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1 d intensification, and maintenance for acute lymphoblastic leukaemia).
2 and survival time, after diagnosis of acute lymphoblastic leukaemia.
3 3%) of 4329 cohort members treated for acute lymphoblastic leukaemia.
4 due to causes other than recurrence of acute lymphoblastic leukaemia.
5 ome (Ph)-negative CD20-positive B-cell acute lymphoblastic leukaemia.
6 nt produced highly disseminated T-cell acute lymphoblastic leukaemia.
7 nts with relapsed or refractory B-cell acute lymphoblastic leukaemia.
8 f choice for continuing therapy of childhood lymphoblastic leukaemia.
9 and toxicity of the two drugs for childhood lymphoblastic leukaemia.
10 O1, and LMO2--in 52 adults with T-cell acute lymphoblastic leukaemia.
11 a good outlook for adults with T-cell acute lymphoblastic leukaemia.
12 Philadelphia-chromosome-positive (Ph+) acute lymphoblastic leukaemia.
13 ata for the pretreatment assessment of acute lymphoblastic leukaemia.
14 or patients receiving chemotherapy for acute lymphoblastic leukaemia.
15 ature myeloblasts, but a minority were acute lymphoblastic leukaemia.
16 y seen in the common form of childhood acute lymphoblastic leukaemia.
17 ly and the UK, who had newly diagnosed acute lymphoblastic leukaemia.
18 211 (85%) participants had B-precursor acute lymphoblastic leukaemia.
19 roves outcomes in patients with B-cell acute lymphoblastic leukaemia.
20 nts with relapsed or refractory B-cell acute lymphoblastic leukaemia.
21 e needed for intermediate-to-high-risk acute lymphoblastic leukaemia.
22 nd 2131 with intermediate-to-high risk acute lymphoblastic leukaemia.
23 l of tisagenlecleucel in children with acute lymphoblastic leukaemia.
24 e and active in paediatric Ph-positive acute lymphoblastic leukaemia.
25 of adults with newly diagnosed B-cell acute lymphoblastic leukaemia.
26 n vivo in mouse models of melanoma and acute lymphoblastic leukaemia.
27 5 years with de-novo BCR-ABL1-negative acute lymphoblastic leukaemia.
28 nts with relapsed or refractory B-cell acute lymphoblastic leukaemia.
29 and relapsed or refractory Ph-positive acute lymphoblastic leukaemia.
30 dren and infants with B-cell precursor acute lymphoblastic leukaemia.
31 to treat patients with relapsed B-cell acute lymphoblastic leukaemia.
32 lts with relapsed or refractory B-cell acute lymphoblastic leukaemia.
33 nts with relapsed or refractory B-cell acute lymphoblastic leukaemia.
34 apy of adults with de novo B-precursor acute lymphoblastic leukaemia.
35 Ireland who were newly diagnosed with acute lymphoblastic leukaemia.
36 ut maintenance treatment for childhood acute lymphoblastic leukaemia.
37 f treatment for children with low-risk acute lymphoblastic leukaemia.
38 ldren with newly diagnosed Ph-positive acute lymphoblastic leukaemia.
39 l in younger children and infants with acute lymphoblastic leukaemia.
40 ldren with acute myeloid leukaemia and acute lymphoblastic leukaemia.
41 lts with relapsed or refractory B-cell acute lymphoblastic leukaemia.
42 erated CAR T cells in a mouse model of acute lymphoblastic leukaemia.
43 lts with relapsed or refractory B-cell acute lymphoblastic leukaemia.
44 iladelphia chromosome-positive (Ph(+)) acute lymphoblastic leukaemia.
45 with Ph-negative CD20-positive B-cell acute lymphoblastic leukaemia.
46 iation and to prevent Notch3-induced T-acute lymphoblastic leukaemia.
47 Nine (27%) of 33 patients had Ph-like acute lymphoblastic leukaemia.
48 nosed Philadelphia chromosome-positive acute lymphoblastic leukaemia.
49 and safety profile of blinatumomab for acute lymphoblastic leukaemia.
50 lts with relapsed or refractory B-cell acute lymphoblastic leukaemia.
51 leukaemia and 30-50% of cases of adult acute lymphoblastic leukaemia.
52 inase in children with newly diagnosed acute lymphoblastic leukaemia.
53 nt of Philadelphia chromosome-positive acute lymphoblastic leukaemia.
