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1 f choice for continuing therapy of childhood lymphoblastic leukaemia.
2 and toxicity of the two drugs for childhood lymphoblastic leukaemia.
3 O1, and LMO2--in 52 adults with T-cell acute lymphoblastic leukaemia.
4 a good outlook for adults with T-cell acute lymphoblastic leukaemia.
5 Philadelphia-chromosome-positive (Ph+) acute lymphoblastic leukaemia.
6 ata for the pretreatment assessment of acute lymphoblastic leukaemia.
7 or patients receiving chemotherapy for acute lymphoblastic leukaemia.
8 ature myeloblasts, but a minority were acute lymphoblastic leukaemia.
9 y seen in the common form of childhood acute lymphoblastic leukaemia.
10 ly and the UK, who had newly diagnosed acute lymphoblastic leukaemia.
11 erated CAR T cells in a mouse model of acute lymphoblastic leukaemia.
12 iation and to prevent Notch3-induced T-acute lymphoblastic leukaemia.
13 nosed Philadelphia chromosome-positive acute lymphoblastic leukaemia.
14 lts with relapsed or refractory B-cell acute lymphoblastic leukaemia.
15 and safety profile of blinatumomab for acute lymphoblastic leukaemia.
16 leukaemia and 30-50% of cases of adult acute lymphoblastic leukaemia.
17 iladelphia chromosome-positive (Ph(+)) acute lymphoblastic leukaemia.
18 inase in children with newly diagnosed acute lymphoblastic leukaemia.
19 nt of Philadelphia chromosome-positive acute lymphoblastic leukaemia.
20 ith chemotherapy-resistant B-precursor acute lymphoblastic leukaemia.
21 ation in children with newly diagnosed acute lymphoblastic leukaemia.
22 ly been implicated in B-cell precursor acute lymphoblastic leukaemia.
23 ntemporary standard-risk protocols for acute lymphoblastic leukaemia.
24 and survival time, after diagnosis of acute lymphoblastic leukaemia.
25 3%) of 4329 cohort members treated for acute lymphoblastic leukaemia.
26 due to causes other than recurrence of acute lymphoblastic leukaemia.
27 nt produced highly disseminated T-cell acute lymphoblastic leukaemia.
28 re found in both acute myelogenous and acute lymphoblastic leukaemias.
30 in children treated for standard risk acute lymphoblastic leukaemia according to contemporary protoc
32 atients were diagnosed with non-B-cell acute lymphoblastic leukaemia, aged at least 8 years, and surv
33 of survival trends for precursor-cell acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemi
34 gical features of paediatric T-lineage acute lymphoblastic leukaemia (ALL) and their impact on treatm
35 tcomes in adult survivors of childhood acute lymphoblastic leukaemia (ALL) and Wilms' tumour to addre
37 omosomal aberrations are a hallmark of acute lymphoblastic leukaemia (ALL) but alone fail to induce l
42 Children with Down syndrome (DS) and acute lymphoblastic leukaemia (ALL) have poorer survival and m
43 inherited predisposition to childhood acute lymphoblastic leukaemia (ALL) identifying a number of ri
44 ted genetic basis of susceptibility to acute lymphoblastic leukaemia (ALL) in children, yet the effec
45 tudies have shown an increased risk of acute lymphoblastic leukaemia (ALL) in young children born by
49 ects on long-term outcome in childhood acute lymphoblastic leukaemia (ALL) of the duration and the in
50 ne-marrow aspirates from children with acute lymphoblastic leukaemia (ALL) remains controversial.
51 sed as first line drugs for paediatric Acute Lymphoblastic Leukaemia (ALL) treatment for more than 40
52 sis and optimum treatment of childhood acute lymphoblastic leukaemia (ALL) with abnormalities of chro
53 as exemplified by the 2% of childhood acute lymphoblastic leukaemia (ALL) with recurrent amplificati
54 of 80% now commonplace for paediatric acute lymphoblastic leukaemia (ALL), and 50% for paediatric ac
55 an essential part in the treatment of acute lymphoblastic leukaemia (ALL), but their optimum doses a
56 te recent advances in the cure rate of acute lymphoblastic leukaemia (ALL), the prognosis for patient
57 ates for children with newly diagnosed acute lymphoblastic leukaemia (ALL), treating relapsed ALL has
68 e children undergoing chemotherapy for acute lymphoblastic leukaemia, although its effects on long-te
69 st that children and young people with acute lymphoblastic leukaemia and 0.01% or more MRD at the end
70 enescence in p53-regulatable models of acute lymphoblastic leukaemia and acute myeloid leukaemia was
71 -9.9 years at the time of diagnosis of acute lymphoblastic leukaemia and had received treatment consi
72 s distinct molecular subsets of T-cell acute lymphoblastic leukaemia and has prognostic relevance in
73 ected in high-grade gliomas, T-lineage acute lymphoblastic leukaemia and medulloblastoma, and a pauci
74 mergence of clonal dominance in T-cell acute lymphoblastic leukaemia and tumour evolution resulting i
75 l component of treatment for childhood acute lymphoblastic leukaemia, and is usually administered int
76 gene has been linked with a subset of acute lymphoblastic leukaemias, and its corresponding protein
78 uses of treatment failure in childhood acute lymphoblastic leukaemia are thought to differ between re
79 Chromosomal abnormalities in childhood acute lymphoblastic leukaemia are well established disease mar
80 716 children treated consecutively for acute lymphoblastic leukaemia at a single academic hospital in
81 tical twins, diagnosed with concordant acute lymphoblastic leukaemia at age 4 years, who shared a sin
82 nalysis, we used data of children with acute lymphoblastic leukaemia at St Jude Children's Research H
83 current cure rate of 80% in childhood acute lymphoblastic leukaemia attests to the effectiveness of
85 years) diagnosed with t(9;22)-negative acute lymphoblastic leukaemia between June 1, 1996, and Jan 1,
86 hat susceptibility to childhood common acute lymphoblastic leukaemia (c-ALL) was associated with an a
89 nhibits the homing of Nalm-6 cells (an acute lymphoblastic leukaemia cell line) to these vessels.
