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1 anced phase Philadelphia chromosome-positive acute myeloid leukaemia).
2 diagnosed paediatric patients with high-risk acute myeloid leukaemia.
3 inib in patients with relapsed or refractory acute myeloid leukaemia.
4 AF9, is required for disease maintenance in acute myeloid leukaemia.
5 .99 years (95% CI 0.2-2.4) for patients with acute myeloid leukaemia.
6 promising treatment method for patients with acute myeloid leukaemia.
7 ond syndrome and myelodysplastic syndrome or acute myeloid leukaemia.
8 orylated BTK in patients with CD117-positive acute myeloid leukaemia.
9 ts with advanced myelodysplastic syndrome or acute myeloid leukaemia.
10 ded for patients with relapsed or refractory acute myeloid leukaemia.
11 diatric patients with relapsed or refractory acute myeloid leukaemia.
12 therapy is not suitable with newly diagnosed acute myeloid leukaemia.
13 to some patients with relapsed or refractory acute myeloid leukaemia.
14 bine in patients with relapsed or refractory acute myeloid leukaemia.
15 hat this dose is also safe for patients with acute myeloid leukaemia.
16 n patients with myelodysplastic syndrome and acute myeloid leukaemia.
17 with high-risk myelodysplastic syndromes and acute myeloid leukaemia.
18 a after myelodysplastic syndrome, or de-novo acute myeloid leukaemia.
19 erated dose was not reached in patients with acute myeloid leukaemia.
20 hemotherapy in cancer, and was developed for acute myeloid leukaemia.
21 s, which protects mice from death related to acute myeloid leukaemia.
22 oncogene-induced differentiation blockade in acute myeloid leukaemia.
23 ematological disorder rapidly progressing to acute myeloid leukaemia.
24 nduction chemotherapy in adult patients with acute myeloid leukaemia.
25 ts with IDH2-mutated, relapsed or refractory acute myeloid leukaemia.
26 ential novel pharmacotherapeutic approach to acute myeloid leukaemia.
27 ntial therapeutic target in t(8;21)-positive acute myeloid leukaemia.
28 therapy in an eight-year-old boy treated for acute myeloid leukaemia.
29 mustards, represent a major risk factor for acute myeloid leukaemia.
30 ype, for example, MLL-AF9 is found mainly in acute myeloid leukaemia.
31 ate with Nf1 gene loss during progression to acute myeloid leukaemia.
32 ytogenetic hallmark for the M4/M5 subtype of acute myeloid leukaemia.
33 CR5 wild-type/Delta32 donor as treatment for acute myeloid leukaemia.
34 nd safe in most older or unfit patients with acute myeloid leukaemia.
35 der) and unfit patients with newly diagnosed acute myeloid leukaemia.
36 with newly diagnosed high-risk or secondary acute myeloid leukaemia.
37 o systems on what constitutes a diagnosis of acute myeloid leukaemia.
38 decline upon ageing and further decrease in acute myeloid leukaemia.
39 n patients with myelodysplastic syndrome and acute myeloid leukaemia.
40 nd all had intermediate-risk or adverse-risk acute myeloid leukaemia.
41 veral haematological malignancies, including acute myeloid leukaemia.
42 r patients with newly diagnosed, mutant-IDH2 acute myeloid leukaemia.
43 efficacy against a xenograft murine model of acute myeloid leukaemia.
44 ard induction chemotherapy for patients with acute myeloid leukaemia.
45 previously untreated patients with high-risk acute myeloid leukaemia.
46 previously untreated patients with high-risk acute myeloid leukaemia.
47 leukaemia and three (8%) had therapy-related acute myeloid leukaemia.
48 mic stem cells (LSCs) and the development of acute myeloid leukaemia.
49 with induction chemotherapy in patients with acute myeloid leukaemia.
50 e-based induction treatment of patients with acute myeloid leukaemia.
51 care for older patients with newly diagnosed acute myeloid leukaemia.
52 ptor CCR5 (CCR5Delta32/Delta32) to treat his acute myeloid leukaemia.
53 tion in patients with relapsed or refractory acute myeloid leukaemia.
54 enzyme as a potential therapeutic target for acute myeloid leukaemia.
55 ated by METTL3 in this way are necessary for acute myeloid leukaemia.
