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1 tin as an effective treatment for MLL-fusion leukaemia".
2 ely transcribed genes that are essential for leukaemia.
3 ial glioma, melanoma and chronic lymphocytic leukaemia.
4 h relapsed or refractory chronic lymphocytic leukaemia.
5 ts with relapsed or refractory acute myeloid leukaemia.
6 h relapsed or refractory chronic lymphocytic leukaemia.
7 red for disease maintenance in acute myeloid leukaemia.
8 ositive and negative prognostic indicator in leukaemia.
9 bination with BET inhibitors, for aggressive leukaemia.
10 h relapsed or refractory chronic lymphocytic leukaemia.
11 ce treatment of del(17p) chronic lymphocytic leukaemia.
12 mg/m(2) in patients with chronic lymphocytic leukaemia.
13 usly untreated patients with chronic myeloid leukaemia.
14 ress this question in chronic myelomonocytic leukaemia.
15 se of its involvement in Ewing's sarcoma and leukaemia.
16 sitively regulates its protein expression in leukaemia.
17 tetramer formation might serve to control NK leukaemia.
18 prevent Notch3-induced T-acute lymphoblastic leukaemia.
19 tment method for patients with acute myeloid leukaemia.
20 d or refractory del(17p) chronic lymphocytic leukaemia.
21 t patients with advanced chronic lymphocytic leukaemia.
22 hromosome (Ph+)-positive chronic myelogenous leukaemia.
23 iteria for T cell large granular lymphocytic leukaemia.
24 patients with chronic-phase chronic myeloid leukaemia.
25 in this way are necessary for acute myeloid leukaemia.
26 n patients with CD117-positive acute myeloid leukaemia.
27 e inhibitor for T315I-mutant BCR-ABL1-driven leukaemia.
28 ts with relapsed or refractory acute myeloid leukaemia.
29 ells in a mouse model of acute lymphoblastic leukaemia.
30 sed or refractory B-cell acute lymphoblastic leukaemia.
31 T1 axis drives cancer progression in myeloid leukaemia.
32 e development of MDS-like disease or myeloid leukaemia.
33 sformed the treatment of chronic lymphocytic leukaemia.
34 with previously treated chronic lymphocytic leukaemia.
35 omosome-positive (Ph(+)) acute lymphoblastic leukaemia.
36 tential therapeutic target for acute myeloid leukaemia.
37 treatment-naive patients with acute myeloid leukaemia.
38 es emergency myelopoiesis and is hijacked in leukaemia.
39 s globally for several subtypes of childhood leukaemia.
40 h relapsed or refractory chronic lymphocytic leukaemia.
41 methylases in AML, especially MLL-rearranged leukaemia.
42 tation therapy in Noonan-syndrome-associated leukaemias.
43 nt to the median mutational burden in common leukaemias.
44 pathy, neutropenic sepsis, and acute myeloid leukaemia]).
45 une 26, 2012, 29 patients with acute myeloid leukaemia (19 newly diagnosed, ten relapsed or refractor
47 nternational Workshop on Chronic Lymphocytic Leukaemia 2008 response criteria modified for treatment-
48 rapy and one patient developed acute myeloid leukaemia 5 months after receiving radioimmunotherapy.
