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1 delayed intensification, and maintenance for acute lymphoblastic leukaemia).
2 by sex and survival time, after diagnosis of acute lymphoblastic leukaemia.
3 556 (13%) of 4329 cohort members treated for acute lymphoblastic leukaemia.
4 were due to causes other than recurrence of acute lymphoblastic leukaemia.
5 hromosome (Ph)-negative CD20-positive B-cell acute lymphoblastic leukaemia.
6 partment produced highly disseminated T-cell acute lymphoblastic leukaemia.
7 patients with relapsed or refractory B-cell acute lymphoblastic leukaemia.
8 1), LMO1, and LMO2--in 52 adults with T-cell acute lymphoblastic leukaemia.
9 onfers a good outlook for adults with T-cell acute lymphoblastic leukaemia.
10 anced Philadelphia-chromosome-positive (Ph+) acute lymphoblastic leukaemia.
11 sion data for the pretreatment assessment of acute lymphoblastic leukaemia.
12 ibed for patients receiving chemotherapy for acute lymphoblastic leukaemia.
13 ng immature myeloblasts, but a minority were acute lymphoblastic leukaemia.
14 quently seen in the common form of childhood acute lymphoblastic leukaemia.
15 om Italy and the UK, who had newly diagnosed acute lymphoblastic leukaemia.
16 211 (85%) participants had B-precursor acute lymphoblastic leukaemia.
17 ies are needed for intermediate-to-high-risk acute lymphoblastic leukaemia.
18 py improves outcomes in patients with B-cell acute lymphoblastic leukaemia.
19 patients with relapsed or refractory B-cell acute lymphoblastic leukaemia.
20 emia and 2131 with intermediate-to-high risk acute lymphoblastic leukaemia.
21 2 trial of tisagenlecleucel in children with acute lymphoblastic leukaemia.
22 is safe and active in paediatric Ph-positive acute lymphoblastic leukaemia.
23 atment of adults with newly diagnosed B-cell acute lymphoblastic leukaemia.
24 vity in vivo in mouse models of melanoma and acute lymphoblastic leukaemia.
25 d 25-65 years with de-novo BCR-ABL1-negative acute lymphoblastic leukaemia.
26 patients with relapsed or refractory B-cell acute lymphoblastic leukaemia.
27 nosed and relapsed or refractory Ph-positive acute lymphoblastic leukaemia.
28 g children and infants with B-cell precursor acute lymphoblastic leukaemia.
29 afely to treat patients with relapsed B-cell acute lymphoblastic leukaemia.
30 in adults with relapsed or refractory B-cell acute lymphoblastic leukaemia.
31 patients with relapsed or refractory B-cell acute lymphoblastic leukaemia.
32 e therapy of adults with de novo B-precursor acute lymphoblastic leukaemia.
33 UK and Ireland who were newly diagnosed with acute lymphoblastic leukaemia.
34 roughout maintenance treatment for childhood acute lymphoblastic leukaemia.
35 year of treatment for children with low-risk acute lymphoblastic leukaemia.
36 in children with newly diagnosed Ph-positive acute lymphoblastic leukaemia.
37 cleucel in younger children and infants with acute lymphoblastic leukaemia.
38 or children with acute myeloid leukaemia and acute lymphoblastic leukaemia.
39 ents with relapsed or refractory B-precursor acute lymphoblastic leukaemia.
40 or outcome in any risk subgroup of childhood acute lymphoblastic leukaemia.
41 nd adults with relapsed or refractory B-cell acute lymphoblastic leukaemia.
42 ly generated CAR T cells in a mouse model of acute lymphoblastic leukaemia.
43 in adults with relapsed or refractory B-cell acute lymphoblastic leukaemia.
44 and Philadelphia chromosome-positive (Ph(+)) acute lymphoblastic leukaemia.
45 adults with Ph-negative CD20-positive B-cell acute lymphoblastic leukaemia.
46 ferentiation and to prevent Notch3-induced T-acute lymphoblastic leukaemia.
47 Nine (27%) of 33 patients had Ph-like acute lymphoblastic leukaemia.
48 y diagnosed Philadelphia chromosome-positive acute lymphoblastic leukaemia.
49 ivity and safety profile of blinatumomab for acute lymphoblastic leukaemia.
50 nd adults with relapsed or refractory B-cell acute lymphoblastic leukaemia.
