ライフサイエンスコーパス: acute lymphoblastic leukemia

1 splantation in Children and Adolescents with Acute Lymphoblastic Leukemia).

2 es are important risk factors for outcome in acute lymphoblastic leukemia.

3 istance to asparaginase therapy in childhood acute lymphoblastic leukemia.

4 owing T cell therapy for relapsed/refractory acute lymphoblastic leukemia.

5 sk factors for pancreatitis in patients with acute lymphoblastic leukemia.

6 pro-B and mature B cells and 184 lncRNAs in acute lymphoblastic leukemia.

7 se of a murine model of BCR-ABL(+) B-lineage acute lymphoblastic leukemia.

8 in DNM2 are common in early T-cell precursor acute lymphoblastic leukemia.

9 terns of RAG1-mediated breaks in human pro-B acute lymphoblastic leukemia.

10 ssion, and the pervasive emergence of T cell acute lymphoblastic leukemia.

11 netic subgroup of childhood B-cell precursor acute lymphoblastic leukemia.

12 re for potentially curable neoplasms such as acute lymphoblastic leukemia.

13 stablished component of induction therapy of acute lymphoblastic leukemia.

14 JAK1 and JAK3 are recurrently mutated in acute lymphoblastic leukemia.

15 dent myeloproliferative neoplasms and B cell acute lymphoblastic leukemia.

16 e in a phase 1 trial for treatment of B cell acute lymphoblastic leukemia.

17 ion of somatic structural DNA alterations in acute lymphoblastic leukemia.

18 ave undergone liver transplants, or who have acute lymphoblastic leukemia.

19 yielded remarkable outcomes in patients with acute lymphoblastic leukemia.

20 rapy who underwent allo-SCT for treatment of acute lymphoblastic leukemia.

21 loped acute leukemias (including four T-cell acute lymphoblastic leukemias), 12 developed Hodgkin lym

22 d in the GRAALL (Group for Research on Adult Acute Lymphoblastic Leukemia) -2003 and -2005 studies.

23 ed reduced rates of cranial radiotherapy for acute lymphoblastic leukemia (85% in the 1970s, 51% in t

24 aginase, a key component in the treatment of acute lymphoblastic leukemia, acts by depleting asparagi

25 loid leukemia and pediatric B-cell precursor acute lymphoblastic leukemia after allogeneic stem cell

26 CD4+:CD8+ composition to adults with B cell acute lymphoblastic leukemia after lymphodepletion chemo

27 ween 2002 and 2007 (including 2,275 cases of acute lymphoblastic leukemia (ALL) and 418 cases of acut

28 MLL-fusion proteins, which could drive both acute lymphoblastic leukemia (ALL) and acute myeloid leu

29 Chromosomal rearrangements are a hallmark of acute lymphoblastic leukemia (ALL) and are important ALL

30 in patients with relapsed/refractory B-cell acute lymphoblastic leukemia (ALL) and chronic lymphocyt

31 sine kinases (TKs) drive pediatric high-risk acute lymphoblastic leukemia (ALL) and confer resistance

32 st common genetic rearrangement in childhood acute lymphoblastic leukemia (ALL) and gives rise to the

33 ontline treatment of virtually all childhood acute lymphoblastic leukemia (ALL) and in many adult ALL

34 The associations between childhood acute lymphoblastic leukemia (ALL) and several proxies o

35 cohort included patients under treatment of acute lymphoblastic leukemia (ALL) and the second is pat

36 Glucocorticoids are important therapy for acute lymphoblastic leukemia (ALL) and their major adver

37 induction failure in patients with pediatric acute lymphoblastic leukemia (ALL) and to identify genet

38 Survivors of childhood acute lymphoblastic leukemia (ALL) are at risk for low b

39 Purpose Survivors of childhood acute lymphoblastic leukemia (ALL) are at risk for neuro

40 Purpose Children with acute lymphoblastic leukemia (ALL) are generally instruc

41 Patients with t(1;19)-positive acute lymphoblastic leukemia (ALL) are prone to central

42 lls to recognize and eliminate CD19-positive acute lymphoblastic leukemia (ALL) blasts, was approved

43 BH3 mimetic drugs may be useful to treat acute lymphoblastic leukemia (ALL) but the sensitivity o

44 el of Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) by combined targeting

