of MLL-rearranged acute myeloid leukaemia (AML) to demonstrate that transforming

86 tial anti-tumour gatekeeper in de novo acute myeloid leukaemia (AML) where it is significantly downre

87 care for newly diagnosed patients with acute myeloid leukaemia (AML) who are 75 years or older, or un

88 sociated genes varies widely, from 4% (acute myeloid leukaemia (AML)) to 19% (ovarian cancer), with a

89 to probe epigenetic vulnerabilities in acute myeloid leukaemia (AML), an aggressive haematopoietic ma

90 Myeloid malignancies, including acute myeloid leukaemia (AML), arise from the expansion of hae

91 as a non-oncogene addiction target in acute myeloid leukaemia (AML), bromodomain and extra terminal

92 in myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML), but the oncogenic changes due t

93 sm involved in cancer pathogenesis and acute myeloid leukaemia (AML), including the hematopoietic reg

94 enes 1 and 2 are frequently mutated in acute myeloid leukaemia (AML), low-grade glioma, cholangiocarc

95 eukaemia (ALL), and 50% for paediatric acute myeloid leukaemia (AML), recent efforts have focused on

96 the role of TEs in the pathogenesis of acute myeloid leukaemia (AML), we studied TE expression in sev

97 observed in about 35% of patients with acute myeloid leukaemia (AML).

98 ed myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML).

99 th myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML).

100 cute lymphoblastic leukaemia (ALL) and acute myeloid leukaemia (AML).

101 of various malignant diseases such as acute myeloid leukaemia (AML).

102 and clinical outcome in patients with Acute Myeloid Leukaemia (AML).

103 pression and frequently deregulated in acute myeloid leukaemia (AML).

104 lastic syndrome (MDS), but are rare in acute myeloid leukaemia (AML).

105 genes, NPM1, is frequently mutated in acute myeloid leukaemia (AML).

106 y patients with relapsed or refractory acute myeloid leukaemia (AML).

107 progenitor cells and in patients with acute myeloid leukaemia (AML).

108 associated with 10-15% of all cases of acute myeloid leukaemia (AML).

109 te lymphoblastic leukaemia (T-ALL) and acute myeloid leukaemia (AML).

110 ara-C is a key agent for treatment of acute myeloid leukaemia (AML); treatment decisions are made ra

111 IDH2 have been identified in gliomas, acute myeloid leukaemias (AML) and chondrosarcomas, and share

112 ronic myelomonocytic leukaemia (CMML), acute myeloid leukaemias (AML) and secondary AML (sAML).

113 vating Nf1 in mouse bone marrow and in acute myeloid leukaemias (AMLs) in which cooperating mutations

114 ly associated with the pathogenesis of acute myeloid leukaemias (AMLs).

115 ible patients had previously untreated acute myeloid leukaemia, an Eastern Cooperative Oncology Group

116 whom 10 (28%) initially presented with acute myeloid leukaemia and 26 (72%) initially presented with

117 fusion gene is a driver oncogene in chronic myeloid leukaemia and 30-50% of cases of adult acute lym

118 cation mutations in FLT3 are common in acute myeloid leukaemia and are associated with rapid relapse

119 bition of Notch signalling ameliorates acute myeloid leukaemia and demonstrates the pathogenic role o

120 s occurred in the placebo group due to acute myeloid leukaemia and depressed level of consciousness.

121 her proteins, previously implicated in acute myeloid leukaemia and development of the palate.

122 ctional dysregulation of these mechanisms in myeloid leukaemia and discuss opportunities for targetin

123 calation cohorts, and 11 patients with acute myeloid leukaemia and four patients with myelodysplastic

124 the BCOR gene have been identified in acute myeloid leukaemia and myelodysplastic syndrome among oth

125 tion with azacitidine in patients with acute myeloid leukaemia and myelodysplastic syndrome was initi

126 treated 93 patients: 35 patients with acute myeloid leukaemia and nine patients with myelodysplastic

127 se activity of PP2A is suppressed in chronic myeloid leukaemia and other malignancies characterised b

128 clusively, restricted to cell lines of acute myeloid leukaemia and prostate cancer that expressed the

129 ients with myelodysplastic syndrome or acute myeloid leukaemia and Shwachman-Diamond syndrome, an inh

130 Six of the 74 patients with acute myeloid leukaemia and six of the 19 patients with myelod

131 e-escalation cohorts, 28 patients with acute myeloid leukaemia and six patients with myelodysplastic

132 s and a high risk of cancer, including acute myeloid leukaemia and squamous cell carcinomas.