49 9, 2014, 41 patients, 36 with acute myeloid leukaemia, a median age of 70 years (IQR 60-75) and two
50 documented diagnosis of chronic lymphocytic leukaemia according to the 2008 International Workshop o
51 h relapsed or refractory chronic lymphocytic leukaemia (according to the 2008 Modified International
52 treatment-naive patients with acute myeloid leukaemia achieved a composite complete response with gu
54 for eight important cancers: acute lymphoid leukaemias, acute myeloid leukaemias, Hodgkin's lymphoma
55 nclude important models for immune response, leukaemia, age-related hearing loss and rheumatoid arthr
56 -naive fit patients with chronic lymphocytic leukaemia (aged 33-81 years) without del(17p) were enrol
57 iagnosed with non-B-cell acute lymphoblastic leukaemia, aged at least 8 years, and survivors with at
59 Survivors of childhood acute lymphoblastic leukaemia (ALL) are at risk for neurocognitive deficits
60 roximately 25% of cases, acute lymphoblastic leukaemia (ALL) cells carry the oncogenic BCR-ABL1 tyros
61 sis of susceptibility to acute lymphoblastic leukaemia (ALL) in children, yet the effects of protein-
62 own an increased risk of acute lymphoblastic leukaemia (ALL) in young children born by caesarean deli
64 nces in the cure rate of acute lymphoblastic leukaemia (ALL), the prognosis for patients with relapse
68 ergoing chemotherapy for acute lymphoblastic leukaemia, although its effects on long-term outcomes is
69 xetine, amitifadine), diabetes (gliclazide), leukaemia (alvocidib), schizophrenia (risperidone, belap
70 ancer cells from patients with acute myeloid leukaemia (AML) and induce the differentiation of RA-low
72 5% CIs for the risk of ALL and acute myeloid leukaemia (AML) in children aged 0-14 years at diagnosis
75 f leukocytes in bone marrow of acute myeloid leukaemia (AML) patients, and the complex immune respons
76 eloid leukaemia cell lines and acute myeloid leukaemia (AML) samples, and downregulated upon granuloc
77 efined model of MLL-rearranged acute myeloid leukaemia (AML) to demonstrate that transforming haemato
78 i-tumour gatekeeper in de novo acute myeloid leukaemia (AML) where it is significantly downregulated.
79 n-oncogene addiction target in acute myeloid leukaemia (AML), bromodomain and extra terminal protein
80 ved in cancer pathogenesis and acute myeloid leukaemia (AML), including the hematopoietic regeneratio
81 of TEs in the pathogenesis of acute myeloid leukaemia (AML), we studied TE expression in several cel
87 53-regulatable models of acute lymphoblastic leukaemia and acute myeloid leukaemia was found to repro
88 utations in FLT3 are common in acute myeloid leukaemia and are associated with rapid relapse and shor
89 patients with acute and chronic lymphocytic leukaemia and B-cell lymphomas, but feasibility, toxicit
91 h relapsed or refractory chronic lymphocytic leukaemia and could allow some patients to maintain resp
92 ource for studying epigenome deregulation in leukaemia and demonstrated the feasibility of large-scal
93 of patients with del17p chronic lymphocytic leukaemia and has been incorporated into treatment algor
94 duced differentiation of acute promyelocytic leukaemia and HL-60 cells, CD38 is one of the earliest a
95 nt cancer cells, including multiple myeloma, leukaemia and lymphoma cells, by activating the BAX/BAK-
96 ff-target sites in human chronic lymphocytic leukaemia and mantle cell lymphoma cell lines, and patie
98 Six of the 74 patients with acute myeloid leukaemia and six of the 19 patients with myelodysplasti
99 demonstrated to have a role in acute myeloid leukaemia and stem cell function, but its role in MDS is
100 ndings identify a dependency factor in acute leukaemia and suggest a mechanistic rationale for disrup
101 onal dominance in T-cell acute lymphoblastic leukaemia and tumour evolution resulting in elevated gro
103 ates and has the ability to cause aggressive leukaemias and lymphomas in non-natural hosts, expresses
104 rs, such as low-grade gliomas, acute myeloid leukaemia, and chondrosarcomas, has been the identificat
105 kaemia, relapsed or refractory acute myeloid leukaemia, and myelodysplastic syndromes; here we report
107 ic transcriptional programs in acute myeloid leukaemia, and suggest that displacement of ENL from chr
108 Here we show that, in acute promyelocytic leukaemia (APL), ILC2s are increased and hyper-activated
109 ositis and T cell large granular lymphocytic leukaemia are rare diseases involving pathogenic cytotox
110 issions in older patients with acute myeloid leukaemia are unavoidable and driven by the illness cour
111 s regardless of their sensitivity, resistant leukaemias are uniformly characterized by their ability
112 ) relapsed or refractory chronic lymphocytic leukaemia (as defined by 2008 Modified International Wor
114 ed data of children with acute lymphoblastic leukaemia at St Jude Children's Research Hospital (Memph
115 diagnosed with and treated for acute myeloid leukaemia at two tertiary care hospitals in the USA.
