ライフサイエンスコーパス: leukaemia

1 reated patients with high-risk acute myeloid leukaemia.

2 33 patients had Ph-like acute lymphoblastic leukaemia.

3 th ABL-class fusion B-cell acute lymphocytic leukaemia.

4 from a diagnosis of bone cancer, lymphoma or leukaemia.

5 three (8%) had therapy-related acute myeloid leukaemia.

6 sed or refractory B-cell acute lymphoblastic leukaemia.

7 t of clinically apparent chronic lymphocytic leukaemia.

8 of relapsed or refractory acute lymphocytic leukaemia.

9 nt approach for patients with advanced-stage leukaemia.

10 ith previously untreated chronic lymphocytic leukaemia.

11 ive CD20-positive B-cell acute lymphoblastic leukaemia.

12 sed or refractory B-cell acute lymphoblastic leukaemia.

13 ith relapsed or refractory acute lymphocytic leukaemia.

14 (LSCs) and the development of acute myeloid leukaemia.

15 chemotherapy in patients with acute myeloid leukaemia.

16 t mutations in RNA splicing factors initiate leukaemia.

17 nts with treatment-naive chronic lymphocytic leukaemia.

18 sociated with an increased risk of childhood leukaemia.

19 d using NGS in patients with chronic myeloid leukaemia.

20 plastic syndromes, or chronic myelomonocytic leukaemia.

21 first-line treatments in chronic lymphocytic leukaemia.

22 an aggressive and fully transplantable acute leukaemia.

23 sed or refractory B-cell acute lymphoblastic leukaemia.

24 hanisms underlies the development of myeloid leukaemia.

25 ith refractory or relapsed acute lymphocytic leukaemia.

26 f function contributes to the development of leukaemia.

27 ion treatment of patients with acute myeloid leukaemia.

28 splastic syndromes or chronic myelomonocytic leukaemia.

29 etroviral therapy use on multiple myeloma or leukaemia.

30 fficacy against mouse models of melanoma and leukaemia.

31 ith previously untreated chronic lymphocytic leukaemia.

32 gkin B-cell lymphoma and chronic lymphocytic leukaemia.

33 inhibitors in patients with chronic myeloid leukaemia.

34 patients with newly diagnosed acute myeloid leukaemia.

35 gkin B-cell lymphoma and chronic lymphocytic leukaemia.

36 ounger fit patients with chronic lymphocytic leukaemia.

37 s (aged >=18 years) with chronic lymphocytic leukaemia.

38 pecial consideration for children with acute leukaemia.

39 ents with IGHV-unmutated chronic lymphocytic leukaemia.

40 5Delta32/Delta32) to treat his acute myeloid leukaemia.

41 egimen for patients with chronic lymphocytic leukaemia.

42 hibitor with activity in chronic lymphocytic leukaemia.

43 iatric patients with high-risk acute myeloid leukaemia.

44 CI 0.2-2.4) for patients with acute myeloid leukaemia.

45 in patients with B-cell acute lymphoblastic leukaemia.

46 sed or refractory B-cell acute lymphoblastic leukaemia.

47 nd myelodysplastic syndrome or acute myeloid leukaemia.

48 ts with relapsed or refractory acute myeloid leukaemia.

49 suitable with newly diagnosed acute myeloid leukaemia.

50 SCT survival outcomes in patients with acute leukaemia.

51 utated, relapsed or refractory acute myeloid leukaemia.

52 ith previously untreated chronic lymphocytic leukaemia.

53 egimen for patients with chronic lymphocytic leukaemia.

54 AR T cells to treat patients with aggressive leukaemia.

55 ive CD20-positive B-cell acute lymphoblastic leukaemia.

56 reated patients with high-risk acute myeloid leukaemia.

57 atment-naive symptomatic chronic lymphocytic leukaemia.

58 expression of cancer-driving genes in acute leukaemia(1).

59 lating each of these processes are common in leukaemia(1,2).

60 eoplasms were lymphoma (74%), myeloma (14%), leukaemia (10%), and sarcoma (2%).