133 as been demonstrated to have a role in acute myeloid leukaemia and stem cell function, but its role i

134 19 (49%) of 39 patients had secondary acute myeloid leukaemia and three (8%) had therapy-related acu

135 vise the current goals of therapy of chronic myeloid leukaemia and to incorporate the influence of th

136 oid leukaemia, 0.959 (0.933-0.986) for acute myeloid leukaemia, and 0.940 (0.897-0.984) for non-Hodgk

137 Further, in blast crisis chronic myeloid leukaemia, and a subset of acute myeloid leukaem

138 in cancers, such as low-grade gliomas, acute myeloid leukaemia, and chondrosarcomas, has been the ide

139 tions, side-effects, and outcomes of chronic myeloid leukaemia, and discusses the possibility of cure

140 B- and mantle-cell lymphomas, chronic myeloid leukaemia, and multiple myeloma, however, expres

141 loid leukaemia, relapsed or refractory acute myeloid leukaemia, and myelodysplastic syndromes; here w

142 atients with myelodysplastic syndrome, acute myeloid leukaemia, and myelofibrosis.

143 oncogenic transcriptional programs in acute myeloid leukaemia, and suggest that displacement of ENL

144 ials have shown promise, especially in acute myeloid leukaemia, and therefore the evaluation of resis

145 ital admissions in older patients with acute myeloid leukaemia are unavoidable and driven by the illn

146 k karyotype, the presence of secondary acute myeloid leukaemia arising from previous myelodysplastic

147 ion of CK2 could be of value in treatment of myeloid leukaemias, as well as other tumour types in whi

148 atients diagnosed with and treated for acute myeloid leukaemia at two tertiary care hospitals in the

149 f health utilities for chronic-phase chronic myeloid leukaemia (base case 0.89, range 0-1) and the an

150 or treatment of relapsed or refractory acute myeloid leukaemia; based on activity data, gilteritinib

151 BI) in adults with advanced refractory acute myeloid leukaemia before allogeneic haemopoietic stem-ce

152 ailable data, and 2 (8%) progressed to acute myeloid leukaemia before receiving treatment.

153 rate the influence of the underlying chronic myeloid leukaemia biology on directing therapeutic manag

154 D117-mediated proliferation of primary acute myeloid leukaemia blast cells (p=0.028).

155 We obtained acute myeloid leukaemia blast cells from 29 patients.

156 We isolated primary acute myeloid leukaemia blast cells from heparinised blood and

157 We obtained acute myeloid leukaemia blast cells from unselected patients a

158 al cells, and proliferation of primary acute myeloid leukaemia blast cells.

159 ients were aged 60 years or older with acute myeloid leukaemia but unsuitable for intensive chemother

160 in human blast crisis CML and de novo acute myeloid leukaemia, but also predicts disease outcome in

161 icacy in myelodysplastic syndromes and acute myeloid leukaemia, but complete tumour responses are inf

162 enrolled patients with a diagnosis of acute myeloid leukaemia by WHO criteria and aged 18-70 years i

163 In contrast, acute myeloid leukaemia cases did not appear to have defects a

164 d data on myelodysplastic syndrome and acute myeloid leukaemia cases from ClinicalTrials.gov.

165 r-related myelodysplastic syndrome and acute myeloid leukaemia cases reported in WHO's pharmacovigila

166 rent types of cancer cells (KU812, a chronic myeloid leukaemia cell line; and DU145, a prostate cance

167 Acetylated C/EBPalpha is enriched in human myeloid leukaemia cell lines and acute myeloid leukaemia

168 TL3 as an essential gene for growth of acute myeloid leukaemia cells in two distinct genetic screens.

169 s a chemotherapy-sensitive subgroup of acute myeloid leukaemia characterised by the presence of the P

170 of PF-04449913 in adult patients with acute myeloid leukaemia, chronic myeloid leukaemia, chronic my

171 tients with acute myeloid leukaemia, chronic myeloid leukaemia, chronic myelomonocytic leukaemia, mye