116 1 (HTLV-1) infection to lethal Adult T-cell Leukaemia (ATL); a progression that is more likely in Ja
117 1, RAEB-2, RAEB-t, or chronic myelomonocytic leukaemia based on local site assessment, and treatment
118 ment of relapsed or refractory acute myeloid leukaemia; based on activity data, gilteritinib at 120 m
119 diatric B-cell precursor acute lymphoblastic leukaemia (BCP-ALL) is the most common cancer of childho
120 dren aged 0-14 years who were diagnosed with leukaemia between Jan 1, 1995, and Dec 31, 2009, and fol
121 ed with t(9;22)-negative acute lymphoblastic leukaemia between June 1, 1996, and Jan 1, 2016, who wit
123 n blast crisis CML and de novo acute myeloid leukaemia, but also predicts disease outcome in patients
124 apy in fit patients with chronic lymphocytic leukaemia, but bendamustine and rituximab is associated
125 myelodysplastic syndromes and acute myeloid leukaemia, but complete tumour responses are infrequent
126 d patients with a diagnosis of acute myeloid leukaemia by WHO criteria and aged 18-70 years inclusive
129 function screen in an MLL-AF4-positive acute leukaemia cell line, we identify ENL as an unrecognized
130 ated C/EBPalpha is enriched in human myeloid leukaemia cell lines and acute myeloid leukaemia (AML) s
133 ssion of CML and promotes BCAA production in leukaemia cells by aminating the branched-chain keto aci
134 e capacity to accumulate in the cytoplasm of leukaemia cells for several days and release their RA pa
135 tive growth inhibition, whereas treatment of leukaemia cells harboring a different oncogenic driver (
137 ukaemia was found to reprogram non-stem bulk leukaemia cells into self-renewing, leukaemia-initiating
139 interactions and promiscuous distribution of leukaemia cells that migrated across the bone marrow, wi
142 eneration-associated WNT10B in AC133(bright) leukaemia cells, although the existence of a specific me
143 ase course and an anergic phenotype of their leukaemia cells, which refers to a state of unresponsive
146 r refractory B-precursor acute lymphoblastic leukaemia characterised by negative prognostic factors.
156 of life of patients with chronic lymphocytic leukaemia (CLL) who do not require systemic therapy.
157 hat has been linked with chronic lymphocytic leukaemia (CLL), but its functions in CLL manifestation
158 proportion of cases with chronic lymphocytic leukaemia (CLL)-phenotype MBL and CD5-negative MBL, as w
162 e association studies of chronic lymphocytic leukaemia (CLL, N = 1,842), Hodgkin lymphoma (HL, N = 1,
164 nd functionally required for chronic myeloid leukaemia (CML) in humans and in mouse models of CML.
169 e-standardised net survival for all lymphoid leukaemias combined ranged from 10.6% (95% CI 3.1-18.2)
171 ewly diagnosed chronic-phase chronic myeloid leukaemia compared with imatinib could not be assessed d
172 l[17p]) in patients with chronic lymphocytic leukaemia confers very poor prognosis when treated with
173 (aged >/=16 years) with acute promyelocytic leukaemia, confirmed by the presence of the PML-RARA tra
174 known role for the cytoplasmic promyelocytic leukaemia (cPML) tumour suppressor in TGF-beta signallin
176 e combination enhanced survival with reduced leukaemia development in secondary transplant recipients
178 ed ETV6 variants were significantly older at leukaemia diagnosis than those without (10.2 years [IQR
179 atients have an increased risk of developing leukaemia, especially juvenile myelomonocytic leukaemia
181 agent oral OTX015 use in patients with acute leukaemia for further phase 2 studies is 80 mg on a 14 d
182 ALL represents a distinct form of high-risk leukaemia, for which new therapeutic approaches should b
183 tio [HR] 0.99 [95% CI 0.83-1.20]; p=0.95) or leukaemia-free survival (HR 0.97 [0.81-1.16]; p=0.71).