61 us diseases including immunodeficiencies and leukaemias(2).

62 FRB fusion-positive B-cell acute lymphocytic leukaemia (43 [88%] of 49 patients).

63 splastic syndromes or chronic myelomonocytic leukaemia; 43 of the enrolled patients were evaluable.

64 980 survivors of acute lymphoblastic leukaemia (50% women, median age at diagnosis 5 years [I

65 420 mg for patients with chronic lymphocytic leukaemia; 560 mg for patients with B-cell non-Hodgkin l

66 ed ABL-class fusion B-cell acute lymphocytic leukaemia (77 from European study groups, 25 from North

67 ase (AAK) expression occurs in acute myeloid leukaemia; AAK inhibition is a promising therapeutic tar

68 sed or refractory B-cell acute lymphoblastic leukaemia achieved overall remission after treatment wit

69 anti-tumour activity in chronic lymphocytic leukaemia, achieving deep remissions by potently inducin

70 f myelodysplastic syndrome and acute myeloid leukaemia across PARP inhibitor groups was 0.73% (95% CI

71 malignancies, including acute lymphoblastic leukaemia, acute myeloid leukaemia (AML) and myelodyspla

72 remission <=6 months) FLT3-ITD acute myeloid leukaemia after standard therapy with or without allogen

73 g to tumour flare and one from acute myeloid leukaemia after study discontinuation.

74 urvivors of testicular cancer, lymphoma, and leukaemia aged 25-50 years with morning total serum test

75 Patients with B-cell acute lymphoblastic leukaemia aged at least 3 years at the time of screening

76 ge of heterocycles, including a complex anti-leukaemia agent and hydrocinnamic acid substrates.

77 Children with acute lymphoblastic leukaemia (ALL) are at increased risk of invasive pneumo

78 sis of susceptibility to acute lymphoblastic leukaemia (ALL) in children.

79 ival above 90% in B-cell acute lymphoblastic leukaemia (ALL) in many study groups, whilst outcomes fo

80 patients with pre-B cell acute lymphoblastic leukaemia (ALL) or B cell lymphomas have revolutionized

81 ion profile of pediatric Acute Lymphoblastic Leukaemia (ALL) patients and the efficacy of two AURKA a

82 patients with childhood acute lymphoblastic leukaemia (ALL).

83 acute lymphoblastic leukaemia, acute myeloid leukaemia (AML) and myelodysplastic syndrome (MDS).

84 ic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) have been advanced paradigms for the can

85 Paediatric acute myeloid leukaemia (AML) is a heterogeneous disease characterised

86 Acute myeloid leukaemia (AML) is a heterogeneous disease characterized

87 Acute myeloid leukaemia (AML) is a malignancy of haematopoietic origin

88 Acute myelogenous leukaemia (AML) is associated with risk factors that are

89 Patients with acute myeloid leukaemia (AML) often achieve remission after therapy, b

90 newly diagnosed patients with acute myeloid leukaemia (AML) who are 75 years or older, or unfit for

91 yeloid malignancies, including acute myeloid leukaemia (AML), arise from the expansion of haematopoie

92 dysplastic syndromes (MDS) and acute myeloid leukaemia (AML), but the oncogenic changes due to these

93 in about 35% of patients with acute myeloid leukaemia (AML).

94 nical outcome in patients with Acute Myeloid Leukaemia (AML).

95 ients had previously untreated acute myeloid leukaemia, an Eastern Cooperative Oncology Group perform

96 33 (92%) of 36 patients (eight of ten with leukaemia and 25 of 26 with myelodysplastic syndrome) we

97 (28%) initially presented with acute myeloid leukaemia and 26 (72%) initially presented with myelodys

98 ears was 11% (95% CI 1-39) for patients with leukaemia and 51% (29-68) for patients with myelodysplas

99 utations in FLT3 are common in acute myeloid leukaemia and are associated with rapid relapse and shor

100 ing activity in advanced chronic lymphocytic leukaemia and B-cell non-Hodgkin lymphoma.

101 ed in the placebo group due to acute myeloid leukaemia and depressed level of consciousness.