172 ades, leukaemia stem cells (LSCs) in chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML

173 Chronic myeloid leukaemia (CML) arises after transformation of a

174 The prognosis of chronic myeloid leukaemia (CML) has improved remarkably over the

175 sed Philadelphia chromosome-positive chronic myeloid leukaemia (CML) in chronic phase after a minimum

176 ivated and functionally required for chronic myeloid leukaemia (CML) in humans and in mouse models of

177 Chronic myeloid leukaemia (CML) is a myeloproliferative disorder

178 Chronic myeloid leukaemia (CML) is driven by the activity of the

179 Chronic Myeloid Leukaemia (CML) is initiated and maintained by t

180 Chronic myeloid leukaemia (CML) is quintessential to this hypoth

181 (TKIs), the treatment of choice for chronic myeloid leukaemia (CML), can cause lower gastrointestina

182 eradicate LSC in chronic phase (CP) chronic myeloid leukaemia (CML).

183 issues in the clinical management of chronic myeloid leukaemia (CML).

184 ilar observations are made on the TCGA acute myeloid leukaemia cohort, confirming the general trends

185 l trials of ibrutinib in patients with acute myeloid leukaemia commence, the data suggest not all pat

186 ent of newly diagnosed chronic-phase chronic myeloid leukaemia compared with imatinib could not be as

187 e risk of myelodysplastic syndrome and acute myeloid leukaemia compared with placebo treatment (Peto

188 Therapeutic advances in chronic myeloid leukaemia continue to circumvent the challenges

189 Chronic myeloid leukaemia continues to instruct us in the mechan

190 inase inhibitors, most patients with chronic myeloid leukaemia could enjoy a near normal life expecta

191 lodysplastic syndromes or oligoblastic acute myeloid leukaemia (defined as blasts >=20% but <=30%) re

192 and t(16;21) that are associated with acute myeloid leukaemia disrupt two closely related genes term

193 In older patients with newly diagnosed acute myeloid leukaemia, efficacy and safety did not differ by

194 g regimen for patients with refractory acute myeloid leukaemia, especially for those transplant centr

195 The outcome acute myeloid leukaemia evolution or disease progression occur

196 f intensive induction chemotherapy for acute myeloid leukaemia (excluding acute promyelocytic leukaem

197 2014, we screened 121 patients with chronic myeloid leukaemia for BCR-ABL1 kinase domain mutation.

198 cases of myelodysplastic syndrome and acute myeloid leukaemia, for which data are scarce.

199 Patients with acute myeloid leukaemia frequently have thrombocytopenia durin

200 Survivors of Hodgkin lymphoma, acute myeloid leukaemia, genitourinary cancers other than blad

201 lts obtained from sequencing a typical acute myeloid leukaemia genome, and its matched normal counter

202 of ETP ALL was similar to that of normal and myeloid leukaemia haematopoietic stem cells.

203 ell activity and an aggressive form of acute myeloid leukaemia harbouring the MLL-AF9 oncogene.

204 it of FLT3 inhibitors in patients with acute myeloid leukaemia has been limited by rapid generation o

205 The management of chronic myeloid leukaemia has been revolutionized by targeted mo

206 less than 10 years, the prognosis of chronic myeloid leukaemia has changed from that of a fatal disea

207 hibitors (TKIs) for the treatment of chronic myeloid leukaemia has changed patient outcome and, conse

208 tandem duplication (FLT3-ITD)-positive acute myeloid leukaemia have a poor prognosis, including high

209 ree remission (TFR) in patients with chronic myeloid leukaemia have discontinued tyrosine kinase inhi

210 Roughly 80% of patients with acute myeloid leukaemia have high activity of Bruton's tyrosin

211 Outcomes for younger patients with acute myeloid leukaemia have moderately improved over the past

212 ovide new insights into the biology of acute myeloid leukaemia, highlight potential therapeutic limit

213 nt cancers: acute lymphoid leukaemias, acute myeloid leukaemias, Hodgkin's lymphomas, non-Hodgkin lym

214 alterations in osteoblasts can induce acute myeloid leukaemia, identify molecular signals leading to

215 In gliomas and acute myeloid leukaemias, IDH1/2 mutations confer gain-of-func

216 Treatment-free remission in chronic myeloid leukaemia-ie, achievement of a sustained deep mo

217 nosomy 7 myelodysplasia progressing to acute myeloid leukaemia in a 53 year old male who presented wi

218 ients (aged >18 years) with refractory acute myeloid leukaemia in active phase of disease, who had re

219 ve overall survival in patients with chronic myeloid leukaemia in chronic phase (CML-CP).

