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1 tion in patients with relapsed or refractory acute myeloid leukaemia.
2 a after myelodysplastic syndrome, or de-novo acute myeloid leukaemia.
3 erated dose was not reached in patients with acute myeloid leukaemia.
4 hemotherapy in cancer, and was developed for acute myeloid leukaemia.
5 s, which protects mice from death related to acute myeloid leukaemia.
6 oncogene-induced differentiation blockade in acute myeloid leukaemia.
7 ematological disorder rapidly progressing to acute myeloid leukaemia.
8 nduction chemotherapy in adult patients with acute myeloid leukaemia.
9 ential novel pharmacotherapeutic approach to acute myeloid leukaemia.
10 ntial therapeutic target in t(8;21)-positive acute myeloid leukaemia.
11 therapy in an eight-year-old boy treated for acute myeloid leukaemia.
12 mustards, represent a major risk factor for acute myeloid leukaemia.
13 the cohort of treatment-naive patients with acute myeloid leukaemia.
14 ype, for example, MLL-AF9 is found mainly in acute myeloid leukaemia.
15 ate with Nf1 gene loss during progression to acute myeloid leukaemia.
16 ytogenetic hallmark for the M4/M5 subtype of acute myeloid leukaemia.
17 inib in patients with relapsed or refractory acute myeloid leukaemia.
18 AF9, is required for disease maintenance in acute myeloid leukaemia.
19 enzyme as a potential therapeutic target for acute myeloid leukaemia.
20 promising treatment method for patients with acute myeloid leukaemia.
21 orylated BTK in patients with CD117-positive acute myeloid leukaemia.
22 ts with advanced myelodysplastic syndrome or acute myeloid leukaemia.
23 ded for patients with relapsed or refractory acute myeloid leukaemia.
24 to some patients with relapsed or refractory acute myeloid leukaemia.
25 bine in patients with relapsed or refractory acute myeloid leukaemia.
26 hat this dose is also safe for patients with acute myeloid leukaemia.
27 ated by METTL3 in this way are necessary for acute myeloid leukaemia.
28 n patients with myelodysplastic syndrome and acute myeloid leukaemia.
29 with high-risk myelodysplastic syndromes and acute myeloid leukaemia.
30 olic encephalopathy, neutropenic sepsis, and acute myeloid leukaemia]).
31 9, 2010, and June 26, 2012, 29 patients with acute myeloid leukaemia (19 newly diagnosed, ten relapse
32 radioimmunotherapy and one patient developed acute myeloid leukaemia 5 months after receiving radioim
33 2013, and Sept 9, 2014, 41 patients, 36 with acute myeloid leukaemia, a median age of 70 years (IQR 6
34 half of older treatment-naive patients with acute myeloid leukaemia achieved a composite complete re
35 advanced myelodysplastic syndrome, secondary acute myeloid leukaemia after myelodysplastic syndrome,
37 ole of the Wnt pathway in the development of acute myeloid leukaemia (AML) and find that the beta-cat
38 bone marrow cancer cells from patients with acute myeloid leukaemia (AML) and induce the differentia
40 o improve outcome in patients with childhood acute myeloid leukaemia (AML) by applying risk-directed
46 os (ORs) and 95% CIs for the risk of ALL and acute myeloid leukaemia (AML) in children aged 0-14 year
55 T3-ITD) are detected in approximately 20% of acute myeloid leukaemia (AML) patients and are associate
57 nal response of leukocytes in bone marrow of acute myeloid leukaemia (AML) patients, and the complex
58 ed in human myeloid leukaemia cell lines and acute myeloid leukaemia (AML) samples, and downregulated
59 e use a well-defined model of MLL-rearranged acute myeloid leukaemia (AML) to demonstrate that transf
60 essential anti-tumour gatekeeper in de novo acute myeloid leukaemia (AML) where it is significantly
61 ity-associated genes varies widely, from 4% (acute myeloid leukaemia (AML)) to 19% (ovarian cancer),
62 roach to probe epigenetic vulnerabilities in acute myeloid leukaemia (AML), an aggressive haematopoie
63 f BRD4 as a non-oncogene addiction target in acute myeloid leukaemia (AML), bromodomain and extra ter
64 echanism involved in cancer pathogenesis and acute myeloid leukaemia (AML), including the hematopoiet
65 IDH) genes 1 and 2 are frequently mutated in acute myeloid leukaemia (AML), low-grade glioma, cholang
66 stic leukaemia (ALL), and 50% for paediatric acute myeloid leukaemia (AML), recent efforts have focus
67 igate the role of TEs in the pathogenesis of acute myeloid leukaemia (AML), we studied TE expression
80 alogue ara-C is a key agent for treatment of acute myeloid leukaemia (AML); treatment decisions are m
81 1) and IDH2 have been identified in gliomas, acute myeloid leukaemias (AML) and chondrosarcomas, and
82 ing chronic myelomonocytic leukaemia (CMML), acute myeloid leukaemias (AML) and secondary AML (sAML).