102 eins, previously implicated in acute myeloid leukaemia and development of the palate.

103 dysregulation of these mechanisms in myeloid leukaemia and discuss opportunities for targeting LSC-sp

104 0), del(17p) or amp1q21, primary plasma cell leukaemia and elevated serum lactate dehydrogenase (two

105 ts with B-cell precursor acute lymphoblastic leukaemia and late bone marrow relapses were treated.

106 Oncogenes that induce the development of leukaemia and lymphoma did not transform Ifitm3(-/-) B c

107 Bloodwise (Formerly Leukaemia and Lymphoma Research) UK, Cancer Research UK,

108 ied clinical cohorts of patients with B cell leukaemia and lymphoma, and identified IFITM3 as a stron

109 everal other countries, for the treatment of leukaemia and lymphoma.

110 ff-target sites in human chronic lymphocytic leukaemia and mantle cell lymphoma cell lines, and patie

111 n relapsed or refractory chronic lymphocytic leukaemia and mantle cell lymphoma, with a recommended p

112 n relapsed or refractory chronic lymphocytic leukaemia and mantle cell lymphoma.

113 R gene have been identified in acute myeloid leukaemia and myelodysplastic syndrome among other cance

114 y, restricted to cell lines of acute myeloid leukaemia and prostate cancer that expressed the full-le

115 th myelodysplastic syndrome or acute myeloid leukaemia and Shwachman-Diamond syndrome, an inherited b

116 and can initiate serially re-transplantable leukaemia and survive chemotherapy in patient-derived xe

117 ) of 39 patients had secondary acute myeloid leukaemia and three (8%) had therapy-related acute myelo

118 (67 patients had B-cell acute lymphoblastic leukaemia and two had B-cell lymphoblastic lymphoma; med

119 e patients had untreated chronic lymphocytic leukaemia and were aged 65 years or older, or older than

120 ical malignancies; in particular, aggressive leukaemias and lymphomas.

121 challenges in caring for patients with acute leukaemias and myeloid neoplasms amid the COVID-19 pande

122 ramework for the care of patients with acute leukaemias and myeloid neoplasms during the COVID-19 pan

123 erations that drive the development of acute leukaemias and other haematopoietic diseases, it has bec

124 y two cancers (gastric non-cardia cancer and leukaemia), and decreased for eight of the 18 additional

125 ysplastic syndrome or chronic myelomonocytic leukaemia); and relapsed or refractory AML.

126 or older, had untreated chronic lymphocytic leukaemia, and coexisting conditions with a cumulative i

127 ldren with newly diagnosed acute lymphocytic leukaemia, and studies suggest that leukaemic cells carr

128 ildhood cancer, $449 million (22.0%) was for leukaemias, and $330 million (16.2%) was for CNS tumours

129 non-Hodgkin lymphoma; 1.77, 1.50-2.09, with leukaemia; and 3.29, 2.59-4.18, with multiple myeloma),

130 gkin B-cell lymphoma and chronic lymphocytic leukaemia; and evaluation of the anti-glycoprotein E hum

131 oma; ovarian; bladder; other female genital; leukaemia; and head and neck cancer.

132 ine oligodeoxynucleotide and one or multiple leukaemia antigens (in the form of a defined peptide ant

133 Data on the risk of multiple myeloma or leukaemia are inconsistent and of low quality but the ri

134 ype, the presence of secondary acute myeloid leukaemia arising from previous myelodysplastic syndrome

135 ation-competent 60S subunits is disrupted in leukaemia-associated ribosomopathies.

136 iagnosed with paediatric acute lymphoblastic leukaemia at St Jude Children's Research Hospital (SJCRH

137 Here we analyse 1,148 patient-derived B-cell leukaemia (B-ALL) samples, and find that individual muta

138 utilities for chronic-phase chronic myeloid leukaemia (base case 0.89, range 0-1) and the annual cos

139 nd/or refractory CD19(+) acute lymphoblastic leukaemia became the first gene therapy to be approved i

140 data, and 2 (8%) progressed to acute myeloid leukaemia before receiving treatment.

