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1 1), LMO1, and LMO2--in 52 adults with T-cell acute lymphoblastic leukaemia.
2 onfers a good outlook for adults with T-cell acute lymphoblastic leukaemia.
3 anced Philadelphia-chromosome-positive (Ph+) acute lymphoblastic leukaemia.
4 sion data for the pretreatment assessment of acute lymphoblastic leukaemia.
5 ibed for patients receiving chemotherapy for acute lymphoblastic leukaemia.
6 ng immature myeloblasts, but a minority were acute lymphoblastic leukaemia.
7 quently seen in the common form of childhood acute lymphoblastic leukaemia.
8 om Italy and the UK, who had newly diagnosed acute lymphoblastic leukaemia.
9 ly generated CAR T cells in a mouse model of acute lymphoblastic leukaemia.
10 ferentiation and to prevent Notch3-induced T-acute lymphoblastic leukaemia.
11 y diagnosed Philadelphia chromosome-positive acute lymphoblastic leukaemia.
12 in adults with relapsed or refractory B-cell acute lymphoblastic leukaemia.
13 ivity and safety profile of blinatumomab for acute lymphoblastic leukaemia.
14 eloid leukaemia and 30-50% of cases of adult acute lymphoblastic leukaemia.
15 and Philadelphia chromosome-positive (Ph(+)) acute lymphoblastic leukaemia.
16 sparaginase in children with newly diagnosed acute lymphoblastic leukaemia.
17 reatment of Philadelphia chromosome-positive acute lymphoblastic leukaemia.
18 ults with chemotherapy-resistant B-precursor acute lymphoblastic leukaemia.
19 preparation in children with newly diagnosed acute lymphoblastic leukaemia.
20 eviously been implicated in B-cell precursor acute lymphoblastic leukaemia.
21 ith contemporary standard-risk protocols for acute lymphoblastic leukaemia.
22 by sex and survival time, after diagnosis of acute lymphoblastic leukaemia.
23 556 (13%) of 4329 cohort members treated for acute lymphoblastic leukaemia.
24 were due to causes other than recurrence of acute lymphoblastic leukaemia.
25 partment produced highly disseminated T-cell acute lymphoblastic leukaemia.
26 ents are found in both acute myelogenous and acute lymphoblastic leukaemias.
28 tcomes in children treated for standard risk acute lymphoblastic leukaemia according to contemporary
29 mours rarely occur in survivors of childhood acute lymphoblastic leukaemia after cranial radiotherapy
30 ible patients were diagnosed with non-B-cell acute lymphoblastic leukaemia, aged at least 8 years, an
31 arison of survival trends for precursor-cell acute lymphoblastic leukaemia (ALL) and acute myeloid le
32 biological features of paediatric T-lineage acute lymphoblastic leukaemia (ALL) and their impact on
33 ial outcomes in adult survivors of childhood acute lymphoblastic leukaemia (ALL) and Wilms' tumour to
35 Chromosomal aberrations are a hallmark of acute lymphoblastic leukaemia (ALL) but alone fail to in
38 c predictor of relapse risk in children with acute lymphoblastic leukaemia (ALL) during remission.
41 ce for inherited predisposition to childhood acute lymphoblastic leukaemia (ALL) identifying a number
42 inherited genetic basis of susceptibility to acute lymphoblastic leukaemia (ALL) in children, yet the
43 trol studies have shown an increased risk of acute lymphoblastic leukaemia (ALL) in young children bo
46 he effects on long-term outcome in childhood acute lymphoblastic leukaemia (ALL) of the duration and
47 in bone-marrow aspirates from children with acute lymphoblastic leukaemia (ALL) remains controversia
48 been used as first line drugs for paediatric Acute Lymphoblastic Leukaemia (ALL) treatment for more t
49 prognosis and optimum treatment of childhood acute lymphoblastic leukaemia (ALL) with abnormalities o
50 genes, as exemplified by the 2% of childhood acute lymphoblastic leukaemia (ALL) with recurrent ampli
51 rvival of 80% now commonplace for paediatric acute lymphoblastic leukaemia (ALL), and 50% for paediat
52 ) play an essential part in the treatment of acute lymphoblastic leukaemia (ALL), but their optimum d
53 Despite recent advances in the cure rate of acute lymphoblastic leukaemia (ALL), the prognosis for p
54 cure rates for children with newly diagnosed acute lymphoblastic leukaemia (ALL), treating relapsed A
64 in some children undergoing chemotherapy for acute lymphoblastic leukaemia, although its effects on l
65 suggest that children and young people with acute lymphoblastic leukaemia and 0.01% or more MRD at t
66 t of senescence in p53-regulatable models of acute lymphoblastic leukaemia and acute myeloid leukaemi
67 ed 1.0-9.9 years at the time of diagnosis of acute lymphoblastic leukaemia and had received treatment
68 defines distinct molecular subsets of T-cell acute lymphoblastic leukaemia and has prognostic relevan
69 ns detected in high-grade gliomas, T-lineage acute lymphoblastic leukaemia and medulloblastoma, and a
70 oma, emergence of clonal dominance in T-cell acute lymphoblastic leukaemia and tumour evolution resul
71 iversal component of treatment for childhood acute lymphoblastic leukaemia, and is usually administer
72 (cdk8) gene has been linked with a subset of acute lymphoblastic leukaemias, and its corresponding pr
74 The causes of treatment failure in childhood acute lymphoblastic leukaemia are thought to differ betw