220 lable for treatment of patients with chronic myeloid leukaemia in chronic phase (CML-CP).

221 ith Philadelphia chromosome-positive chronic myeloid leukaemia in chronic phase and Eastern Cooperati

222 s frontline therapy in patients with chronic myeloid leukaemia in chronic phase in relation to the pr

223 Optimal management of patients with chronic myeloid leukaemia in chronic phase with suboptimal cytog

224 l, randomised trial in patients with chronic myeloid leukaemia in chronic phase with suboptimal cytog

225 ted patients (aged >/=18 years) with chronic myeloid leukaemia in first chronic phase who had receive

226 ited patients (aged >=18 years) with chronic myeloid leukaemia in first chronic phase, who had receiv

227 ligible patients were 18-70 years, had acute myeloid leukaemia in first or consecutive complete haema

228 ressive, fully-penetrant and cell-autonomous myeloid leukaemia in mice, pointing to a causative role

229 atopoietic differentiation and induced acute myeloid leukaemia in murine models.

230 in the USA for the treatment of mIDH1 acute myeloid leukaemia in newly diagnosed patients ineligible

231 r good value as frontline therapy in chronic myeloid leukaemia in order to achieve sustained deep mol

232 12 patients received treatment for acute myeloid leukaemia-including the two patients initially d

233 ents with myelodysplastic syndromes or acute myeloid leukaemia, increased beta-catenin signalling and

234 Acute myeloid leukaemia is a fatal disease for most patients.

235 Acute myeloid leukaemia is a highly malignant haematopoietic t

236 Chronic myeloid leukaemia is a paradigmatic haematopoietic stem

237 eer-unrelated donor HCT for refractory acute myeloid leukaemia is not inferior to that of patients re

238 erated by the t(8;21) translocation in acute myeloid leukaemia, is a transcription factor implicated

239 Meta-analysis of the acute myeloid leukaemia, low-grade glioma, cholangiocarcinoma

240 In mouse transplantation acute myeloid leukaemia models, a deficiency in intracellular

241 second primary brain tumour (n=1), and acute myeloid leukaemia (n=1), and in the placebo group were a

242 of myelodysplastic syndrome (n=99) and acute myeloid leukaemia (n=79) related to PARP inhibitor thera

243 x patients (6%) receiving momelotinib (acute myeloid leukaemia [n=2], respiratory failure [n=2, with

244 Patients with acute myeloid leukaemia of any subtype except M3 and M7 were s

245 2-22 years with relapsed or refractory acute myeloid leukaemia or acute leukaemia of ambiguous lineag

246 We included patients with acute myeloid leukaemia or acute lymphocytic leukaemia, who re

247 chemotherapy), and had newly diagnosed acute myeloid leukaemia or high-risk myelodysplastic syndrome,

248 sible in patients with newly diagnosed acute myeloid leukaemia or high-risk myelodysplastic syndrome.

249 abine in patients with newly diagnosed acute myeloid leukaemia or high-risk myelodysplastic syndrome.

250 2a if they had relapsed or refractory acute myeloid leukaemia or myelodysplastic syndrome with bone

251 y given guadecitabine in patients with acute myeloid leukaemia or myelodysplastic syndrome.

252 CT for older or comorbid patients with acute myeloid leukaemia or myelodysplastic syndrome.

253 ber of older or comorbid patients with acute myeloid leukaemia or myelodysplastic syndrome.

254 plasm, the presence of therapy-related acute myeloid leukaemia, or being 65 years or older.

255 vo versus secondary or therapy-related acute myeloid leukaemia, or TP53(mut) status.

256 ndrome and myelodysplastic syndrome or acute myeloid leukaemia owing to both therapy-resistant diseas

257 Using leukaemia cell lines and primary acute myeloid leukaemia patient samples, we show that low expr

258 sequencing and standard RNA-Seq for chronic myeloid leukaemia patient samples.