91 ith relapsed or refractory B-precursor acute lymphoblastic leukaemia characterised by negative progno
92 im of the Dana-Farber Cancer Institute Acute Lymphoblastic Leukaemia Consortium Protocol 05-001 (DFCI
93 bone in osteoarthritis and in Pax5 in acute lymphoblastic leukaemia, demonstrate that PhenomeExpress
94 For example, eIF4A promotes T-cell acute lymphoblastic leukaemia development in vivo and is requi
96 ntelligent decision support system for acute lymphoblastic leukaemia diagnosis from microscopic blood
98 ation of prophylactic radiotherapy for acute lymphoblastic leukaemia except in patients at high risk
99 s aged 1-18 years with newly diagnosed acute lymphoblastic leukaemia from 11 consortium sites in the
100 ecture and evolution of 20 pediatric B-acute lymphoblastic leukaemias from diagnosis to relapse.
101 r understanding of the pathobiology of acute lymphoblastic leukaemia, fuelled by emerging molecular t
102 Treatment of patients with paediatric acute lymphoblastic leukaemia has evolved such that the risk o
103 Although survival of children with acute lymphoblastic leukaemia has improved greatly in the past
105 e fusion gene BCR:Abl, associated with acute lymphoblastic leukaemia, has previously been characteris
106 ith relapsed or refractory B-precursor acute lymphoblastic leukaemia have an unfavourable prognosis.
109 now demonstrate that in contrast to B-acute lymphoblastic leukaemia, human T-ALL samples largely use
110 ctory or relapsed CD22-positive B-cell acute lymphoblastic leukaemia in a standard 3 + 3 phase 1 stud
111 with Philadelphia chromosome-positive acute lymphoblastic leukaemia in this continuing phase 2 trial
112 have examined this issue in childhood acute lymphoblastic leukaemia in which the ETV6-RUNX1 gene fus
113 Our findings showed that childhood acute lymphoblastic leukaemia is frequently initiated by a chr
115 f patients with relapsed or refractory acute lymphoblastic leukaemia is poor and new treatments are n
121 ite matter alterations in survivors of acute lymphoblastic leukaemia possibly resulting in restricted
122 thout cranial radiation, for childhood acute lymphoblastic leukaemia predicted higher risk for long-t
123 lastic leukaemia study groups assessed acute lymphoblastic leukaemia protocols to address toxic effec
124 of IRM in the United Kingdom Childhood Acute Lymphoblastic Leukaemia Randomised Trial 2003 (UKALL 200
127 phi method, 15 international childhood acute lymphoblastic leukaemia study groups assessed acute lymp
129 phoid-myeloid) in patients with T-cell acute lymphoblastic leukaemia (T-ALL) and acute myeloid leukae
130 studied a mouse model of human T-cell acute lymphoblastic leukaemia (T-ALL) and used intravital micr
133 xpression is seen in the majority of T-acute lymphoblastic leukaemia (T-ALL) patients with specific t
135 ecently recognized as a form of T-cell acute lymphoblastic leukaemia (T-ALL) with a poor prognosis.
136 NOTCH1 is frequently mutated in T-cell acute lymphoblastic leukaemia (T-ALL), and can stimulate T-ALL
137 Akt signalling are prevalent in T-cell acute lymphoblastic leukaemia (T-ALL), and often coexist.
138 cer cell lines, including human T-cell acute lymphoblastic leukaemia (T-ALL), have exceptional sensit
143 high survival rates for children with acute lymphoblastic leukaemia, their outcome is often counterb
144 ents that take place in the genesis of acute lymphoblastic leukaemia, to enhance the clinical applica
145 long-term adult survivors of childhood acute lymphoblastic leukaemia treated with chemotherapy alone
148 es in long-term survivors of childhood acute lymphoblastic leukaemia treated with chemotherapy withou
149 effects in children with standard-risk acute lymphoblastic leukaemia treated with contemporary protoc
150 n the overall assessment of outcome of acute lymphoblastic leukaemia treatment, these expert opinion-
152 iated pancreatitis to asparaginase, 18 acute lymphoblastic leukaemia trial groups merged data for thi
153 eated Philadelphia chromosome-positive acute lymphoblastic leukaemia were sequentially enrolled.
154 aged 1-18 years with first relapse of acute lymphoblastic leukaemia were stratified into high-risk,
155 long-term continuing treatment for childhood lymphoblastic leukaemia, whereas 6-thioguanine has been
157 estigated the outcome of children with acute lymphoblastic leukaemia who relapsed on present therapeu
158 me (Ph)-positive or Ph-negative B-cell acute lymphoblastic leukaemia who were due to receive first or
159 rrow samples from 19 patients with Ph+ acute lymphoblastic leukaemia who were enrolled into a phase I
160 om 1725 children with B-cell precursor acute lymphoblastic leukaemia who were included in the UK Medi
162 rs) with relapsed or refractory B-cell acute lymphoblastic leukaemia (with CD22 expression on at leas
163 lt T-ALL treated on the United Kingdom Acute Lymphoblastic Leukaemia XII (UKALLXII)/Eastern Cooperati
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