45 issue in the context of TEL-AML1-associated acute lymphoblastic leukemia (ALL) by profiling a refine

46 Childhood acute lymphoblastic leukemia (ALL) can often be traced t

47 fusion accounts for <1% of B-cell precursor acute lymphoblastic leukemia (ALL) cases and occurs with

48 Acute lymphoblastic leukemia (ALL) cells reside in the b

49 of nucleotide biosynthesis in ATR-inhibited acute lymphoblastic leukemia (ALL) cells reveals substan

50 Primary adult acute lymphoblastic leukemia (ALL) cells treated with vi

51 nges in P-glycoprotein overexpressing T-cell acute lymphoblastic leukemia (ALL) cells, which escaped

52 In those days, acute myeloid leukemia and acute lymphoblastic leukemia (ALL) could not be distingu

53 e (Ph)-negative relapsed or refractory (r/r) acute lymphoblastic leukemia (ALL) eventually resulting

54 With cure rates of childhood acute lymphoblastic leukemia (ALL) exceeding 85%, there

55 Survivors of childhood acute lymphoblastic leukemia (ALL) exhibit increased rat

56 igh-titer anti-MV antibody in 16 adults with acute lymphoblastic leukemia (ALL) following treatments

57 cell transplantation (HCT) of patients with acute lymphoblastic leukemia (ALL) identifies patients a

58 Outcome of childhood acute lymphoblastic leukemia (ALL) improved greatly by i

59 The distinct nature of acute lymphoblastic leukemia (ALL) in adults, evidenced

60 hromosomes is an uncommon genetic feature of acute lymphoblastic leukemia (ALL) in both children and

61 ed several susceptibility loci for childhood acute lymphoblastic leukemia (ALL) in populations of Eur

62 Prognosis of Philadelphia-positive (Ph(+)) acute lymphoblastic leukemia (ALL) in the elderly has im

63 e complete response (CR) rate in adults with acute lymphoblastic leukemia (ALL) is 80% to 90%, and th

64 Ph-like acute lymphoblastic leukemia (ALL) is a genetically defi

65 Philadelphia chromosome-like (Ph-like) acute lymphoblastic leukemia (ALL) is a high-risk subtyp

66 Philadelphia chromosome (Ph)-like acute lymphoblastic leukemia (ALL) is a high-risk subtyp

67 Purpose Philadelphia chromosome (Ph) -like acute lymphoblastic leukemia (ALL) is a high-risk subtyp

68 T-cell acute lymphoblastic leukemia (ALL) is a rare disease in

69 Early T-cell precursor (ETP) acute lymphoblastic leukemia (ALL) is a recently describ

70 Purpose Early thymic precursor (ETP) acute lymphoblastic leukemia (ALL) is an immunophenotypi

71 Therapy for childhood acute lymphoblastic leukemia (ALL) is associated with 5-

72 Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) is characterized by a

73 MP) during maintenance therapy for childhood acute lymphoblastic leukemia (ALL) is critical for susta

74 TCF3-HLF-positive acute lymphoblastic leukemia (ALL) is currently incurabl

75 Acute lymphoblastic leukemia (ALL) is the commonest chil

76 Acute lymphoblastic leukemia (ALL) is the most common ch

77 Acute lymphoblastic leukemia (ALL) is the most common ch

78 Acute lymphoblastic leukemia (ALL) is the most common pe

79 hip of mode of delivery to risk of childhood acute lymphoblastic leukemia (ALL) is uncertain.

80 Patients with B-lineage acute lymphoblastic leukemia (ALL) may also have the CD2

81 ether a higher BMI at diagnosis of pediatric acute lymphoblastic leukemia (ALL) or acute myeloid leuk

82 A total of 68 survivors of childhood acute lymphoblastic leukemia (ALL) or brain tumor (BT) w

83 evaluate treatment outcomes in children with acute lymphoblastic leukemia (ALL) over the past 3 decad

84 Increased understanding of pediatric acute lymphoblastic leukemia (ALL) pathobiology has led

85 e first active transcriptional profiles from acute lymphoblastic leukemia (ALL) patients acquired her

86 The outcome for pediatric acute lymphoblastic leukemia (ALL) patients who relapse

87 dual disease (MRD) in B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) patients with a sensi

88 Acute lymphoblastic leukemia (ALL) persisting or relapsi

89 olescent and young adult (AYA) patients with acute lymphoblastic leukemia (ALL) poses unique challeng

90 Relapsed and refractory acute lymphoblastic leukemia (ALL) remains difficult to

91 in Philadelphia chromosome-positive (Ph(+)) acute lymphoblastic leukemia (ALL) remains undefined.