54 ith chemotherapy-resistant B-precursor acute lymphoblastic leukaemia.
55 ation in children with newly diagnosed acute lymphoblastic leukaemia.
56 ly been implicated in B-cell precursor acute lymphoblastic leukaemia.
57 ntemporary standard-risk protocols for acute lymphoblastic leukaemia.
58 re found in both acute myelogenous and acute lymphoblastic leukaemias.
59 ineage antigen, such as CD19 in B cell acute lymphoblastic leukaemia(1,2), the broader applicability
60 tients had newly diagnosed Ph-positive acute lymphoblastic leukaemia, 14 [23%] had relapsed or refrac
61 ients with newly diagnosed Ph-positive acute lymphoblastic leukaemia, 33 (87%) of 38 evaluable patien
62 gnificant association was observed for acute lymphoblastic leukaemia (4.25, -4.19 to 19.32, n=49) or
67 in children treated for standard risk acute lymphoblastic leukaemia according to contemporary protoc
68 elapsed or refractory B-cell precursor acute lymphoblastic leukaemia according to licensed indication
69 nts with relapsed or refractory B-cell acute lymphoblastic leukaemia achieved overall remission after
70 haematological malignancies, including acute lymphoblastic leukaemia, acute myeloid leukaemia (AML) a
73 atients were diagnosed with non-B-cell acute lymphoblastic leukaemia, aged at least 8 years, and surv
74 of survival trends for precursor-cell acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemi
75 gical features of paediatric T-lineage acute lymphoblastic leukaemia (ALL) and their impact on treatm
76 tcomes in adult survivors of childhood acute lymphoblastic leukaemia (ALL) and Wilms' tumour to addre
79 omosomal aberrations are a hallmark of acute lymphoblastic leukaemia (ALL) but alone fail to induce l
84 Although children and adolescents with acute lymphoblastic leukaemia (ALL) have high survival rates,
85 Children with Down syndrome (DS) and acute lymphoblastic leukaemia (ALL) have poorer survival and m
86 inherited predisposition to childhood acute lymphoblastic leukaemia (ALL) identifying a number of ri
87 utions to the evolutionary dynamics of Acute Lymphoblastic Leukaemia (ALL) in children with Down synd
88 ted genetic basis of susceptibility to acute lymphoblastic leukaemia (ALL) in children, yet the effec
90 r overall survival above 90% in B-cell acute lymphoblastic leukaemia (ALL) in many study groups, whil
91 tudies have shown an increased risk of acute lymphoblastic leukaemia (ALL) in young children born by
97 ects on long-term outcome in childhood acute lymphoblastic leukaemia (ALL) of the duration and the in
98 als involving patients with pre-B cell acute lymphoblastic leukaemia (ALL) or B cell lymphomas have r
99 e mRNA expression profile of pediatric Acute Lymphoblastic Leukaemia (ALL) patients and the efficacy
100 ne-marrow aspirates from children with acute lymphoblastic leukaemia (ALL) remains controversial.
101 ns that facilitate primary disease and Acute Lymphoblastic Leukaemia (ALL) survival after induction c
102 sed as first line drugs for paediatric Acute Lymphoblastic Leukaemia (ALL) treatment for more than 40
103 sis and optimum treatment of childhood acute lymphoblastic leukaemia (ALL) with abnormalities of chro
104 as exemplified by the 2% of childhood acute lymphoblastic leukaemia (ALL) with recurrent amplificati
105 Philadelphia chromosome-like (Ph-like) acute lymphoblastic leukaemia (ALL), a high-risk subtype chara
106 of 80% now commonplace for paediatric acute lymphoblastic leukaemia (ALL), and 50% for paediatric ac
107 an essential part in the treatment of acute lymphoblastic leukaemia (ALL), but their optimum doses a
108 te recent advances in the cure rate of acute lymphoblastic leukaemia (ALL), the prognosis for patient
109 ates for children with newly diagnosed acute lymphoblastic leukaemia (ALL), treating relapsed ALL has
110 samples from patients with paediatric acute lymphoblastic leukaemia (ALL), we show that ALL epigenom
122 e children undergoing chemotherapy for acute lymphoblastic leukaemia, although its effects on long-te
123 st that children and young people with acute lymphoblastic leukaemia and 0.01% or more MRD at the end
124 the experimental group) with low-risk acute lymphoblastic leukaemia and 2131 with intermediate-to-hi
125 enescence in p53-regulatable models of acute lymphoblastic leukaemia and acute myeloid leukaemia was
126 promising results in the treatment of acute lymphoblastic leukaemia and aggressive B cell lymphoma.