56 the cohort of treatment-naive patients with acute myeloid leukaemia.
57 olic encephalopathy, neutropenic sepsis, and acute myeloid leukaemia]).
58 9, 2010, and June 26, 2012, 29 patients with acute myeloid leukaemia (19 newly diagnosed, ten relapse
59 radioimmunotherapy and one patient developed acute myeloid leukaemia 5 months after receiving radioim
60 2013, and Sept 9, 2014, 41 patients, 36 with acute myeloid leukaemia, a median age of 70 years (IQR 6
61 d aurora A kinase (AAK) expression occurs in acute myeloid leukaemia; AAK inhibition is a promising t
62 75 years and had a pathological diagnosis of acute myeloid leukaemia according to WHO 2008 criteria,
63 half of older treatment-naive patients with acute myeloid leukaemia achieved a composite complete re
64 he incidence of myelodysplastic syndrome and acute myeloid leukaemia across PARP inhibitor groups was
65 advanced myelodysplastic syndrome, secondary acute myeloid leukaemia after myelodysplastic syndrome,
66 site complete remission <=6 months) FLT3-ITD acute myeloid leukaemia after standard therapy with or w
67 rred, one owing to tumour flare and one from acute myeloid leukaemia after study discontinuation.
69 tings, and strongly recommended if the novel acute myeloid leukaemia agent is administered in combina
70 ole of the Wnt pathway in the development of acute myeloid leukaemia (AML) and find that the beta-cat
71 bone marrow cancer cells from patients with acute myeloid leukaemia (AML) and induce the differentia
72 es, including acute lymphoblastic leukaemia, acute myeloid leukaemia (AML) and myelodysplastic syndro
74 o improve outcome in patients with childhood acute myeloid leukaemia (AML) by applying risk-directed
77 CaSR influences the location of MLL-AF9(+) acute myeloid leukaemia (AML) cells within this niche an
81 LSCs) in chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) have been advanced paradig
83 os (ORs) and 95% CIs for the risk of ALL and acute myeloid leukaemia (AML) in children aged 0-14 year
98 T3-ITD) are detected in approximately 20% of acute myeloid leukaemia (AML) patients and are associate
100 nal response of leukocytes in bone marrow of acute myeloid leukaemia (AML) patients, and the complex
103 ed in human myeloid leukaemia cell lines and acute myeloid leukaemia (AML) samples, and downregulated
104 e use a well-defined model of MLL-rearranged acute myeloid leukaemia (AML) to demonstrate that transf
105 essential anti-tumour gatekeeper in de novo acute myeloid leukaemia (AML) where it is significantly
106 rd of care for newly diagnosed patients with acute myeloid leukaemia (AML) who are 75 years or older,
107 ity-associated genes varies widely, from 4% (acute myeloid leukaemia (AML)) to 19% (ovarian cancer),
108 roach to probe epigenetic vulnerabilities in acute myeloid leukaemia (AML), an aggressive haematopoie
110 f BRD4 as a non-oncogene addiction target in acute myeloid leukaemia (AML), bromodomain and extra ter
111 ommon in myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML), but the oncogenic changes
112 echanism involved in cancer pathogenesis and acute myeloid leukaemia (AML), including the hematopoiet
113 IDH) genes 1 and 2 are frequently mutated in acute myeloid leukaemia (AML), low-grade glioma, cholang
114 stic leukaemia (ALL), and 50% for paediatric acute myeloid leukaemia (AML), recent efforts have focus
115 igate the role of TEs in the pathogenesis of acute myeloid leukaemia (AML), we studied TE expression
130 alogue ara-C is a key agent for treatment of acute myeloid leukaemia (AML); treatment decisions are m
131 1) and IDH2 have been identified in gliomas, acute myeloid leukaemias (AML) and chondrosarcomas, and
132 ing chronic myelomonocytic leukaemia (CMML), acute myeloid leukaemias (AML) and secondary AML (sAML).