92 of concept data by profiling 60 drugs on 68 acute lymphoblastic leukemia (ALL) samples mostly from r

93 thereby generating a model of t(4;11) pro-B acute lymphoblastic leukemia (ALL) that fully recapitula

94 udy evaluated the efficacy of pediatric-like acute lymphoblastic leukemia (ALL) therapy in adults wit

95 Induction therapy for childhood acute lymphoblastic leukemia (ALL) traditionally include

96 Survivors of childhood acute lymphoblastic leukemia (ALL) treated with CNS-dire

97 Acute lymphoblastic leukemia (ALL) typically originates

98 conomic position (SEP) and risk of childhood acute lymphoblastic leukemia (ALL) were investigated usi

99 phia chromosome-positive (Ph(+)) B-precursor acute lymphoblastic leukemia (ALL) who progress after fa

100 Infant acute lymphoblastic leukemia (ALL) with MLL rearrangemen

101 following induction therapy in patients with acute lymphoblastic leukemia (ALL) with relapse and mort

102 tent sensitivity of many high-risk childhood acute lymphoblastic leukemia (ALL) xenografts to navitoc

103 In a panel of 7 patient-derived pediatric acute lymphoblastic leukemia (ALL) xenografts, PR-104 sh

104 blood cells, in CSF samples at diagnosis of acute lymphoblastic leukemia (ALL), a uniform CSF and ri

105 anial radiotherapy (CRT) in the treatment of acute lymphoblastic leukemia (ALL), adult survivors of c

106 Philadelphia chromosome (Ph)-like acute lymphoblastic leukemia (ALL), also referred to as

107 ids are universally used in the treatment of acute lymphoblastic leukemia (ALL), and resistance to gl

108 key component in the treatment of pediatric acute lymphoblastic leukemia (ALL), but can induce serio

109 n is a promising target for immunotherapy of acute lymphoblastic leukemia (ALL), but CD19(-) relapses

110 s an integral part of treatment of childhood acute lymphoblastic leukemia (ALL), but it is associated

111 In acute lymphoblastic leukemia (ALL), central nervous syst

112 ce, and fitness among survivors of childhood acute lymphoblastic leukemia (ALL), especially those tre

113 n factor IKAROS, are a hallmark of high-risk acute lymphoblastic leukemia (ALL), however the role of

114 omosome (Ph)-negative B-cell precursor (BCP) acute lymphoblastic leukemia (ALL), often comprising sma

115 widely performed in children with high-risk acute lymphoblastic leukemia (ALL), the influence of don

116 lays an etiologic role in the development of acute lymphoblastic leukemia (ALL), the most common chil

117 ranscriptome sequencing of 231 children with acute lymphoblastic leukemia (ALL), we identified 58 put

118 t a tumor suppressive role for PTEN in pre-B acute lymphoblastic leukemia (ALL), we induced Cre-media

119 mise in the clinic to treat refractory CD19+ acute lymphoblastic leukemia (ALL).

120 opoietic transcription factors are common in acute lymphoblastic leukemia (ALL).

121 iting toxicity in the treatment of pediatric acute lymphoblastic leukemia (ALL).

122 sitive dyes in patient-derived xenografts of acute lymphoblastic leukemia (ALL).

123 six genes that are associated with childhood acute lymphoblastic leukemia (ALL).

124 her clinical contexts, including JAK-mutated acute lymphoblastic leukemia (ALL).

125 ow represent the normal counterpart for most acute lymphoblastic leukemia (ALL).

126 leading cause of mortality in children with acute lymphoblastic leukemia (ALL).

127 with Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL).

128 mbination chemotherapy regimens in pediatric acute lymphoblastic leukemia (ALL).

129 amethasone response in pediatric B-precursor acute lymphoblastic leukemia (ALL).

130 tients with leukemia or lymphoma, especially acute lymphoblastic leukemia (ALL).