127 -9.9 years at the time of diagnosis of acute lymphoblastic leukaemia and had received treatment consi
128 s distinct molecular subsets of T-cell acute lymphoblastic leukaemia and has prognostic relevance in
129 ve high-risk (KMT2A-rearranged) infant acute lymphoblastic leukaemia and historically poor outcomes d
130 lly on first-line decisions for B-cell acute lymphoblastic leukaemia and how to best personalise trea
131 st common genetic subtype of childhood acute lymphoblastic leukaemia and is associated with a good ou
132 13, 228 patients with B-cell precursor acute lymphoblastic leukaemia and late bone marrow relapses we
133 ected in high-grade gliomas, T-lineage acute lymphoblastic leukaemia and medulloblastoma, and a pauci
135 ears) with newly diagnosed Ph-positive acute lymphoblastic leukaemia and performance status of at lea
136 he common genetic subtype of childhood acute lymphoblastic leukaemia and testicular seminoma, differ
137 mergence of clonal dominance in T-cell acute lymphoblastic leukaemia and tumour evolution resulting i
138 7, 69 patients (67 patients had B-cell acute lymphoblastic leukaemia and two had B-cell lymphoblastic
139 receiving therapy for newly diagnosed acute lymphoblastic leukaemia and who received either primary
140 %) of 38 patients had KMT2A-rearranged acute lymphoblastic leukaemia, and 25 (66%) had relapsed after
141 l component of treatment for childhood acute lymphoblastic leukaemia, and is usually administered int
142 had relapsed or refractory Ph-positive acute lymphoblastic leukaemia, and six [10%] had chronic myelo
143 nt of Philadelphia chromosome-positive acute lymphoblastic leukaemia, and the introduction of immunot
144 phia chromosome-positive (Ph-positive) acute lymphoblastic leukaemia, and their combination might be
145 gene has been linked with a subset of acute lymphoblastic leukaemias, and its corresponding protein
146 ofloxacin during induction therapy for acute lymphoblastic leukaemia appeared to increase the short-t
148 uses of treatment failure in childhood acute lymphoblastic leukaemia are thought to differ between re
149 Chromosomal abnormalities in childhood acute lymphoblastic leukaemia are well established disease mar
151 716 children treated consecutively for acute lymphoblastic leukaemia at a single academic hospital in
152 tical twins, diagnosed with concordant acute lymphoblastic leukaemia at age 4 years, who shared a sin
153 treated for acute myeloid leukaemia or acute lymphoblastic leukaemia at Children's Healthcare of Atla
154 nalysis were diagnosed with paediatric acute lymphoblastic leukaemia at St Jude Children's Research H
155 nalysis, we used data of children with acute lymphoblastic leukaemia at St Jude Children's Research H
156 der with relapsed or refractory B-cell acute lymphoblastic leukaemia, at least 5% of blasts in the bo
157 current cure rate of 80% in childhood acute lymphoblastic leukaemia attests to the effectiveness of
158 owing CART-19 immunotherapy for B-cell acute lymphoblastic leukaemia (B-ALL), many patients relapse d
159 -risk, intermediate-risk, or high-risk acute lymphoblastic leukaemia based on minimal residual diseas
161 ith relapsed and/or refractory CD19(+) acute lymphoblastic leukaemia became the first gene therapy to
162 years) diagnosed with t(9;22)-negative acute lymphoblastic leukaemia between June 1, 1996, and Jan 1,
163 ct of a more profound understanding of acute lymphoblastic leukaemia biology, innovations in measurab
165 kable clinical success to treat B cell acute lymphoblastic leukaemia by harnessing a patient's own T
166 hat susceptibility to childhood common acute lymphoblastic leukaemia (c-ALL) was associated with an a
169 nhibits the homing of Nalm-6 cells (an acute lymphoblastic leukaemia cell line) to these vessels.
