ライフサイエンスコーパス: myeloid leukaemia

1 n patients with relapsed or refractory acute myeloid leukaemia.

2 e patients with relapsed or refractory acute myeloid leukaemia.

3 n patients with relapsed or refractory acute myeloid leukaemia.

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

5 ents with myelodysplastic syndrome and acute myeloid leukaemia.

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

7 igh-risk myelodysplastic syndromes and acute myeloid leukaemia.

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

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

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

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

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

13 ne-induced differentiation blockade in acute myeloid leukaemia.

14 ogical disorder rapidly progressing to acute myeloid leukaemia.

15 on chemotherapy in adult patients with acute myeloid leukaemia.

16 novel pharmacotherapeutic approach to acute myeloid leukaemia.

17 cell disorder myelodysplastic syndromes and myeloid leukaemia.

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

19 levated in several cancers including chronic myeloid leukaemia.

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

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

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

23 for patients in the chronic phase of chronic myeloid leukaemia.

24 ed with distinct types of acute lymphoid and myeloid leukaemia.

25 or example, MLL-AF9 is found mainly in acute myeloid leukaemia.

26 n, NUP214, has also been implicated in human myeloid leukaemia.

27 th Nf1 gene loss during progression to acute myeloid leukaemia.

28 etic hallmark for the M4/M5 subtype of acute myeloid leukaemia.

29 uction pathway is often deregulated in human myeloid leukaemia.

30 as a potential therapeutic target for acute myeloid leukaemia.

31 n patients with relapsed or refractory acute myeloid leukaemia.

32 is required for disease maintenance in acute myeloid leukaemia.

33 n previously untreated patients with chronic myeloid leukaemia.

34 ing treatment method for patients with acute myeloid leukaemia.

35 iagnosed patients with chronic-phase chronic myeloid leukaemia.

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

37 h advanced myelodysplastic syndrome or acute myeloid leukaemia.

38 r patients with relapsed or refractory acute myeloid leukaemia.

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

40 vated by proviral integration in BXH2 murine myeloid leukaemias.

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

42 0, and June 26, 2012, 29 patients with acute myeloid leukaemia (19 newly diagnosed, ten relapsed or r

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

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

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

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

47 In acute myeloid leukaemia age is such an important factor that i

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

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

50 The association between acute myeloid leukaemia (AML) and the aberrant expression of H

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

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

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

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

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

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

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

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

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

60 Acute myeloid leukaemia (AML) is a major haematopoietic malign

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

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

63 Murine radiation-induced acute myeloid leukaemia (AML) is characterized by loss of one

64 Acute myeloid leukaemia (AML) is characterized by subpopulatio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 ng myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML).

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

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

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

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

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

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

95 on t(9;11), the majority of cases were acute myeloid leukaemias (AMLs) involving immature myeloblasts

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

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

98 nstrated in acute myeloid leukaemia, chronic myeloid leukaemia and acute lymphoid leukaemia, suggesti

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

100 Recently, studies of acute myeloid leukaemia and cutaneous T cell lymphoma patients

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

121 n genes, including one associated with acute myeloid leukaemia arising from the recurrent translocati

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

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

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

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

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

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

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

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

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

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

132 Smac sensitized human acute myeloid leukaemia blasts to cytochrome c-induced activat

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

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

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

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

137 or this study the well characterised chronic myeloid leukaemia cell line KYO-1 was selected and oligo

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

139 )(p11;q11-12), is found in both lymphoma and myeloid leukaemia cells from these patients, supporting

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

141 helial cells, and also following exposure of myeloid leukaemia cells to etoposide.

142 at highest levels in the testis and certain myeloid leukaemia cells.

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

144 -1 DNA methylation was demonstrated in acute myeloid leukaemia, chronic myeloid leukaemia and acute l

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

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

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

148 In chronic myeloid leukaemia (CML) expression of the chimeric tyros

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

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

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

152 Chronic myeloid leukaemia (CML) is a clonal disorder of the plur

153 Chronic myeloid leukaemia (CML) is a myeloproliferative disorder

154 Chronic myeloid leukaemia (CML) is characterized by the presence

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

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

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

158 ided a curative treatment option for chronic myeloid leukaemia (CML) over the past 20-30 years.

159 yrosine kinase inhibitor imatinib in chronic myeloid leukaemia (CML) serves as a model for molecularl

160 Chronic myeloid leukaemia (CML), a hematopoietic stem cell disor

161 The clonogenic cells of chronic myeloid leukaemia (CML), unlike normal haemopoietic prog

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

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

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

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

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

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

168 Chronic myeloid leukaemia continues to instruct us in the mechan

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

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

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

172 The outcome acute myeloid leukaemia evolution or disease progression occur

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

174 abnormality associated primarily with acute myeloid leukaemia (FAB M2 and M4).

175 In acute myeloid leukaemia, for instance, response to therapy is

176 studies identify HOXA9 as an important human myeloid leukaemia gene and suggest an important role for

177 ormation and identify a number of new murine myeloid leukaemia genes.

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

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

180 an important role for nucleoporins in human myeloid leukaemia given that a second nucleoporin, NUP21

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

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

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

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

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

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

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

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

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

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

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

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

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

194 Retroviruses induce myeloid leukaemia in BXH-2 mice by the insertional mutat

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

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

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

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

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

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

201 ed to prevent relapse in patients with acute myeloid leukaemia in first remission.

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

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

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

205 Chronic myeloid leukaemia is a haemopoietic stem cell disorder,

206 Acute myeloid leukaemia is a highly malignant haematopoietic t

207 Chronic myeloid leukaemia is a paradigmatic haematopoietic stem

208 for this is that in older patients the acute myeloid leukaemia is more likely to have arisen from a p

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

210 ich is also a fusion partner of MLL in acute myeloid leukaemia, is a member of a family of novel GTP

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

212 tudy, we used the p53 negative human chronic myeloid leukaemia K562 cell line.

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

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

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

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

217 2a if they had relapsed or refractory acute myeloid leukaemia or myelodysplastic syndrome with bone

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

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

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

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

222 )(p15;p15) translocation found in some human myeloid leukaemia patients.

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

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

225 252 adults with relapsed or refractory acute myeloid leukaemia received oral gilteritinib once daily

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

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

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

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

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

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

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

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

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

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

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

237 in the Medical Research Council's 10th acute myeloid leukaemia trial (MRC AML 10), which was open to

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

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

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

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

242 imatinib is used in the treatment of chronic myeloid leukaemia, where it targets the intracellular Bc

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

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

245 5 years) patients with treatment-naive acute myeloid leukaemia who were not candidates for intensive

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

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

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

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