83 inactivating Nf1 in mouse bone marrow and in acute myeloid leukaemias (AMLs) in which cooperating mut
84 location t(9;11), the majority of cases were acute myeloid leukaemias (AMLs) involving immature myelo
86 duplication mutations in FLT3 are common in acute myeloid leukaemia and are associated with rapid re
88 l inhibition of Notch signalling ameliorates acute myeloid leukaemia and demonstrates the pathogenic
89 ose-escalation cohorts, and 11 patients with acute myeloid leukaemia and four patients with myelodysp
90 ombination with azacitidine in patients with acute myeloid leukaemia and myelodysplastic syndrome was
91 ed and treated 93 patients: 35 patients with acute myeloid leukaemia and nine patients with myelodysp
93 5 dose-escalation cohorts, 28 patients with acute myeloid leukaemia and six patients with myelodyspl
94 alities and a high risk of cancer, including acute myeloid leukaemia and squamous cell carcinomas.
95 tein has been demonstrated to have a role in acute myeloid leukaemia and stem cell function, but its
96 lymphoid leukaemia, 0.959 (0.933-0.986) for acute myeloid leukaemia, and 0.940 (0.897-0.984) for non
97 certain cancers, such as low-grade gliomas, acute myeloid leukaemia, and chondrosarcomas, has been t
98 te myeloid leukaemia, relapsed or refractory acute myeloid leukaemia, and myelodysplastic syndromes;
100 ulates oncogenic transcriptional programs in acute myeloid leukaemia, and suggest that displacement o
101 cal trials have shown promise, especially in acute myeloid leukaemia, and therefore the evaluation of
102 y hospital admissions in older patients with acute myeloid leukaemia are unavoidable and driven by th
103 l human genes, including one associated with acute myeloid leukaemia arising from the recurrent trans
104 lder patients diagnosed with and treated for acute myeloid leukaemia at two tertiary care hospitals i
105 rget for treatment of relapsed or refractory acute myeloid leukaemia; based on activity data, gilteri
106 ion (TBI) in adults with advanced refractory acute myeloid leukaemia before allogeneic haemopoietic s
113 ivated in human blast crisis CML and de novo acute myeloid leukaemia, but also predicts disease outco
114 wn efficacy in myelodysplastic syndromes and acute myeloid leukaemia, but complete tumour responses a
115 We enrolled patients with a diagnosis of acute myeloid leukaemia by WHO criteria and aged 18-70 y
117 fy METTL3 as an essential gene for growth of acute myeloid leukaemia cells in two distinct genetic sc
118 emia is a chemotherapy-sensitive subgroup of acute myeloid leukaemia characterised by the presence of
119 Apaf-1 DNA methylation was demonstrated in acute myeloid leukaemia, chronic myeloid leukaemia and a
120 study of PF-04449913 in adult patients with acute myeloid leukaemia, chronic myeloid leukaemia, chro
121 Similar observations are made on the TCGA acute myeloid leukaemia cohort, confirming the general t
122 linical trials of ibrutinib in patients with acute myeloid leukaemia commence, the data suggest not a
123 (8;21) and t(16;21) that are associated with acute myeloid leukaemia disrupt two closely related gene
124 tioning regimen for patients with refractory acute myeloid leukaemia, especially for those transplant
126 urse of intensive induction chemotherapy for acute myeloid leukaemia (excluding acute promyelocytic l
130 e results obtained from sequencing a typical acute myeloid leukaemia genome, and its matched normal c
131 stem-cell activity and an aggressive form of acute myeloid leukaemia harbouring the MLL-AF9 oncogene.