141 ulk sequencing can provide information about leukaemia biology and prognosis, it cannot distinguish w

142 mon in bladder cancers, paediatric sarcomas, leukaemias, brain tumours and other cancer types.

143 re aged 60 years or older with acute myeloid leukaemia but unsuitable for intensive chemotherapy (or

144 s that are suspected of initiating childhood leukaemia by releasing factors that cause DNA damage in

145 n myelodysplastic syndrome and acute myeloid leukaemia cases from ClinicalTrials.gov.

146 d myelodysplastic syndrome and acute myeloid leukaemia cases reported in WHO's pharmacovigilance data

147 se for proteomic patterns in AML, a guide to leukaemia cell line selection, and a broadly applicable

148 es of cancer cells (KU812, a chronic myeloid leukaemia cell line; and DU145, a prostate cancer cell l

149 Using leukaemia cell lines and primary acute myeloid leukaemia

150 Moreover, leukaemia cell lines show limited proteomic similarities

151 c profiling of 205 patients with AML and 111 leukaemia cell lines.

152 shown to be expressed on chronic lymphocytic leukaemia cells and on the surface of newly formed vesse

153 otent cytotoxicity against NPM1c(+)HLA-A2(+) leukaemia cells and primary AML blasts, but not NPM1c(-)

154 rates and corresponding genomic patterns of leukaemia cells from 107 patients with CLL, spanning dec

155 rimary AML blasts, but not NPM1c(-)HLA-A2(+) leukaemia cells or HLA-A2(-) tumour cells.

156 LL and/or the responses of non-malignant and leukaemia cells to therapy; shared pathways for drug act

157 and patient-derived xenotransplants bearing leukaemia cells with low ferroportin expression.

158 a phenotypic feature of chronic lymphocytic leukaemia cells, can skew B cell development in mice, mo

159 Chronic lymphocytic leukaemia (CLL) is a highly informative model for cancer

160 olent growth dynamics of chronic lymphocytic leukaemia (CLL) to analyse the growth rates and correspo

161 h relapsed or refractory chronic lymphocytic leukaemia (CLL) who are on targeted therapies.

162 Chronic lymphocytic leukaemia (CLL), the most frequent type of leukaemia in

163 imentally, we focused on chronic lymphocytic leukaemia (CLL), where MIM showed high overall expressio

164 ukaemia stem cells (LSCs) in chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) have b

165 the treatment of choice for chronic myeloid leukaemia (CML), can cause lower gastrointestinal (GI) t

166 f myelodysplastic syndrome and acute myeloid leukaemia compared with placebo treatment (Peto OR 2.63

167 herapy for children with acute lymphoblastic leukaemia, conditions now predominately include musculos

168 stic syndromes or oligoblastic acute myeloid leukaemia (defined as blasts >=20% but <=30%) refractory

169 nts with treatment-naive chronic lymphocytic leukaemia done at 142 academic and community hospitals i

170 he 2017 European Conference on Infections in Leukaemia (ECIL 7) after a review of the literature on t

171 n deficiency treatment, demonstrates an anti-leukaemia effect in vitro and in vivo.

172 patients with newly diagnosed acute myeloid leukaemia, efficacy and safety did not differ by the 5-d

173 RB fusion-positive) B-cell acute lymphocytic leukaemia enrolled in clinical trials of multidrug chemo

174 ents with IGHV-unmutated chronic lymphocytic leukaemia enrolled on the CLL8 trial of the German Chron

175 ), seven (7%) of 100 had primary plasma cell leukaemia, five (5%) of 100 had t(14;20), four (4%) of 1

176 e screened 121 patients with chronic myeloid leukaemia for BCR-ABL1 kinase domain mutation.

177 as done in three (33%) of nine patients with leukaemia for whom surveillance status was confirmed and

178 f myelodysplastic syndrome and acute myeloid leukaemia, for which data are scarce.