51 eloid leukaemia and 30-50% of cases of adult acute lymphoblastic leukaemia.
52 sparaginase in children with newly diagnosed acute lymphoblastic leukaemia.
53 reatment of Philadelphia chromosome-positive acute lymphoblastic leukaemia.
54 ults with chemotherapy-resistant B-precursor acute lymphoblastic leukaemia.
55 preparation in children with newly diagnosed acute lymphoblastic leukaemia.
56 eviously been implicated in B-cell precursor acute lymphoblastic leukaemia.
57 ith contemporary standard-risk protocols for acute lymphoblastic leukaemia.
58 ents are found in both acute myelogenous and acute lymphoblastic leukaemias.
59 able lineage antigen, such as CD19 in B cell acute lymphoblastic leukaemia(1,2), the broader applicab
60 7%] patients had newly diagnosed Ph-positive acute lymphoblastic leukaemia, 14 [23%] had relapsed or
61 Of patients with newly diagnosed Ph-positive acute lymphoblastic leukaemia, 33 (87%) of 38 evaluable
62 No significant association was observed for acute lymphoblastic leukaemia (4.25, -4.19 to 19.32, n=4
67 tcomes in children treated for standard risk acute lymphoblastic leukaemia according to contemporary
68 for relapsed or refractory B-cell precursor acute lymphoblastic leukaemia according to licensed indi
69 patients with relapsed or refractory B-cell acute lymphoblastic leukaemia achieved overall remission
70 radic haematological malignancies, including acute lymphoblastic leukaemia, acute myeloid leukaemia (
71 mours rarely occur in survivors of childhood acute lymphoblastic leukaemia after cranial radiotherapy
73 ible patients were diagnosed with non-B-cell acute lymphoblastic leukaemia, aged at least 8 years, an
74 arison of survival trends for precursor-cell acute lymphoblastic leukaemia (ALL) and acute myeloid le
75 biological features of paediatric T-lineage acute lymphoblastic leukaemia (ALL) and their impact on
76 ial outcomes in adult survivors of childhood acute lymphoblastic leukaemia (ALL) and Wilms' tumour to
79 Chromosomal aberrations are a hallmark of acute lymphoblastic leukaemia (ALL) but alone fail to in
82 c predictor of relapse risk in children with acute lymphoblastic leukaemia (ALL) during remission.
86 ce for inherited predisposition to childhood acute lymphoblastic leukaemia (ALL) identifying a number
87 ontributions to the evolutionary dynamics of Acute Lymphoblastic Leukaemia (ALL) in children with Dow
88 inherited genetic basis of susceptibility to acute lymphoblastic leukaemia (ALL) in children, yet the
90 5-year overall survival above 90% in B-cell acute lymphoblastic leukaemia (ALL) in many study groups
91 trol studies have shown an increased risk of acute lymphoblastic leukaemia (ALL) in young children bo
96 he effects on long-term outcome in childhood acute lymphoblastic leukaemia (ALL) of the duration and
97 al trials involving patients with pre-B cell acute lymphoblastic leukaemia (ALL) or B cell lymphomas
98 ted the mRNA expression profile of pediatric Acute Lymphoblastic Leukaemia (ALL) patients and the eff
99 in bone-marrow aspirates from children with acute lymphoblastic leukaemia (ALL) remains controversia
100 ptations that facilitate primary disease and Acute Lymphoblastic Leukaemia (ALL) survival after induc
101 been used as first line drugs for paediatric Acute Lymphoblastic Leukaemia (ALL) treatment for more t
102 prognosis and optimum treatment of childhood acute lymphoblastic leukaemia (ALL) with abnormalities o
103 genes, as exemplified by the 2% of childhood acute lymphoblastic leukaemia (ALL) with recurrent ampli
105 rvival of 80% now commonplace for paediatric acute lymphoblastic leukaemia (ALL), and 50% for paediat
106 ) play an essential part in the treatment of acute lymphoblastic leukaemia (ALL), but their optimum d
107 Despite recent advances in the cure rate of acute lymphoblastic leukaemia (ALL), the prognosis for p
108 cure rates for children with newly diagnosed acute lymphoblastic leukaemia (ALL), treating relapsed A
109 ity in samples from patients with paediatric acute lymphoblastic leukaemia (ALL), we show that ALL ep
120 in some children undergoing chemotherapy for acute lymphoblastic leukaemia, although its effects on l
121 suggest that children and young people with acute lymphoblastic leukaemia and 0.01% or more MRD at t
122 481 in the experimental group) with low-risk acute lymphoblastic leukaemia and 2131 with intermediate
123 t of senescence in p53-regulatable models of acute lymphoblastic leukaemia and acute myeloid leukaemi
124 howing promising results in the treatment of acute lymphoblastic leukaemia and aggressive B cell lymp
125 ed 1.0-9.9 years at the time of diagnosis of acute lymphoblastic leukaemia and had received treatment
126 defines distinct molecular subsets of T-cell acute lymphoblastic leukaemia and has prognostic relevan
127 hom have high-risk (KMT2A-rearranged) infant acute lymphoblastic leukaemia and historically poor outc
128 cifically on first-line decisions for B-cell acute lymphoblastic leukaemia and how to best personalis
129 the most common genetic subtype of childhood acute lymphoblastic leukaemia and is associated with a g
130 28, 2013, 228 patients with B-cell precursor acute lymphoblastic leukaemia and late bone marrow relap
131 ns detected in high-grade gliomas, T-lineage acute lymphoblastic leukaemia and medulloblastoma, and a
132 d and/or refractory B cell lymphomas, B cell acute lymphoblastic leukaemia and multiple myeloma.