133 inactivating Nf1 in mouse bone marrow and in acute myeloid leukaemias (AMLs) in which cooperating mut
134 location t(9;11), the majority of cases were acute myeloid leukaemias (AMLs) involving immature myelo
136 Eligible patients had previously untreated acute myeloid leukaemia, an Eastern Cooperative Oncology
137 s, of whom 10 (28%) initially presented with acute myeloid leukaemia and 26 (72%) initially presented
138 duplication mutations in FLT3 are common in acute myeloid leukaemia and are associated with rapid re
140 l inhibition of Notch signalling ameliorates acute myeloid leukaemia and demonstrates the pathogenic
141 deaths occurred in the placebo group due to acute myeloid leukaemia and depressed level of conscious
142 to other proteins, previously implicated in acute myeloid leukaemia and development of the palate.
143 ose-escalation cohorts, and 11 patients with acute myeloid leukaemia and four patients with myelodysp
144 ons in the BCOR gene have been identified in acute myeloid leukaemia and myelodysplastic syndrome amo
145 ombination with azacitidine in patients with acute myeloid leukaemia and myelodysplastic syndrome was
146 ed and treated 93 patients: 35 patients with acute myeloid leukaemia and nine patients with myelodysp
147 id leukaemia at dose level two; and six with acute myeloid leukaemia and one with myelodysplastic syn
148 not exclusively, restricted to cell lines of acute myeloid leukaemia and prostate cancer that express
149 of patients with myelodysplastic syndrome or acute myeloid leukaemia and Shwachman-Diamond syndrome,
151 5 dose-escalation cohorts, 28 patients with acute myeloid leukaemia and six patients with myelodyspl
152 alities and a high risk of cancer, including acute myeloid leukaemia and squamous cell carcinomas.
153 tein has been demonstrated to have a role in acute myeloid leukaemia and stem cell function, but its
155 lymphoid leukaemia, 0.959 (0.933-0.986) for acute myeloid leukaemia, and 0.940 (0.897-0.984) for non
156 ylating agent, ten (16%) had therapy-related acute myeloid leukaemia, and 11 (18%) had TP53 mutations
157 r older and had newly diagnosed, mutant-IDH2 acute myeloid leukaemia, and an Eastern Cooperative Onco
158 criteria, no previous induction therapy for acute myeloid leukaemia, and an Eastern Cooperative Onco
159 certain cancers, such as low-grade gliomas, acute myeloid leukaemia, and chondrosarcomas, has been t
160 8 years or older, had relapsed or refractory acute myeloid leukaemia, and had an Eastern Cooperative
161 te myeloid leukaemia, relapsed or refractory acute myeloid leukaemia, and myelodysplastic syndromes;
163 ulates oncogenic transcriptional programs in acute myeloid leukaemia, and suggest that displacement o
164 cal trials have shown promise, especially in acute myeloid leukaemia, and therefore the evaluation of
165 y hospital admissions in older patients with acute myeloid leukaemia are unavoidable and driven by th
166 se-risk karyotype, the presence of secondary acute myeloid leukaemia arising from previous myelodyspl
167 l human genes, including one associated with acute myeloid leukaemia arising from the recurrent trans
168 (three with multiple myeloma and three with acute myeloid leukaemia at dose level one; three with ac
169 loid leukaemia at dose level one; three with acute myeloid leukaemia at dose level two; and six with
170 lder patients diagnosed with and treated for acute myeloid leukaemia at two tertiary care hospitals i
171 rget for treatment of relapsed or refractory acute myeloid leukaemia; based on activity data, gilteri
172 ion (TBI) in adults with advanced refractory acute myeloid leukaemia before allogeneic haemopoietic s
173 d unavailable data, and 2 (8%) progressed to acute myeloid leukaemia before receiving treatment.
180 le patients were aged 60 years or older with acute myeloid leukaemia but unsuitable for intensive che
181 ivated in human blast crisis CML and de novo acute myeloid leukaemia, but also predicts disease outco
182 wn efficacy in myelodysplastic syndromes and acute myeloid leukaemia, but complete tumour responses a
183 We enrolled patients with a diagnosis of acute myeloid leukaemia by WHO criteria and aged 18-70 y
186 tracted data on myelodysplastic syndrome and acute myeloid leukaemia cases from ClinicalTrials.gov.