131 nic transformation in mouse models for pre-B acute lymphoblastic leukemia (ALL).

132 MCV) and two occurrences of B cell-precursor acute lymphoblastic leukemia (ALL).

133 nosed Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL).

134 (MP) is the mainstay of curative therapy for acute lymphoblastic leukemia (ALL).

135 adults with relapsed/refractory B-precursor acute lymphoblastic leukemia (ALL).

136 ne nucleotide [TGN] levels) in children with acute lymphoblastic leukemia (ALL).

137 nce contributes to poor outcome in pediatric acute lymphoblastic leukemia (ALL).

138 ) is a central component in the treatment of acute lymphoblastic leukemia (ALL).

139 se issues in mouse transplantation models of acute lymphoblastic leukemia (ALL).

140 aginase is a chemotherapy drug used to treat acute lymphoblastic leukemia (ALL).

141 stance for children with relapsed/refractory acute lymphoblastic leukemia (ALL).

142 e has been associated with risk of childhood acute lymphoblastic leukemia (ALL).

143 disease (MRD) in 48 patients with childhood acute lymphoblastic leukemia (ALL).

144 mortality in pediatric patients treated for acute lymphoblastic leukemia (ALL).

145 Asparaginase is used to treat acute lymphoblastic leukemia (ALL); however, hypersensit

146 ing to 4 disease categories: AML (n = 5310); acute lymphoblastic leukemia (ALL, n = 1883); chronic my

147 The cohort included patients with acute lymphoblastic leukemia (ALL; n = 47), chronic lymp

148 pressing cells induces development of T-cell acute lymphoblastic leukemia and lymphoma, but not other

149 imethyltransferase, are enriched in relapsed acute lymphoblastic leukemia and MLL-rearranged acute le

150 nd deletions in ribosomal proteins in T-cell acute lymphoblastic leukemia and solid tumors, further e

151 th reduced late mortality among survivors of acute lymphoblastic leukemia and Wilms' tumor.

152 oma, relapsed or refractory B-cell precursor acute lymphoblastic leukemia, and acute myeloid leukemia

153 ts with acute myeloid leukemia (AML), T-cell acute lymphoblastic leukemia, and myelodysplastic syndro

154 omains, the same two hotspots seen in T-cell acute lymphoblastic leukemias, and led to pathway activa

155 n, we report that CD10, also known as common acute lymphoblastic leukemia antigen, neutral endopeptid

156 s of NOTCH1 (a well-known oncogene in T-cell acute lymphoblastic leukemia) are present in approximate

157 d with those of acute myeloid leukemia and T-acute lymphoblastic leukemia, as well as the transcripto

158 aired B cell development, followed by B cell acute lymphoblastic leukemia at 100% incidence and with

159 ukemic progression of both B cell and T cell acute lymphoblastic leukemia (B-ALL and T-ALL, respectiv

160 Infant B-cell acute lymphoblastic leukemia (B-ALL) accounts for 10% of

161 d development are a hallmark of B-progenitor acute lymphoblastic leukemia (B-ALL) and most commonly i

162 re associated with poor outcome in B lineage acute lymphoblastic leukemia (B-ALL) and occur in >70% o

163 ed the role of CD9 in the dissemination of B acute lymphoblastic leukemia (B-ALL) cells, by stably do

164 We treated 7 patients with B-cell acute lymphoblastic leukemia (B-ALL) harboring rearrange

165 cts in relapsed and/or refractory pre-B cell acute lymphoblastic leukemia (B-ALL), but antigen loss i

166 neage leukemia-rearranged (MLL-rearranged) B-acute lymphoblastic leukemia (B-ALL), which constitutes

167 y is much less effective against Ph(+)B-cell acute lymphoblastic leukemia (B-ALL).

168 indicates poor prognosis in precursor B-cell acute lymphoblastic leukemia (B-ALL).

169 of patients with relapsed/refractory B cell acute lymphoblastic leukemia (B-ALL).

170 netic hallmark of an aggressive infant pro-B-acute lymphoblastic leukemia (B-ALL).

171 occurs frequently in human progenitor B-cell acute lymphoblastic leukemia (B-ALL).

172 s highly prognostic in pediatric B-precursor acute lymphoblastic leukemia (B-ALL).