133 <18 years) with newly diagnosed Ph-positive acute lymphoblastic leukaemia and performance status of
134 ding the common genetic subtype of childhood acute lymphoblastic leukaemia and testicular seminoma, d
135 oma, emergence of clonal dominance in T-cell acute lymphoblastic leukaemia and tumour evolution resul
136 8, 2017, 69 patients (67 patients had B-cell acute lymphoblastic leukaemia and two had B-cell lymphob
137 years) receiving therapy for newly diagnosed acute lymphoblastic leukaemia and who received either pr
138 29 (76%) of 38 patients had KMT2A-rearranged acute lymphoblastic leukaemia, and 25 (66%) had relapsed
139 iversal component of treatment for childhood acute lymphoblastic leukaemia, and is usually administer
140 [23%] had relapsed or refractory Ph-positive acute lymphoblastic leukaemia, and six [10%] had chronic
141 reatment of Philadelphia chromosome-positive acute lymphoblastic leukaemia, and the introduction of i
142 iladelphia chromosome-positive (Ph-positive) acute lymphoblastic leukaemia, and their combination mig
143 (cdk8) gene has been linked with a subset of acute lymphoblastic leukaemias, and its corresponding pr
144 or levofloxacin during induction therapy for acute lymphoblastic leukaemia appeared to increase the s
146 The causes of treatment failure in childhood acute lymphoblastic leukaemia are thought to differ betw
149 om of 716 children treated consecutively for acute lymphoblastic leukaemia at a single academic hospi
150 e identical twins, diagnosed with concordant acute lymphoblastic leukaemia at age 4 years, who shared
151 years treated for acute myeloid leukaemia or acute lymphoblastic leukaemia at Children's Healthcare o
152 this analysis were diagnosed with paediatric acute lymphoblastic leukaemia at St Jude Children's Rese
153 inal analysis, we used data of children with acute lymphoblastic leukaemia at St Jude Children's Rese
154 or older with relapsed or refractory B-cell acute lymphoblastic leukaemia, at least 5% of blasts in
155 The current cure rate of 80% in childhood acute lymphoblastic leukaemia attests to the effectivene
156 Following CART-19 immunotherapy for B-cell acute lymphoblastic leukaemia (B-ALL), many patients rel
157 ng low-risk, intermediate-risk, or high-risk acute lymphoblastic leukaemia based on minimal residual
159 ults with relapsed and/or refractory CD19(+) acute lymphoblastic leukaemia became the first gene ther
160 -17.9 years) diagnosed with t(9;22)-negative acute lymphoblastic leukaemia between June 1, 1996, and
161 product of a more profound understanding of acute lymphoblastic leukaemia biology, innovations in me
163 remarkable clinical success to treat B cell acute lymphoblastic leukaemia by harnessing a patient's
164 ting that susceptibility to childhood common acute lymphoblastic leukaemia (c-ALL) was associated wit
167 XCR4 inhibits the homing of Nalm-6 cells (an acute lymphoblastic leukaemia cell line) to these vessel
169 ents with relapsed or refractory B-precursor acute lymphoblastic leukaemia characterised by negative
170 on of cranial radiotherapy for children with acute lymphoblastic leukaemia, conditions now predominat
171 The aim of the Dana-Farber Cancer Institute Acute Lymphoblastic Leukaemia Consortium Protocol 05-001
172 Patients with newly diagnosed Ph-positive acute lymphoblastic leukaemia could be spared the toxici