187 hibitor-related myelodysplastic syndrome and acute myeloid leukaemia cases reported in WHO's pharmaco
188 2 notably inhibits survival/proliferation of acute myeloid leukaemia cells and promotes their myeloid
189 fy METTL3 as an essential gene for growth of acute myeloid leukaemia cells in two distinct genetic sc
190 emia is a chemotherapy-sensitive subgroup of acute myeloid leukaemia characterised by the presence of
191 Apaf-1 DNA methylation was demonstrated in acute myeloid leukaemia, chronic myeloid leukaemia and a
192 study of PF-04449913 in adult patients with acute myeloid leukaemia, chronic myeloid leukaemia, chro
193 Similar observations are made on the TCGA acute myeloid leukaemia cohort, confirming the general t
194 linical trials of ibrutinib in patients with acute myeloid leukaemia commence, the data suggest not a
195 sed the risk of myelodysplastic syndrome and acute myeloid leukaemia compared with placebo treatment
196 sed the risk of myelodysplastic syndrome and acute myeloid leukaemia compared with placebo treatment
197 sk myelodysplastic syndromes or oligoblastic acute myeloid leukaemia (defined as blasts >=20% but <=3
198 (8;21) and t(16;21) that are associated with acute myeloid leukaemia disrupt two closely related gene
200 tioning regimen for patients with refractory acute myeloid leukaemia, especially for those transplant
202 urse of intensive induction chemotherapy for acute myeloid leukaemia (excluding acute promyelocytic l
205 luding cases of myelodysplastic syndrome and acute myeloid leukaemia, for which data are scarce.
207 utuzumab-ibrutinib group (n=1 due to each of acute myeloid leukaemia, fungal encephalitis, small-cell
209 e results obtained from sequencing a typical acute myeloid leukaemia genome, and its matched normal c
210 stem-cell activity and an aggressive form of acute myeloid leukaemia harbouring the MLL-AF9 oncogene.
211 benefit of FLT3 inhibitors in patients with acute myeloid leukaemia has been limited by rapid genera
212 ernal tandem duplication (FLT3-ITD)-positive acute myeloid leukaemia have a poor prognosis, including
215 ngs provide new insights into the biology of acute myeloid leukaemia, highlight potential therapeutic
216 mportant cancers: acute lymphoid leukaemias, acute myeloid leukaemias, Hodgkin's lymphomas, non-Hodgk
217 enetic alterations in osteoblasts can induce acute myeloid leukaemia, identify molecular signals lead
220 ve, monosomy 7 myelodysplasia progressing to acute myeloid leukaemia in a 53 year old male who presen
221 or patients (aged >18 years) with refractory acute myeloid leukaemia in active phase of disease, who
222 ged >=18 years) with a WHO 2016 diagnosis of acute myeloid leukaemia in complete remission or complet
223 Eligible patients were 18-70 years, had acute myeloid leukaemia in first or consecutive complete
226 proved in the USA for the treatment of mIDH1 acute myeloid leukaemia in newly diagnosed patients inel
228 f patients with myelodysplastic syndromes or acute myeloid leukaemia, increased beta-catenin signalli
229 ensification II, and intensification III for acute myeloid leukaemia; induction, consolidation, inter
232 ation for this is that in older patients the acute myeloid leukaemia is more likely to have arisen fr
233 volunteer-unrelated donor HCT for refractory acute myeloid leukaemia is not inferior to that of patie
234 ne, which is also a fusion partner of MLL in acute myeloid leukaemia, is a member of a family of nove
235 in generated by the t(8;21) translocation in acute myeloid leukaemia, is a transcription factor impli
236 phase, and Philadelphia chromosome-positive acute myeloid leukaemia-is associated with poor outcomes
238 ere aged 18-65 years with a new diagnosis of acute myeloid leukaemia, mixed phenotype acute leukaemia
240 2), a second primary brain tumour (n=1), and acute myeloid leukaemia (n=1), and in the placebo group
241 cases of myelodysplastic syndrome (n=99) and acute myeloid leukaemia (n=79) related to PARP inhibitor
242 for six patients (6%) receiving momelotinib (acute myeloid leukaemia [n=2], respiratory failure [n=2,
244 aged 2-22 years with relapsed or refractory acute myeloid leukaemia or acute leukaemia of ambiguous
246 18 years and older, and had newly diagnosed acute myeloid leukaemia or high-risk myelodysplastic syn
247 nsive chemotherapy), and had newly diagnosed acute myeloid leukaemia or high-risk myelodysplastic syn
248 is feasible in patients with newly diagnosed acute myeloid leukaemia or high-risk myelodysplastic syn
249 cytarabine in patients with newly diagnosed acute myeloid leukaemia or high-risk myelodysplastic syn
250 1 and 2a if they had relapsed or refractory acute myeloid leukaemia or myelodysplastic syndrome with
251 neously given guadecitabine in patients with acute myeloid leukaemia or myelodysplastic syndrome.