184 nce, duration of response, overall survival, leukaemia-free survival, and pharmacokinetics will be re
185 Survivors of Hodgkin lymphoma, acute myeloid leukaemia, genitourinary cancers other than bladder canc
186 ples collected from UK Children's Cancer and Leukaemia Group (CCLG) treatment centres (UK), collabora
189 T3 inhibitors in patients with acute myeloid leukaemia has been limited by rapid generation of resist
190 t-free survival (TFS) in chronic lymphocytic leukaemia have been investigated, most have proven eithe
191 obal inequalities in survival from childhood leukaemia have narrowed with time but remain very wide f
192 th 17p deletion (del17p) chronic lymphocytic leukaemia have poor responses and survival after chemoim
193 espite high-hyperdiploid acute lymphoblastic leukaemia (HD-ALL) being the most common subgroup of pae
194 rs: acute lymphoid leukaemias, acute myeloid leukaemias, Hodgkin's lymphomas, non-Hodgkin lymphomas,
196 adelphia chromosome-positive chronic myeloid leukaemia in chronic phase and Eastern Cooperative Oncol
197 management of patients with chronic myeloid leukaemia in chronic phase with suboptimal cytogenetic r
198 mised trial in patients with chronic myeloid leukaemia in chronic phase with suboptimal cytogenetic r
199 ents (aged >/=18 years) with chronic myeloid leukaemia in first chronic phase who had received TKI fo
201 ne [2%] patient with fatal acute lymphocytic leukaemia in the lenalidomide group and one patient (3%)
202 molecule inhibitors (2i) in the presence of leukaemia inhibitory factor (LIF) (hereafter termed 2i/L
206 eukaemia, especially juvenile myelomonocytic leukaemia (JMML), a childhood myeloproliferative neoplas
208 tidase) that are over-expressed by resistant leukaemia lymphoblasts, thereby impairing drug activity
210 Japanese patients with relapsed adult T-cell leukaemia-lymphoma and other peripheral T-cell lymphomas
212 umented diagnosis of aggressive adult T-cell leukaemia-lymphoma or other peripheral T-cell lymphoma s
213 assessable patients (nine with adult T-cell leukaemia-lymphoma, four with other peripheral T-cell ly
215 Survivors of childhood acute lymphoblastic leukaemia might benefit from preventive cognitive or beh
217 rimary brain tumour (n=1), and acute myeloid leukaemia (n=1), and in the placebo group were a brain h
218 ts (6%) receiving momelotinib (acute myeloid leukaemia [n=2], respiratory failure [n=2, with one cons
220 reviously treated del17p chronic lymphocytic leukaemia or small lymphocytic lymphoma received oral ib
222 144 patients with del17p chronic lymphocytic leukaemia or small lymphocytic lymphoma who received at
223 s of age) who had active chronic lymphocytic leukaemia or small lymphocytic lymphoma with measurable
227 r cancer, non-Hodgkin lymphoma, lung cancer, leukaemia other than acute myeloid, central nervous syst
228 ntly in children and AYAs for acute lymphoid leukaemia (p<0.0001) and non-Hodgkin lymphoma (p<0.0001
229 To explain the mechanistic role of ENL in leukaemia pathogenesis and dynamic transcription control
230 Natural killer cells from acute myeloid leukaemia patients (AML-NK) show a dramatic impairment i
233 he cytoplasmic localization of promyelocytic leukaemia (PML) is mediated by its nuclear export in a c
234 radiation, for childhood acute lymphoblastic leukaemia predicted higher risk for long-term neurobehav
236 2HG oncogenicity in glioma and acute myeloid leukaemia progression, with the promise for innovative d
237 ia study groups assessed acute lymphoblastic leukaemia protocols to address toxic effects that were t
238 d or refractory del(17p) chronic lymphocytic leukaemia, providing a new therapeutic option for this v
239 when age-standardised survival for lymphoid leukaemias ranged from 52.4% (95% CI 42.8-61.9) in Cali,
240 s (PMCs) from BALB/c mice and Rat Basophilic Leukaemia (RBL-2H3) MCs led to significant killing of L.