173 ondral bone in osteoarthritis and in Pax5 in acute lymphoblastic leukaemia, demonstrate that PhenomeE
175 s an intelligent decision support system for acute lymphoblastic leukaemia diagnosis from microscopic
176 ractory or relapsed blood cancers, including acute lymphoblastic leukaemia, diffuse large B cell lymp
177 ith Ph-positive chronic myeloid leukaemia or acute lymphoblastic leukaemia (eligible only for the pha
178 y of post-induction treatment of Ph-positive acute lymphoblastic leukaemia (EsPhALL) open-label, sing
180 elimination of prophylactic radiotherapy for acute lymphoblastic leukaemia except in patients at high
181 patients with B cell non-Hodgkin lymphoma or acute lymphoblastic leukaemia for CAR T cell therapy, an
182 atients aged 1-18 years with newly diagnosed acute lymphoblastic leukaemia from 11 consortium sites i
183 architecture and evolution of 20 pediatric B-acute lymphoblastic leukaemias from diagnosis to relapse
184 in our understanding of the pathobiology of acute lymphoblastic leukaemia, fuelled by emerging molec
185 ents with relapsed or refractory Ph-positive acute lymphoblastic leukaemia had an overall response.
191 unique fusion gene BCR:Abl, associated with acute lymphoblastic leukaemia, has previously been chara
192 ults with relapsed or refractory B-precursor acute lymphoblastic leukaemia have an unfavourable progn
195 on, we now demonstrate that in contrast to B-acute lymphoblastic leukaemia, human T-ALL samples large
196 refractory or relapsed CD22-positive B-cell acute lymphoblastic leukaemia in a standard 3 + 3 phase
198 ioned allogeneic HSCT in older patients with acute lymphoblastic leukaemia in first complete remissio
199 be used frequently for high-risk adults with acute lymphoblastic leukaemia in first complete remissio
201 tients with Philadelphia chromosome-positive acute lymphoblastic leukaemia in this continuing phase 2
202 ere we have examined this issue in childhood acute lymphoblastic leukaemia in which the ETV6-RUNX1 ge
205 therapy in patients older than 40 years with acute lymphoblastic leukaemia is poor and myeloablative
206 osis of patients with relapsed or refractory acute lymphoblastic leukaemia is poor and new treatments
208 th syngeneic and humanized mouse models of B-acute lymphoblastic leukaemia/lymphoma, and enhanced con
209 Considering the rapid pace of evolution in acute lymphoblastic leukaemia management, novel trial de
212 mong patients with intermediate-to-high-risk acute lymphoblastic leukaemia, no difference was observe
216 gnosed or relapsed or refractory Ph-positive acute lymphoblastic leukaemia or chronic myeloid leukaem
217 nts with newly diagnosed, Ph-negative B-cell acute lymphoblastic leukaemia or lymphoblastic lymphoma
220 for the treatment of B cell lymphomas and/or acute lymphoblastic leukaemia or multiple myeloma incorp
221 aged 1-30 years) with relapsed or refractory acute lymphoblastic leukaemia or non-Hodgkin lymphoma.
223 fic white matter alterations in survivors of acute lymphoblastic leukaemia possibly resulting in rest
224 o younger than 18 years with newly diagnosed acute lymphoblastic leukaemia (pre-B cell or T cell) or
225 nt, without cranial radiation, for childhood acute lymphoblastic leukaemia predicted higher risk for
226 ymphoblastic leukaemia study groups assessed acute lymphoblastic leukaemia protocols to address toxic
227 rials in patients with low-risk or high-risk acute lymphoblastic leukaemia provides uncertainty.