179 Patients with acute myeloid leukaemia frequently have thrombocytopenia during induct

180 Chronic Lymphocytic Leukaemia Global Research Foundation and the National In

181 e 30 years, survivors of acute lymphoblastic leukaemia had, on average, 5.4 (95% CI 5.1-5.8) grade 1-

182 uplication (FLT3-ITD)-positive acute myeloid leukaemia have a poor prognosis, including high frequenc

183 ssion (TFR) in patients with chronic myeloid leukaemia have discontinued tyrosine kinase inhibitor (T

184 omes for younger patients with acute myeloid leukaemia have moderately improved over the past two dec

185 th ABL-class fusion B-cell acute lymphocytic leukaemia have poor outcomes when treated with regimens

186 ecting epigenetic regulation and splicing in leukaemia, how these processes influence one another to

187 Treatment-free remission in chronic myeloid leukaemia-ie, achievement of a sustained deep molecular

188 c leukaemia (CLL), the most frequent type of leukaemia in adults, is a lymphoproliferative disorder t

189 ine therapy in patients with chronic myeloid leukaemia in chronic phase in relation to the probabilit

190 ients (aged >=18 years) with chronic myeloid leukaemia in first chronic phase, who had received TKI t

191 patients were 18-70 years, had acute myeloid leukaemia in first or consecutive complete haematologica

192 Cs are defined by their capacity to initiate leukaemia in immunocompromised mice(4).

193 USA for the treatment of mIDH1 acute myeloid leukaemia in newly diagnosed patients ineligible for int

194 alue as frontline therapy in chronic myeloid leukaemia in order to achieve sustained deep molecular r

195 th ABL-class fusion B-cell acute lymphocytic leukaemia in the pre-tyrosine-kinase inhibitor era.

196 mutational precursors of chronic lymphocytic leukaemia (including trisomy 12, loss of chromosomes 13q

197 atients received treatment for acute myeloid leukaemia-including the two patients initially diagnosed

198 erlying molecular mechanisms, we reveal that leukaemia inhibitory factor (LIF) is a key paracrine fac

199 in self-renewal of mESCs in combination with leukaemia inhibitory factor and regulates the formation

200 ta might contribute to the first hit towards leukaemia initiation by bystander-like signalling to foe

201 principal driver defines a central event in leukaemia initiation.

202 active for patients with chronic lymphocytic leukaemia irrespective of IGHV mutation status but requi

203 Acute myeloid leukaemia is a fatal disease for most patients.

204 n as part of conditioning regimens for acute leukaemia is progressively declining because of concerns

205 Common childhood acute leukaemia is thought to be caused by two hits, the first

206 Patients with haematological malignancies (leukaemia, lymphoma, and myeloma) had a more severe COVI

207 tched on primary cancer diagnosis, including leukaemia, lymphoma, CNS tumours, neuroblastoma, Wilms t

208 ligible participants had been diagnosed with leukaemia, lymphoma, malignant CNS tumours, neuroblastom

209 me H3K9M mice succumbed to aggressive T cell leukaemia/lymphoma, while H3K36M mice exhibited differen

210 dification is catalyzed by the mixed lineage leukaemia (MLL) family of histone methyltransferases inc

211 In acute lymphoblastic leukaemia, MLPA has been used in research studies to ide

212 cant reduction of disease burden in a murine leukaemia model and patient-derived xenotransplants bear

213 le patients had a haematological malignancy (leukaemia, myelodysplastic syndrome, or lymphoma), were

214 dysplastic syndrome (n=99) and acute myeloid leukaemia (n=79) related to PARP inhibitor therapy were

215 one dose of study drug (chronic lymphocytic leukaemia, n=21; mantle cell lymphoma, n=21).

216 2 (50%) had adverse genetic risk by European Leukaemia Network classification.