171 ith relapsed or refractory B-precursor acute lymphoblastic leukaemia characterised by negative progno
172 cranial radiotherapy for children with acute lymphoblastic leukaemia, conditions now predominately in
173 im of the Dana-Farber Cancer Institute Acute Lymphoblastic Leukaemia Consortium Protocol 05-001 (DFCI
174 ients with newly diagnosed Ph-positive acute lymphoblastic leukaemia could be spared the toxicities a
175 bone in osteoarthritis and in Pax5 in acute lymphoblastic leukaemia, demonstrate that PhenomeExpress
176 For example, eIF4A promotes T-cell acute lymphoblastic leukaemia development in vivo and is requi
178 ntelligent decision support system for acute lymphoblastic leukaemia diagnosis from microscopic blood
179 y or relapsed blood cancers, including acute lymphoblastic leukaemia, diffuse large B cell lymphoma,
180 -positive chronic myeloid leukaemia or acute lymphoblastic leukaemia (eligible only for the phase 1 s
181 ost-induction treatment of Ph-positive acute lymphoblastic leukaemia (EsPhALL) open-label, single-arm
183 ation of prophylactic radiotherapy for acute lymphoblastic leukaemia except in patients at high risk
184 ts with B cell non-Hodgkin lymphoma or acute lymphoblastic leukaemia for CAR T cell therapy, and outl
185 s aged 1-18 years with newly diagnosed acute lymphoblastic leukaemia from 11 consortium sites in the
186 ecture and evolution of 20 pediatric B-acute lymphoblastic leukaemias from diagnosis to relapse.
187 r understanding of the pathobiology of acute lymphoblastic leukaemia, fuelled by emerging molecular t
191 Treatment of patients with paediatric acute lymphoblastic leukaemia has evolved such that the risk o
192 Although survival of children with acute lymphoblastic leukaemia has improved greatly in the past
194 e fusion gene BCR:Abl, associated with acute lymphoblastic leukaemia, has previously been characteris
195 ith relapsed or refractory B-precursor acute lymphoblastic leukaemia have an unfavourable prognosis.
198 now demonstrate that in contrast to B-acute lymphoblastic leukaemia, human T-ALL samples largely use
199 ctory or relapsed CD22-positive B-cell acute lymphoblastic leukaemia in a standard 3 + 3 phase 1 stud
201 allogeneic HSCT in older patients with acute lymphoblastic leukaemia in first complete remission prov
202 d frequently for high-risk adults with acute lymphoblastic leukaemia in first complete remission.
203 atients with intermediate-to-high-risk acute lymphoblastic leukaemia in the control group were more l
204 with Philadelphia chromosome-positive acute lymphoblastic leukaemia in this continuing phase 2 trial
205 have examined this issue in childhood acute lymphoblastic leukaemia in which the ETV6-RUNX1 gene fus
206 Our findings showed that childhood acute lymphoblastic leukaemia is frequently initiated by a chr
208 y in patients older than 40 years with acute lymphoblastic leukaemia is poor and myeloablative alloge
209 f patients with relapsed or refractory acute lymphoblastic leukaemia is poor and new treatments are n
211 geneic and humanized mouse models of B-acute lymphoblastic leukaemia/lymphoma, and enhanced control o
212 idering the rapid pace of evolution in acute lymphoblastic leukaemia management, novel trial designs
215 atients with intermediate-to-high-risk acute lymphoblastic leukaemia, no difference was observed in 5
219 or relapsed or refractory Ph-positive acute lymphoblastic leukaemia or chronic myeloid leukaemia in
220 th newly diagnosed, Ph-negative B-cell acute lymphoblastic leukaemia or lymphoblastic lymphoma with C
223 e treatment of B cell lymphomas and/or acute lymphoblastic leukaemia or multiple myeloma incorporate
226 ite matter alterations in survivors of acute lymphoblastic leukaemia possibly resulting in restricted
227 ger than 18 years with newly diagnosed acute lymphoblastic leukaemia (pre-B cell or T cell) or lympho
228 thout cranial radiation, for childhood acute lymphoblastic leukaemia predicted higher risk for long-t
229 lastic leukaemia study groups assessed acute lymphoblastic leukaemia protocols to address toxic effec
231 of IRM in the United Kingdom Childhood Acute Lymphoblastic Leukaemia Randomised Trial 2003 (UKALL 200
233 ith relapsed or refractory B-precursor acute lymphoblastic leukaemia remain poor, underlining the nee
235 ty of life for survivors of paediatric acute lymphoblastic leukaemia requires continued medical surve
238 phia chromosome-positive (Ph-positive) acute lymphoblastic leukaemia significantly improved with the
239 phi method, 15 international childhood acute lymphoblastic leukaemia study groups assessed acute lymp
240 Relapsed Paediatric CD19+ and/or CD22+ Acute Lymphoblastic Leukaemia] study, NCT02443831), a third of
242 phoid-myeloid) in patients with T-cell acute lymphoblastic leukaemia (T-ALL) and acute myeloid leukae
243 studied a mouse model of human T-cell acute lymphoblastic leukaemia (T-ALL) and used intravital micr
248 xpression is seen in the majority of T-acute lymphoblastic leukaemia (T-ALL) patients with specific t
251 ecently recognized as a form of T-cell acute lymphoblastic leukaemia (T-ALL) with a poor prognosis.