228 cases of IRM in the United Kingdom Childhood Acute Lymphoblastic Leukaemia Randomised Trial 2003 (UKA
230 ents with relapsed or refractory B-precursor acute lymphoblastic leukaemia remain poor, underlining t
232 quality of life for survivors of paediatric acute lymphoblastic leukaemia requires continued medical
235 iladelphia chromosome-positive (Ph-positive) acute lymphoblastic leukaemia significantly improved wit
236 he Delphi method, 15 international childhood acute lymphoblastic leukaemia study groups assessed acut
237 Risk/Relapsed Paediatric CD19+ and/or CD22+ Acute Lymphoblastic Leukaemia] study, NCT02443831), a th
239 ke lymphoid-myeloid) in patients with T-cell acute lymphoblastic leukaemia (T-ALL) and acute myeloid
240 ere we studied a mouse model of human T-cell acute lymphoblastic leukaemia (T-ALL) and used intravita
245 opic expression is seen in the majority of T-acute lymphoblastic leukaemia (T-ALL) patients with spec
247 been recently recognized as a form of T-cell acute lymphoblastic leukaemia (T-ALL) with a poor progno
249 PI3K)/Akt signalling are prevalent in T-cell acute lymphoblastic leukaemia (T-ALL), and often coexist
250 of inappropriate NOTCH1 signalling in T-cell acute lymphoblastic leukaemia (T-ALL), and the involveme
251 of cancer cell lines, including human T-cell acute lymphoblastic leukaemia (T-ALL), have exceptional
256 ho were aged 0-18 years with newly diagnosed acute lymphoblastic leukaemia that was subsequently in c
257 (36 with B-cell lymphoma and 15 with B-cell acute lymphoblastic leukaemia), the overall response rat
258 re are high survival rates for children with acute lymphoblastic leukaemia, their outcome is often co
259 ophylaxis, given to paediatric patients with acute lymphoblastic leukaemia to prevent infections duri
260 ise events that take place in the genesis of acute lymphoblastic leukaemia, to enhance the clinical a
261 actors among patients with high hyperdiploid acute lymphoblastic leukaemia treated on UKALL2003.
265 outcomes in long-term survivors of childhood acute lymphoblastic leukaemia treated with chemotherapy
266 gy in long-term adult survivors of childhood acute lymphoblastic leukaemia treated with chemotherapy
267 late effects in children with standard-risk acute lymphoblastic leukaemia treated with contemporary
269 In the overall assessment of outcome of acute lymphoblastic leukaemia treatment, these expert op
271 -associated pancreatitis to asparaginase, 18 acute lymphoblastic leukaemia trial groups merged data f
272 was similar to that of previous Ph-positive acute lymphoblastic leukaemia trials despite the limited
273 Patients with de-novo BCR-ABL1-positive acute lymphoblastic leukaemia were eligible if they were
274 opy numbers at diagnosis of B cell precursor acute lymphoblastic leukaemia were highly correlated wit
275 patients with relapsed or refractory B-cell acute lymphoblastic leukaemia were identified as prelimi
276 141 paediatric patients with newly diagnosed acute lymphoblastic leukaemia were registered to this st
277 y untreated Philadelphia chromosome-positive acute lymphoblastic leukaemia were sequentially enrolled
278 tients aged 1-18 years with first relapse of acute lymphoblastic leukaemia were stratified into high-
279 549 for acute myeloid leukaemia and 4062 for acute lymphoblastic leukaemia) were extracted, processed
280 Participants in UKALL14 had B-cell or T-cell acute lymphoblastic leukaemia, were aged 25-65 years (BC
281 the treatment of adults with newly diagnosed acute lymphoblastic leukaemia, which adds to previously
283 ildren aged 1-18 years with B-cell precursor acute lymphoblastic leukaemia who had late bone marrow r
284 d outcomes of children with B-cell precursor acute lymphoblastic leukaemia who had late bone marrow r
285 CD19-positive relapsed or refractory B-cell acute lymphoblastic leukaemia who had morphological rela
286 We investigated the outcome of children with acute lymphoblastic leukaemia who relapsed on present th
287 romosome (Ph)-positive or Ph-negative B-cell acute lymphoblastic leukaemia who were due to receive fi
288 one-marrow samples from 19 patients with Ph+ acute lymphoblastic leukaemia who were enrolled into a p
289 ata from 1725 children with B-cell precursor acute lymphoblastic leukaemia who were included in the U
292 18 years) with relapsed or refractory B-cell acute lymphoblastic leukaemia (with CD22 expression on a
293 ents with relapsed or refractory B-precursor acute lymphoblastic leukaemia, with the median overall s
294 th adult T-ALL treated on the United Kingdom Acute Lymphoblastic Leukaemia XII (UKALLXII)/Eastern Coo