259 Treatment of a T315I chronic myeloid leukaemia patient with axitinib resulted in a ra

260 Natural killer cells from acute myeloid leukaemia patients (AML-NK) show a dramatic impa

261 ASXL2 is frequently mutated in acute myeloid leukaemia patients with t(8;21).

262 shown to be upregulated in a subset of acute myeloid leukaemia patients, conferring susceptibility fo

263 nic myeloid leukaemia, and a subset of acute myeloid leukaemias, PRH is aberrantly localised and its

264 bute to 2HG oncogenicity in glioma and acute myeloid leukaemia progression, with the promise for inno

265 252 adults with relapsed or refractory acute myeloid leukaemia received oral gilteritinib once daily

266 lodysplastic syndromes or oligoblastic acute myeloid leukaemia refractory to hypomethylating agents.

267 lodysplastic syndromes or oligoblastic acute myeloid leukaemia refractory to hypomethylating agents.

268 horts of patients with treatment-naive acute myeloid leukaemia, relapsed or refractory acute myeloid

269 y risk of myelodysplastic syndrome and acute myeloid leukaemia related to PARP inhibition versus plac

270 cases of myelodysplastic syndrome and acute myeloid leukaemia related to PARP inhibitor therapy were

271 e risk of myelodysplastic syndrome and acute myeloid leukaemia related to PARP inhibitors, via a syst

272 r children with relapsed or refractory acute myeloid leukaemia remain poor.

273 ve chemotherapy regimens used to treat acute myeloid leukaemia routinely result in serious infections

274 led and included in the study: 28 with acute myeloid leukaemia, six with myelodysplastic syndrome, fi

275 Older adults (>/=60 years of age) with acute myeloid leukaemia spend a substantial proportion of thei

276 to cancer progression and the development of myeloid leukaemia stem cell therapeutic resistance.

277 in the treatment of newly diagnosed chronic myeloid leukaemia suggest that this first-generation tyr

278 s with heavily relapsed and refractory acute myeloid leukaemia suggests that this combination should

279 Therapy-related acute myeloid leukaemia (t-AML) and therapy-related myelodyspl

280 oss in alkylating chemotherapy-related acute myeloid leukaemia (t-AML) suggests that DNA mismatch rep

281 ib has shown potent activity against chronic myeloid leukaemia that is resistant to available treatme

282 ntres with myelodysplastic syndrome or acute myeloid leukaemia that was refractory to or had relapsed

283 al understanding of the BTK pathway in acute myeloid leukaemia to identify clinically relevant diagno

284 cutive patients newly diagnosed with chronic myeloid leukaemia treated with first-line tyrosine kinas

285 Standfirst | In 2018, the acute myeloid leukaemia treatment landscape expanded notably,

286 Patient-derived acute myeloid leukaemia tumour cells exhibit high sensitivity

287 iac arrest (one [1%]), therapy-related acute myeloid leukaemia (two [3%]), and haematopoietic stem-ce

288 myelodysplastic syndrome, five with chronic myeloid leukaemia (two with chronic-phase and three with

289 e risk of myelodysplastic syndrome and acute myeloid leukaemia versus placebo treatment.

290 s of acute lymphoblastic leukaemia and acute myeloid leukaemia was found to reprogram non-stem bulk l

291 transcriptomes from 982 patients with acute myeloid leukaemia, we identified frequent overlap of mut

292 Eligible patients with acute myeloid leukaemia were aged 18 years of age or older and

293 developed myelodysplastic syndrome or acute myeloid leukaemia were eligible without additional restr

294 ients with myelodysplastic syndrome or acute myeloid leukaemia who are thrombocytopenic and unable to

295 d patients aged 18 years or older with acute myeloid leukaemia who either were refractory to inductio

296 5 years) patients with treatment-naive acute myeloid leukaemia who were not candidates for intensive

297 rdingly, we propose that patients with acute myeloid leukaemia whose blast cells express CD117 should

298 progenitors leading to development of acute myeloid leukaemia with common chromosomal aberrations an

299 y is feasible for some patients with chronic myeloid leukaemia with deep molecular responses; however

300 had a treatment-related adverse event (acute myeloid leukaemia) with an outcome of death.