252 eic HSCT for older or comorbid patients with acute myeloid leukaemia or myelodysplastic syndrome.
253 ng number of older or comorbid patients with acute myeloid leukaemia or myelodysplastic syndrome.
254 ve neoplasm, the presence of therapy-related acute myeloid leukaemia, or being 65 years or older.
256 ond syndrome and myelodysplastic syndrome or acute myeloid leukaemia owing to both therapy-resistant
260 K4 is shown to be upregulated in a subset of acute myeloid leukaemia patients, conferring susceptibil
261 s chronic myeloid leukaemia, and a subset of acute myeloid leukaemias, PRH is aberrantly localised an
263 contribute to 2HG oncogenicity in glioma and acute myeloid leukaemia progression, with the promise fo
264 three (1%) of 354 patients in the VMP group (acute myeloid leukaemia, pulmonary embolism, and bacteri
265 2015, 252 adults with relapsed or refractory acute myeloid leukaemia received oral gilteritinib once
266 th myelodysplastic syndromes or oligoblastic acute myeloid leukaemia refractory to hypomethylating ag
267 th myelodysplastic syndromes or oligoblastic acute myeloid leukaemia refractory to hypomethylating ag
268 in cohorts of patients with treatment-naive acute myeloid leukaemia, relapsed or refractory acute my
269 summary risk of myelodysplastic syndrome and acute myeloid leukaemia related to PARP inhibition versu
270 iBase, cases of myelodysplastic syndrome and acute myeloid leukaemia related to PARP inhibitor therap
271 ate the risk of myelodysplastic syndrome and acute myeloid leukaemia related to PARP inhibitors, via
273 ntensive chemotherapy regimens used to treat acute myeloid leukaemia routinely result in serious infe
274 enrolled and included in the study: 28 with acute myeloid leukaemia, six with myelodysplastic syndro
276 atients with heavily relapsed and refractory acute myeloid leukaemia suggests that this combination s
278 MSH2 loss in alkylating chemotherapy-related acute myeloid leukaemia (t-AML) suggests that DNA mismat
279 cal centres with myelodysplastic syndrome or acute myeloid leukaemia that was refractory to or had re
280 ological understanding of the BTK pathway in acute myeloid leukaemia to identify clinically relevant
282 imens in the Medical Research Council's 10th acute myeloid leukaemia trial (MRC AML 10), which was op
284 , cardiac arrest (one [1%]), therapy-related acute myeloid leukaemia (two [3%]), and haematopoietic s
286 models of acute lymphoblastic leukaemia and acute myeloid leukaemia was found to reprogram non-stem
287 ses of transcriptomes from 982 patients with acute myeloid leukaemia, we identified frequent overlap
289 me who developed myelodysplastic syndrome or acute myeloid leukaemia were eligible without additional
290 with newly diagnosed high-risk or secondary acute myeloid leukaemia were enrolled and randomly assig
292 t 30, 2021, 36 patients with newly diagnosed acute myeloid leukaemia were enrolled; the median age wa
293 tic syndrome, 19 with relapsed or refractory acute myeloid leukaemia) were enrolled in phase 1; no pa
294 hown preliminary activity as a treatment for acute myeloid leukaemia when combined with azacitidine.
295 Patients with myelodysplastic syndrome or acute myeloid leukaemia who are thrombocytopenic and una
296 nrolled patients aged 18 years or older with acute myeloid leukaemia who either were refractory to in
297 (>/=65 years) patients with treatment-naive acute myeloid leukaemia who were not candidates for inte
298 Accordingly, we propose that patients with acute myeloid leukaemia whose blast cells express CD117
299 mphoid progenitors leading to development of acute myeloid leukaemia with common chromosomal aberrati