173 ) during early B-cell development and B-cell acute lymphoblastic leukemia (B-ALL).

174 K2) to eradicate disease in high-risk B-cell acute lymphoblastic leukemia (B-ALL).

175 tivity against relapsed/refractory B-lineage acute lymphoblastic leukemia (B-ALL).

176 plays an important role in pre-BCR(+) B cell acute lymphoblastic leukemia (B-ALL).

177 chemotherapy for childhood B-cell precursor acute lymphoblastic leukemia (B-ALL).

178 n factor STAT5 has a critical role in B cell acute lymphoblastic leukemia (B-ALL).

179 estigated DNA methylomes of pediatric B-cell acute lymphoblastic leukemias (B-ALLs) using whole-genom

180 ng, including the high-risk subset of B cell acute lymphoblastic leukemias (B-ALLs) with CRLF2 rearra

181 of secondary genetic events in human B-cell acute lymphoblastic leukemias (B-ALLs), illustrating the

182 B cell precursor acute lymphoblastic leukemia (BCP ALL) is the most commo

183 ly, 20% to 30% of pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) could not be clas

184 advance in the treatment of B-cell precursor acute lymphoblastic leukemia (BCP-ALL).

185 en with relapsed/refractory B-cell precursor acute lymphoblastic leukemia (BCP-ALL).

186 tical for cure of childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL).

187 n in relapsed or refractory B-cell precursor acute lymphoblastic leukemia (BCP-ALL).

188 BCR-ABL1(+) precursor B-cell acute lymphoblastic leukemia (BCR-ABL1(+) B-ALL) is an a

189 cancers and primary, patient-derived B-cell acute lymphoblastic leukemia blasts compared with standa

190 Patients with B cell precursor acute lymphoblastic leukemia (BPL) respond well to chemo

191 g CD19 (CAR-19) have potent activity against acute lymphoblastic leukemia, but fewer results supporti

192 airy cell leukemia and in some children with acute lymphoblastic leukemia, but have been much less ef

193 el recurrent fusion gene in B-cell precursor acute lymphoblastic leukemia, but the function of the en

194 i formation in human PBMCs (lymphocytes) and acute lymphoblastic leukemia CCRF-CEM cells documented s

195 o malignant transformation because B-lineage acute lymphoblastic leukemia cells display a pronounced

196 Inhibition of Hsp72 in acute lymphoblastic leukemia cells resulted in increased

197 Central nervous system acute lymphoblastic leukemia (CNS-ALL) is a major clinic

198 Acute lymphoblastic leukemia developed in 2 of the 29 pa

199 inib (in the European Study for Philadelphia-Acute Lymphoblastic Leukemia [EsPhALL]).

200 diatric-inspired Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) protocol yielded a

201 n et al from the Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) show that young to

202 the intensified Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL)-2003/2005 trials.

203 r children and young adults with high-risk B-acute lymphoblastic leukemia has improved significantly,

204 cies such as non-Hodgkin lymphoma (B-NHL) or acute lymphoblastic leukemia have a poor prognosis.

205 Children with acute myeloid leukemia, infant acute lymphoblastic leukemia, hepatoblastoma, and malign

206 male) the most common initial diagnoses were acute lymphoblastic leukemia, Hodgkin lymphoma, and astr

207 The genomic lesions that characterize acute lymphoblastic leukemia in childhood include recurr

208 270 children enrolled in clinical trials for acute lymphoblastic leukemia in Guatemala, Singapore and

209 with Amerindian ancestry and higher risk of acute lymphoblastic leukemia in Hispanics.

210 hort of 5,185 children and young adults with acute lymphoblastic leukemia, including 117 (2.3%) who w

211 ified T cell therapy for relapsed/refractory acute lymphoblastic leukemia is leading to expanded use

212 The prognosis for adults with relapsed acute lymphoblastic leukemia is poor.

213 LL-AR-03 trial (Treatment of High Risk Adult Acute Lymphoblastic Leukemia [LAL-AR/2003]) assigned ado

214 The limited available data suggest that an "acute lymphoblastic leukemia-like" regimen followed by a

215 Early T-cell precursor (ETP) acute lymphoblastic leukemia/lymphoma (ALL/LBL) is a rec

216 rotein Rpl22 is a tumor suppressor in T-cell acute lymphoblastic leukemia/lymphoma (T-ALL), and that