217 refractory acute myeloid leukaemia or acute leukaemia of ambiguous lineage with adequate organ funct

218 Patients with acute myeloid leukaemia of any subtype except M3 and M7 were stratifie

219 In B cell leukaemia, oncogenic kinases phosphorylate IFITM3 at Tyr

220 Moreover, the presumption that familial leukaemias only present in childhood is no longer true,

221 y once daily (420 mg for chronic lymphocytic leukaemia or 560 mg for mantle cell lymphoma) until dise

222 rs with relapsed or refractory acute myeloid leukaemia or acute leukaemia of ambiguous lineage with a

223 We included patients with acute myeloid leukaemia or acute lymphocytic leukaemia, who received a

224 n HTLV-1 infected people will develop severe leukaemia or an ALS-like motor disease, unless a therapy

225 rapy), and had newly diagnosed acute myeloid leukaemia or high-risk myelodysplastic syndrome, and an

226 patients with newly diagnosed acute myeloid leukaemia or high-risk myelodysplastic syndrome.

227 patients with newly diagnosed acute myeloid leukaemia or high-risk myelodysplastic syndrome.

228 osed, Ph-negative B-cell acute lymphoblastic leukaemia or lymphoblastic lymphoma with CD20 expression

229 in patients with certain subtypes of B cell leukaemia or lymphoma, with promising efficacy also demo

230 or refractory high-risk chronic lymphocytic leukaemia or mantle cell lymphoma often do not derive du

231 h relapsed or refractory chronic lymphocytic leukaemia or mantle cell lymphoma, with an Eastern Coope

232 w pathology was done if available to confirm leukaemia or myelodysplastic syndrome diagnosis.

233 lder or comorbid patients with acute myeloid leukaemia or myelodysplastic syndrome.

234 lder or comorbid patients with acute myeloid leukaemia or myelodysplastic syndrome.

235 er with histologically confirmed lymphocytic leukaemia or relapsed or refractory B-cell non-Hodgkin l

236 or refractory high-risk chronic lymphocytic leukaemia or small lymphocytic lymphoma (del17p or del11

237 or refractory high-risk chronic lymphocytic leukaemia or small lymphocytic lymphoma (del17p or del11

238 untreated patients with chronic lymphocytic leukaemia or small lymphocytic lymphoma independent of h

239 patients with high-risk chronic lymphocytic leukaemia or small lymphocytic lymphoma, 13 (33%) of 40

240 ith previously untreated chronic lymphocytic leukaemia or small lymphocytic lymphoma, either aged 65

241 ingle-agent ibrutinib in chronic lymphocytic leukaemia or small lymphocytic lymphoma, follicular lymp

242 inutuzumab in first-line chronic lymphocytic leukaemia or small lymphocytic lymphoma.

243 53%) of 36 patients with chronic lymphocytic leukaemia or small lymphocytic lymphoma; incidence of gr

244 -escalation cohort (n=14 chronic lymphocytic leukaemia or small lymphocytic lymphoma; n=10 B-cell non

245 se-expansion cohort (n=9 chronic lymphocytic leukaemia or small lymphocytic lymphoma; n=13 B-cell non

246 he presence of therapy-related acute myeloid leukaemia, or being 65 years or older.

247 s secondary or therapy-related acute myeloid leukaemia, or TP53(mut) status.

248 nd myelodysplastic syndrome or acute myeloid leukaemia owing to both therapy-resistant disease and tr

249 ukaemia cell lines and primary acute myeloid leukaemia patient samples, we show that low expression o

250 ing and standard RNA-Seq for chronic myeloid leukaemia patient samples.

251 be upregulated in a subset of acute myeloid leukaemia patients, conferring susceptibility for IRAK4

252 tive prevention and treatment strategies for leukaemia predisposition in patients with Shwachman-Diam

253 ata to inform surveillance and treatment for leukaemia predisposition syndromes are scarce and recomm

254 epigenetic state and splicing in a subset of leukaemias, provide functional evidence that mutations i

255 stic syndromes or oligoblastic acute myeloid leukaemia refractory to hypomethylating agents.

256 stic syndromes or oligoblastic acute myeloid leukaemia refractory to hypomethylating agents.

257 f myelodysplastic syndrome and acute myeloid leukaemia related to PARP inhibition versus placebo trea

258 f myelodysplastic syndrome and acute myeloid leukaemia related to PARP inhibitor therapy were extract

259 f myelodysplastic syndrome and acute myeloid leukaemia related to PARP inhibitors, via a systematic r

260 en with relapsed or refractory acute myeloid leukaemia remain poor.