241 ts with relapsed or refractory acute myeloid leukaemia received oral gilteritinib once daily in one o
242 ition triggers acute MYC repression in human leukaemias regardless of their sensitivity, resistant le
243 patients with treatment-naive acute myeloid leukaemia, relapsed or refractory acute myeloid leukaemi
244 h relapsed or refractory chronic lymphocytic leukaemia requiring treatment who had measurable lymphad
245 plication of this technology to human B cell leukaemias reveals different levels of karyotype heterog
246 therapy regimens used to treat acute myeloid leukaemia routinely result in serious infections, largel
247 ults (>/=60 years of age) with acute myeloid leukaemia spend a substantial proportion of their life i
248 Hedgehog (Hh) pathway represents a potential leukaemia stem cell (LSC)-directed therapy which may com
249 international childhood acute lymphoblastic leukaemia study groups assessed acute lymphoblastic leuk
251 Survival for childhood acute lymphoblastic leukaemia surpasses 90% with contemporary therapy; howev
252 se model of human T-cell acute lymphoblastic leukaemia (T-ALL) and used intravital microscopy to moni
254 ying nanoparticles can efficiently introduce leukaemia-targeting CAR genes into T-cell nuclei, thereb
255 hown potent activity against chronic myeloid leukaemia that is resistant to available treatment, alth
256 0 mg dose established in chronic lymphocytic leukaemia, the study was amended on Dec 9, 2009, to chan
257 rates for children with acute lymphoblastic leukaemia, their outcome is often counterbalanced by the
258 We excluded those with acute promyelocytic leukaemia, those seen only for a one-time consultation w
259 , advanced breast cancer, colorectal cancer, leukaemia, thyroid cancer, and non-Hodgkin lymphomas are
260 ould allow patients with chronic lymphocytic leukaemia to receive clinical benefit from the drug via
261 m survivors of childhood acute lymphoblastic leukaemia treated with chemotherapy without cranial radi
262 assessment of outcome of acute lymphoblastic leukaemia treatment, these expert opinion-based definiti
265 itis to asparaginase, 18 acute lymphoblastic leukaemia trial groups merged data for this observationa
267 e insertion, somatically acquired in primary leukaemia tumour genomes, reveals that it nucleates form
268 he authors show that, in acute promyelocytic leukaemia, tumour-activated ILC2s secrete IL-13 to induc
269 s (four pneumonia, three chronic lymphocytic leukaemia, two Richter's syndrome, two sepsis, and one e
270 MiSL between the IDH1 mutation and ACACA in leukaemia using gene targeting and patient-derived xenog
273 s of different genera: HTLV-1, HIV-1, murine leukaemia virus (MLV), avian sarcoma leucosis virus (ASL
274 te lymphoblastic leukaemia and acute myeloid leukaemia was found to reprogram non-stem bulk leukaemia
276 2015, 314 patients with chronic lymphocytic leukaemia were enrolled and randomly assigned to receive
277 h relapsed or refractory chronic lymphocytic leukaemia were enrolled from 15 sites across the USA.
278 or older with untreated chronic lymphocytic leukaemia were randomly assigned, via an interactive voi
279 untreated patients with chronic lymphocytic leukaemia were screened for the study; 379 (81%) were no
280 differences in 5-year survival for childhood leukaemia were still large as recently as 2005-09, when
281 ere eligible if they had chronic lymphocytic leukaemia; were aged 18 years or older; had been treated
283 or non-proliferative chronic myelomonocytic leukaemia (white blood cell count <13 000/muL), and had
284 recurrent or progressive chronic lymphocytic leukaemia who are in complete or partial response after
285 etoclax in patients with chronic lymphocytic leukaemia who are refractory to or relapse during or aft
286 first-line patients with chronic lymphocytic leukaemia who do not achieve minimal residual disease ne
287 option for patients with chronic lymphocytic leukaemia who do not have access to kinase inhibitors.
288 ts aged 18 years or older with acute myeloid leukaemia who either were refractory to induction therap
289 ly untreated progressive chronic lymphocytic leukaemia who had an Eastern Cooperative Oncology Group
291 ve or Ph-negative B-cell acute lymphoblastic leukaemia who were due to receive first or second salvag
292 patients with treatment-naive acute myeloid leukaemia who were not candidates for intensive chemothe
293 h relapsed or refractory chronic lymphocytic leukaemia whose disease progressed during or after disco
294 phenotypically confirmed chronic lymphocytic leukaemia with active disease, who responded to chemoimm
295 sible for some patients with chronic myeloid leukaemia with deep molecular responses; however, patien
296 identifies patients with chronic lymphocytic leukaemia with poor outcome after first-line chemoimmuno
297 sed or refractory B-cell acute lymphoblastic leukaemia (with CD22 expression on at least 70% of blast
299 649 cases), and the most common cancers were leukaemia (WSR 46.4), followed by CNS tumours (WSR 28.2)
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