217 ells, double-deficient mice developed T cell acute lymphoblastic leukemia/lymphoma, which originated

218 ildren's Oncology Group trials P9404 (T-cell acute lymphoblastic leukemia/lymphoma; n = 537), P9425 (

219 in other hematologic malignancies, including acute lymphoblastic leukemia, natural killer/T-cell lymp

220 B-cell NHL, HL, and acute lymphoblastic leukemia occur at a high rate and ea

221 BMT recipients with acute myeloid leukemia, acute lymphoblastic leukemia, or myelodysplastic syndrom

222 BCR-ABL(+) acute lymphoblastic leukemia patients have transient res

223 commonly occurs in T-ALL and relapsed B-cell acute lymphoblastic leukemia patients, and is associated

224 Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph(+) ALL) is currently tr

225 tients with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph(+) ALL) undergoing main

226 Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) is initiated and

227 Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL) is a high-ris

228 Philadelphia chromosome (Ph)-like B-cell acute lymphoblastic leukemia (Ph-like ALL) is associated

229 Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL) is characteri

230 reatment of Philadelphia chromosome-negative acute lymphoblastic leukemia (Ph-neg ALL) do not appear

231 l age, but no associations were observed for acute lymphoblastic leukemia, plasma cell neoplasms, or

232 s a hallmark of BCR-ABL1(+) precursor B cell acute lymphoblastic leukemia (pre-B ALL).

233 ics and biology of infant and childhood PreB acute lymphoblastic leukemia (PreB-ALL), initiated by di

234 screens of 123 mammary tumors and 20 B-cell acute lymphoblastic leukemias, respectively.

235 patients with high-risk genetics and T-cell acute lymphoblastic leukemia responded more slowly.

236 activity as a single agent, particularly for acute lymphoblastic leukemia, resulting in its US Food a

237 ients with advanced non-Hodgkin lymphoma and acute lymphoblastic leukemia safely underwent hematopoie

238 Finally, analysis of Myc-induced T cell acute lymphoblastic leukemia showed that cells are arres

239 ia (sRR = 2.07; 95% CI: 1.34, 3.20) than for acute lymphoblastic leukemia (sRR = 1.49; 95% CI: 1.07,

240 = 2.34, 95% CI: 1.72, 3.18; n = 6) than for acute lymphoblastic leukemia (sRR = 1.57; 95% CI: 1.21,

241 We mapped insulated neighborhoods in T cell acute lymphoblastic leukemia (T-ALL) and found that tumo

242 OTCH1 mutations are frequent in human T-cell acute lymphoblastic leukemia (T-ALL) and Notch inhibitor

243 This causes rapid onset of acute lymphoblastic leukemia (T-ALL) and progressive dev

244 cells effectively eliminate malignant T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoma

245 ne kinase is mutated in 10% to 16% of T-cell acute lymphoblastic leukemia (T-ALL) cases.

246 Here, we report that T-cell acute lymphoblastic leukemia (T-ALL) cells are character

247 Primary T-cell acute lymphoblastic leukemia (T-ALL) cells require strom

248 ll migration has been demonstrated in T cell acute lymphoblastic leukemia (T-ALL) cells upon calcineu

249 n aberrant transcriptional program in T-cell acute lymphoblastic leukemia (T-ALL) cells.

250 ed Notch signaling is associated with T-cell Acute Lymphoblastic Leukemia (T-ALL) development and pro

251 Current chemotherapies for T cell acute lymphoblastic leukemia (T-ALL) efficiently reduce

252 rved the development of a spontaneous T-cell acute lymphoblastic leukemia (T-ALL) in these animals.