261 apsed or refractory B-cell acute lymphocytic leukaemia, reported between Jan 1, 2012, and April 14, 2

262 survivors of paediatric acute lymphoblastic leukaemia requires continued medical surveillance, couns

263 and 3D chromatin interaction data for these leukaemia risk loci suggests deregulation of B-cell deve

264 e between SNP6.0 and MLPA CNA calling on 143 leukaemia samples from two UK trials; comparing 1,287 ca

265 the rest of the UKCCMP cohort, patients with leukaemia showed a significantly increased case-fatality

266 CA016672, and the MD Anderson Cancer Center Leukaemia SPORE CA100632 from the National Cancer Instit

267 For two decades, leukaemia stem cells (LSCs) in chronic myeloid leukaemia

268 Leukaemia stem cells (LSCs) underlie cancer therapy resi

269 ing to an inability to effectively eradicate leukaemia stem cells (LSCs)(1).

270 CLL8 trial of the German Chronic Lymphocytic Leukaemia Study Group who were treated between July 21,

271 eavily relapsed and refractory acute myeloid leukaemia suggests that this combination should be teste

272 timate phenotype in these different familial leukaemia syndromes.

273 CH1 signalling in T-cell acute lymphoblastic leukaemia (T-ALL), and the involvement of BCL6 in other

274 nd the involvement of BCL6 in other types of leukaemia, this study is important to our understanding

275 g survivors of childhood acute lymphoblastic leukaemia treated over time.

276 outcomes of patients with acute lymphocytic leukaemia treated with anti-CD19 CAR T cells and identif

277 atients newly diagnosed with chronic myeloid leukaemia treated with first-line tyrosine kinase inhibi

278 on regimen for frontline chronic lymphocytic leukaemia treatment in younger fit patients.

279 Standfirst | In 2018, the acute myeloid leukaemia treatment landscape expanded notably, with the

280 gh changes in paediatric acute lymphoblastic leukaemia treatment protocols have improved overall surv

281 st (one [1%]), therapy-related acute myeloid leukaemia (two [3%]), and haematopoietic stem-cell trans

282 blished in patients with chronic lymphocytic leukaemia unrestricted by prognostic marker status.

283 f myelodysplastic syndrome and acute myeloid leukaemia versus placebo treatment.

284 The human T-cell leukaemia virus type 1 (HTLV-1) subtype c is endemic to

285 iptomes from 982 patients with acute myeloid leukaemia, we identified frequent overlap of mutations i

286 Here, using mouse models of leukaemia, we show that CARs provoke reversible antigen

287 man AML as well as syngeneic mouse models of leukaemia, we show that ligands of the danger detector N

288 ed myelodysplastic syndrome or acute myeloid leukaemia were eligible without additional restriction.

289 , 2018, 85 patients with chronic lymphocytic leukaemia were enrolled.

290 duct and no abnormal clonal proliferation or leukaemia were reported after gene therapy.

291 ed the relative rates of chronic lymphocytic leukaemia (which is more common among European individua

292 ommon among European individuals) and T cell leukaemia (which is more common among Japanese individua

293 rs with B-cell precursor acute lymphoblastic leukaemia who had late bone marrow relapses.

294 en with B-cell precursor acute lymphoblastic leukaemia who had late bone marrow relapses.

295 ents with IGHV-unmutated chronic lymphocytic leukaemia who might substantially benefit from treatment

296 nce or alloreactivity in patients with acute leukaemia who received a myeloablative 10/10 HLA-matched

297 acute myeloid leukaemia or acute lymphocytic leukaemia, who received a HSCT at any age from an unrela

298 ts with B-cell precursor acute lymphoblastic leukaemia with late bone marrow relapses and low minimal

299 rated into clinical trials for patients with leukaemia with low ferroportin levels.

300 years) fit patients with chronic lymphocytic leukaemia with mutated IGHV.