132 benefit of FLT3 inhibitors in patients with acute myeloid leukaemia has been limited by rapid genera
134 ngs provide new insights into the biology of acute myeloid leukaemia, highlight potential therapeutic
135 mportant cancers: acute lymphoid leukaemias, acute myeloid leukaemias, Hodgkin's lymphomas, non-Hodgk
136 enetic alterations in osteoblasts can induce acute myeloid leukaemia, identify molecular signals lead
138 ve, monosomy 7 myelodysplasia progressing to acute myeloid leukaemia in a 53 year old male who presen
139 or patients (aged >18 years) with refractory acute myeloid leukaemia in active phase of disease, who
142 f patients with myelodysplastic syndromes or acute myeloid leukaemia, increased beta-catenin signalli
144 ation for this is that in older patients the acute myeloid leukaemia is more likely to have arisen fr
145 volunteer-unrelated donor HCT for refractory acute myeloid leukaemia is not inferior to that of patie
146 ne, which is also a fusion partner of MLL in acute myeloid leukaemia, is a member of a family of nove
147 in generated by the t(8;21) translocation in acute myeloid leukaemia, is a transcription factor impli
150 2), a second primary brain tumour (n=1), and acute myeloid leukaemia (n=1), and in the placebo group
151 for six patients (6%) receiving momelotinib (acute myeloid leukaemia [n=2], respiratory failure [n=2,
152 1 and 2a if they had relapsed or refractory acute myeloid leukaemia or myelodysplastic syndrome with
153 neously given guadecitabine in patients with acute myeloid leukaemia or myelodysplastic syndrome.
156 s chronic myeloid leukaemia, and a subset of acute myeloid leukaemias, PRH is aberrantly localised an
157 contribute to 2HG oncogenicity in glioma and acute myeloid leukaemia progression, with the promise fo
158 2015, 252 adults with relapsed or refractory acute myeloid leukaemia received oral gilteritinib once
159 in cohorts of patients with treatment-naive acute myeloid leukaemia, relapsed or refractory acute my
160 ntensive chemotherapy regimens used to treat acute myeloid leukaemia routinely result in serious infe
161 enrolled and included in the study: 28 with acute myeloid leukaemia, six with myelodysplastic syndro
164 MSH2 loss in alkylating chemotherapy-related acute myeloid leukaemia (t-AML) suggests that DNA mismat
165 cal centres with myelodysplastic syndrome or acute myeloid leukaemia that was refractory to or had re
166 ological understanding of the BTK pathway in acute myeloid leukaemia to identify clinically relevant
167 imens in the Medical Research Council's 10th acute myeloid leukaemia trial (MRC AML 10), which was op
169 models of acute lymphoblastic leukaemia and acute myeloid leukaemia was found to reprogram non-stem
171 Patients with myelodysplastic syndrome or acute myeloid leukaemia who are thrombocytopenic and una
172 nrolled patients aged 18 years or older with acute myeloid leukaemia who either were refractory to in
173 (>/=65 years) patients with treatment-naive acute myeloid leukaemia who were not candidates for inte
174 Accordingly, we propose that patients with acute myeloid leukaemia whose blast cells express CD117
175 mphoid progenitors leading to development of acute myeloid leukaemia with common chromosomal aberrati
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