253 T-cell acute lymphoblastic leukemia (T-ALL) is a heterogeneous

254 T-cell acute lymphoblastic leukemia (T-ALL) is a highly prolife

255 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive ch

256 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive fo

257 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive ma

258 T-cell immunophenotype of acute lymphoblastic leukemia (T-ALL) is an uncommon aggr

259 Risk stratification in childhood T-cell acute lymphoblastic leukemia (T-ALL) is mainly based on

260 Spontaneous T-cell acute lymphoblastic leukemia (T-ALL) occurred in 100% of

261 was recently implicated in pediatric T-cell acute lymphoblastic leukemia (T-ALL) patients and murine

262 More than half of T-cell acute lymphoblastic leukemia (T-ALL) patients harbor gai

263 Pediatric T-acute lymphoblastic leukemia (T-ALL) patients often disp

264 tion factor is mutated in a subset of T-cell acute lymphoblastic leukemia (T-ALL) patients, and RUNX1

265 otential of siRNNs as therapeutic tools in T-acute lymphoblastic leukemia (T-ALL) using T-ALL cell li

266 B2 is an oncogenic driver of immature T-cell acute lymphoblastic leukemia (T-ALL), a heterogenic subg

267 umor suppressors, are hallmarks of T-lineage acute lymphoblastic leukemia (T-ALL), but detailed genom

268 receptors compared with wild type in T cell acute lymphoblastic leukemia (T-ALL), but its administra

269 These tumors resemble human T-cell acute lymphoblastic leukemia (T-ALL), in that they predo

270 The role of the microenvironment in T cell acute lymphoblastic leukemia (T-ALL), or any acute leuke

271 s what role Wnt signaling may play in T-cell acute lymphoblastic leukemia (T-ALL), we used a stably i

272 ions of LMO2, a prominent oncogene in T-cell acute lymphoblastic leukemia (T-ALL).

273 cure rate of patients suffering from T-cell acute lymphoblastic leukemia (T-ALL).

274 most notable example being NOTCH1 in T-cell acute lymphoblastic leukemia (T-ALL).

275 s exemplified by LIM-only 2 (LMO2) in T-cell acute lymphoblastic leukemia (T-ALL).

276 ion" mutants of Notch1 NRR associated with T Acute lymphoblastic Leukemia (T-ALL).

277 is pathway functions in the progression of T acute lymphoblastic leukemia (T-ALL).

278 ing mutations in NOTCH1 are common in T cell acute lymphoblastic leukemia (T-ALL).

279 co-expressed with activated NOTCH1 in T cell acute lymphoblastic leukemia (T-ALL).

280 ntial for Notch-mediated induction of T-cell acute lymphoblastic leukemia (T-ALL).

281 enic driver and therapeutic target in T-cell acute lymphoblastic leukemia (T-ALL).

282 gain of function mutations, including T-cell acute lymphoblastic leukemia (T-ALL).

283 al microRNAs (miRNAs) in Notch-driven T-cell acute lymphoblastic leukemias (T-ALLs) has recently been

284 SCL/TAL1 (stem cell leukemia/T-cell acute lymphoblastic leukemia [T-ALL] 1) is an essential

285 omes in patients with relapsed or refractory acute lymphoblastic leukemia than does standard therapy.

286 et al. describe rare, non-cycling blasts in acute lymphoblastic leukemia that combine the phenotypes

287 assigned adults with relapsed or refractory acute lymphoblastic leukemia to receive either inotuzuma

288 Survivors of childhood acute lymphoblastic leukemia treated on contemporary che

289 hirty-nine subjects with relapsed/refractory acute lymphoblastic leukemia treated with chimeric antig

290 Chronic Myeloid Leukemia Evaluation and Ph(+)Acute Lymphoblastic Leukemia trial, including 231 patien

291 have been made in the treatment of pediatric acute lymphoblastic leukemia, up to one of five patients

292 adults with relapsed or refractory B-lineage acute lymphoblastic leukemia was conducted using a CD19

293 cells from 6 patients with B-progenitor cell acute lymphoblastic leukemia, we demonstrate that patien

294 election approach in a murine model of Ph(+) acute lymphoblastic leukemia, we indeed find that tempor

295 as their Arf-null counterparts in generating acute lymphoblastic leukemia when infused into unconditi

296 s with acute myelogenous leukemia and B-cell acute lymphoblastic leukemia whose tumors harbor point m

297 The response rate was highest for acute lymphoblastic leukemia, with four of five patients

298 ethotrexate for the treatment of high-risk B-acute lymphoblastic leukemia, with no increase in acute

299 lasting antitumor responses against systemic acute lymphoblastic leukemia xenografts.

300 ector function of human NK cells in a B-cell acute lymphoblastic leukemia xenotransplants model.