252 NOTCH1 is frequently mutated in T-cell acute lymphoblastic leukaemia (T-ALL), and can stimulate T-ALL
253 Akt signalling are prevalent in T-cell acute lymphoblastic leukaemia (T-ALL), and often coexist.
254 ppropriate NOTCH1 signalling in T-cell acute lymphoblastic leukaemia (T-ALL), and the involvement of
255 cer cell lines, including human T-cell acute lymphoblastic leukaemia (T-ALL), have exceptional sensit
261 e aged 0-18 years with newly diagnosed acute lymphoblastic leukaemia that was subsequently in continu
262 ith B-cell lymphoma and 15 with B-cell acute lymphoblastic leukaemia), the overall response rate was
263 high survival rates for children with acute lymphoblastic leukaemia, their outcome is often counterb
264 xis, given to paediatric patients with acute lymphoblastic leukaemia to prevent infections during ind
265 ents that take place in the genesis of acute lymphoblastic leukaemia, to enhance the clinical applica
270 long-term adult survivors of childhood acute lymphoblastic leukaemia treated with chemotherapy alone
271 es in long-term survivors of childhood acute lymphoblastic leukaemia treated with chemotherapy withou
272 effects in children with standard-risk acute lymphoblastic leukaemia treated with contemporary protoc
274 n the overall assessment of outcome of acute lymphoblastic leukaemia treatment, these expert opinion-
276 iated pancreatitis to asparaginase, 18 acute lymphoblastic leukaemia trial groups merged data for thi
277 imilar to that of previous Ph-positive acute lymphoblastic leukaemia trials despite the limited use o
278 atients with de-novo BCR-ABL1-positive acute lymphoblastic leukaemia were eligible if they were aged
279 mbers at diagnosis of B cell precursor acute lymphoblastic leukaemia were highly correlated with subs
280 nts with relapsed or refractory B-cell acute lymphoblastic leukaemia were identified as preliminary r
281 ediatric patients with newly diagnosed acute lymphoblastic leukaemia were registered to this study.
282 eated Philadelphia chromosome-positive acute lymphoblastic leukaemia were sequentially enrolled.
283 aged 1-18 years with first relapse of acute lymphoblastic leukaemia were stratified into high-risk,
284 r acute myeloid leukaemia and 4062 for acute lymphoblastic leukaemia) were extracted, processed, and
285 ipants in UKALL14 had B-cell or T-cell acute lymphoblastic leukaemia, were aged 25-65 years (BCR-ABL1
286 long-term continuing treatment for childhood lymphoblastic leukaemia, whereas 6-thioguanine has been
287 eatment of adults with newly diagnosed acute lymphoblastic leukaemia, which adds to previously publis
289 aged 1-18 years with B-cell precursor acute lymphoblastic leukaemia who had late bone marrow relapse
290 omes of children with B-cell precursor acute lymphoblastic leukaemia who had late bone marrow relapse
291 positive relapsed or refractory B-cell acute lymphoblastic leukaemia who had morphological relapse or
292 estigated the outcome of children with acute lymphoblastic leukaemia who relapsed on present therapeu
293 me (Ph)-positive or Ph-negative B-cell acute lymphoblastic leukaemia who were due to receive first or
294 rrow samples from 19 patients with Ph+ acute lymphoblastic leukaemia who were enrolled into a phase I
295 om 1725 children with B-cell precursor acute lymphoblastic leukaemia who were included in the UK Medi
298 rs) with relapsed or refractory B-cell acute lymphoblastic leukaemia (with CD22 expression on at leas
299 ith relapsed or refractory B-precursor acute lymphoblastic leukaemia, with the median overall surviva
300 lt T-ALL treated on the United Kingdom Acute Lymphoblastic Leukaemia XII (UKALLXII)/Eastern Cooperati