76 om of 716 children treated consecutively for acute lymphoblastic leukaemia at a single academic hospi
77 e identical twins, diagnosed with concordant acute lymphoblastic leukaemia at age 4 years, who shared
78 inal analysis, we used data of children with acute lymphoblastic leukaemia at St Jude Children's Rese
79 The current cure rate of 80% in childhood acute lymphoblastic leukaemia attests to the effectivene
81 -17.9 years) diagnosed with t(9;22)-negative acute lymphoblastic leukaemia between June 1, 1996, and
82 ting that susceptibility to childhood common acute lymphoblastic leukaemia (c-ALL) was associated wit
85 XCR4 inhibits the homing of Nalm-6 cells (an acute lymphoblastic leukaemia cell line) to these vessel
87 ents with relapsed or refractory B-precursor acute lymphoblastic leukaemia characterised by negative
88 The aim of the Dana-Farber Cancer Institute Acute Lymphoblastic Leukaemia Consortium Protocol 05-001
89 ondral bone in osteoarthritis and in Pax5 in acute lymphoblastic leukaemia, demonstrate that PhenomeE
91 s an intelligent decision support system for acute lymphoblastic leukaemia diagnosis from microscopic
93 elimination of prophylactic radiotherapy for acute lymphoblastic leukaemia except in patients at high
94 atients aged 1-18 years with newly diagnosed acute lymphoblastic leukaemia from 11 consortium sites i
95 architecture and evolution of 20 pediatric B-acute lymphoblastic leukaemias from diagnosis to relapse
96 in our understanding of the pathobiology of acute lymphoblastic leukaemia, fuelled by emerging molec
100 unique fusion gene BCR:Abl, associated with acute lymphoblastic leukaemia, has previously been chara
101 ults with relapsed or refractory B-precursor acute lymphoblastic leukaemia have an unfavourable progn
104 on, we now demonstrate that in contrast to B-acute lymphoblastic leukaemia, human T-ALL samples large
105 refractory or relapsed CD22-positive B-cell acute lymphoblastic leukaemia in a standard 3 + 3 phase
106 tients with Philadelphia chromosome-positive acute lymphoblastic leukaemia in this continuing phase 2
107 ere we have examined this issue in childhood acute lymphoblastic leukaemia in which the ETV6-RUNX1 ge
110 osis of patients with relapsed or refractory acute lymphoblastic leukaemia is poor and new treatments
114 aged 1-30 years) with relapsed or refractory acute lymphoblastic leukaemia or non-Hodgkin lymphoma.
116 fic white matter alterations in survivors of acute lymphoblastic leukaemia possibly resulting in rest
117 nt, without cranial radiation, for childhood acute lymphoblastic leukaemia predicted higher risk for
118 ymphoblastic leukaemia study groups assessed acute lymphoblastic leukaemia protocols to address toxic
119 cases of IRM in the United Kingdom Childhood Acute Lymphoblastic Leukaemia Randomised Trial 2003 (UKA
122 he Delphi method, 15 international childhood acute lymphoblastic leukaemia study groups assessed acut
124 ke lymphoid-myeloid) in patients with T-cell acute lymphoblastic leukaemia (T-ALL) and acute myeloid
125 ere we studied a mouse model of human T-cell acute lymphoblastic leukaemia (T-ALL) and used intravita
128 opic expression is seen in the majority of T-acute lymphoblastic leukaemia (T-ALL) patients with spec
129 been recently recognized as a form of T-cell acute lymphoblastic leukaemia (T-ALL) with a poor progno
131 PI3K)/Akt signalling are prevalent in T-cell acute lymphoblastic leukaemia (T-ALL), and often coexist
132 of cancer cell lines, including human T-cell acute lymphoblastic leukaemia (T-ALL), have exceptional
136 re are high survival rates for children with acute lymphoblastic leukaemia, their outcome is often co
137 ise events that take place in the genesis of acute lymphoblastic leukaemia, to enhance the clinical a
138 outcomes in long-term survivors of childhood acute lymphoblastic leukaemia treated with chemotherapy
139 gy in long-term adult survivors of childhood acute lymphoblastic leukaemia treated with chemotherapy
142 late effects in children with standard-risk acute lymphoblastic leukaemia treated with contemporary
143 In the overall assessment of outcome of acute lymphoblastic leukaemia treatment, these expert op
145 -associated pancreatitis to asparaginase, 18 acute lymphoblastic leukaemia trial groups merged data f
146 y untreated Philadelphia chromosome-positive acute lymphoblastic leukaemia were sequentially enrolled
147 tients aged 1-18 years with first relapse of acute lymphoblastic leukaemia were stratified into high-
149 We investigated the outcome of children with acute lymphoblastic leukaemia who relapsed on present th
150 romosome (Ph)-positive or Ph-negative B-cell acute lymphoblastic leukaemia who were due to receive fi
151 one-marrow samples from 19 patients with Ph+ acute lymphoblastic leukaemia who were enrolled into a p
152 ata from 1725 children with B-cell precursor acute lymphoblastic leukaemia who were included in the U
154 18 years) with relapsed or refractory B-cell acute lymphoblastic leukaemia (with CD22 expression on a
155 th adult T-ALL treated on the United Kingdom Acute Lymphoblastic Leukaemia XII (UKALLXII)/Eastern Coo
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