ライフサイエンスコーパス: lymphoblastic

1 With time in culture, lymphoblastic cell lines (LCLs) from two affected indivi

2 of survival trends for precursor-cell acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemi

3 Survivors of childhood acute lymphoblastic leukaemia (ALL) are at risk for neurocogni

4 In approximately 25% of cases, acute lymphoblastic leukaemia (ALL) cells carry the oncogenic

5 ted genetic basis of susceptibility to acute lymphoblastic leukaemia (ALL) in children, yet the effec

6 tudies have shown an increased risk of acute lymphoblastic leukaemia (ALL) in young children born by

7 sed as first line drugs for paediatric Acute Lymphoblastic Leukaemia (ALL) treatment for more than 40

8 te recent advances in the cure rate of acute lymphoblastic leukaemia (ALL), the prognosis for patient

9 marked success in relapsed pre-B-cell acute lymphoblastic leukaemia (ALL).

10 earrangements are initiating events in acute lymphoblastic leukaemia (ALL).

11 tion is rarely suspected for childhood acute lymphoblastic leukaemia (ALL).

12 cur in over 80% of cases of pre-B-cell acute lymphoblastic leukaemia (ALL).

13 Paediatric B-cell precursor acute lymphoblastic leukaemia (BCP-ALL) is the most common can

14 Despite high-hyperdiploid acute lymphoblastic leukaemia (HD-ALL) being the most common s

15 studied a mouse model of human T-cell acute lymphoblastic leukaemia (T-ALL) and used intravital micr

16 rs) with relapsed or refractory B-cell acute lymphoblastic leukaemia (with CD22 expression on at leas

17 enescence in p53-regulatable models of acute lymphoblastic leukaemia and acute myeloid leukaemia was

18 mergence of clonal dominance in T-cell acute lymphoblastic leukaemia and tumour evolution resulting i

19 nalysis, we used data of children with acute lymphoblastic leukaemia at St Jude Children's Research H

20 years) diagnosed with t(9;22)-negative acute lymphoblastic leukaemia between June 1, 1996, and Jan 1,

21 en consistently expressed on B-lineage acute lymphoblastic leukaemia cells.

22 ith relapsed or refractory B-precursor acute lymphoblastic leukaemia characterised by negative progno

23 ntelligent decision support system for acute lymphoblastic leukaemia diagnosis from microscopic blood

24 s aged 1-18 years with newly diagnosed acute lymphoblastic leukaemia from 11 consortium sites in the

25 ith relapsed or refractory B-precursor acute lymphoblastic leukaemia have an unfavourable prognosis.

26 with Philadelphia chromosome-positive acute lymphoblastic leukaemia in this continuing phase 2 trial

27 Survivors of childhood acute lymphoblastic leukaemia might benefit from preventive co

28 thout cranial radiation, for childhood acute lymphoblastic leukaemia predicted higher risk for long-t

29 lastic leukaemia study groups assessed acute lymphoblastic leukaemia protocols to address toxic effec

30 phi method, 15 international childhood acute lymphoblastic leukaemia study groups assessed acute lymp

31 Survival for childhood acute lymphoblastic leukaemia surpasses 90% with contemporary

32 es in long-term survivors of childhood acute lymphoblastic leukaemia treated with chemotherapy withou

33 n the overall assessment of outcome of acute lymphoblastic leukaemia treatment, these expert opinion-

34 consensus algorithms for reporting on acute lymphoblastic leukaemia treatment.

35 iated pancreatitis to asparaginase, 18 acute lymphoblastic leukaemia trial groups merged data for thi

36 me (Ph)-positive or Ph-negative B-cell acute lymphoblastic leukaemia who were due to receive first or

37 atients were diagnosed with non-B-cell acute lymphoblastic leukaemia, aged at least 8 years, and surv

38 e children undergoing chemotherapy for acute lymphoblastic leukaemia, although its effects on long-te

39 l component of treatment for childhood acute lymphoblastic leukaemia, and is usually administered int

40 high survival rates for children with acute lymphoblastic leukaemia, their outcome is often counterb

41 iation and to prevent Notch3-induced T-acute lymphoblastic leukaemia.

42 nosed Philadelphia chromosome-positive acute lymphoblastic leukaemia.

43 erated CAR T cells in a mouse model of acute lymphoblastic leukaemia.

44 lts with relapsed or refractory B-cell acute lymphoblastic leukaemia.

45 iladelphia chromosome-positive (Ph(+)) acute lymphoblastic leukaemia.

46 uced rates of cranial radiotherapy for acute lymphoblastic leukemia (85% in the 1970s, 51% in the 198

47 usion proteins, which could drive both acute lymphoblastic leukemia (ALL) and acute myeloid leukemia

48 somal rearrangements are a hallmark of acute lymphoblastic leukemia (ALL) and are important ALL initi

49 tients with relapsed/refractory B-cell acute lymphoblastic leukemia (ALL) and chronic lymphocytic leu

50 inases (TKs) drive pediatric high-risk acute lymphoblastic leukemia (ALL) and confer resistance to st

51 e treatment of virtually all childhood acute lymphoblastic leukemia (ALL) and in many adult ALL patie

52 The associations between childhood acute lymphoblastic leukemia (ALL) and several proxies of earl

53 t included patients under treatment of acute lymphoblastic leukemia (ALL) and the second is patients

54 cocorticoids are important therapy for acute lymphoblastic leukemia (ALL) and their major adverse eff

55 ion failure in patients with pediatric acute lymphoblastic leukemia (ALL) and to identify genetic abn

56 Survivors of childhood acute lymphoblastic leukemia (ALL) are at risk for low bone mi

57 Purpose Survivors of childhood acute lymphoblastic leukemia (ALL) are at risk for neurocognit

58 Purpose Children with acute lymphoblastic leukemia (ALL) are generally instructed to

59 recognize and eliminate CD19-positive acute lymphoblastic leukemia (ALL) blasts, was approved for us

60 3 mimetic drugs may be useful to treat acute lymphoblastic leukemia (ALL) but the sensitivity of prim

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

62 in the context of TEL-AML1-associated acute lymphoblastic leukemia (ALL) by profiling a refined prog

63 n accounts for <1% of B-cell precursor acute lymphoblastic leukemia (ALL) cases and occurs within the

64 Acute lymphoblastic leukemia (ALL) cells reside in the bone ma

65 cleotide biosynthesis in ATR-inhibited acute lymphoblastic leukemia (ALL) cells reveals substantial r

66 Primary adult acute lymphoblastic leukemia (ALL) cells treated with vincrist

67 those days, acute myeloid leukemia and acute lymphoblastic leukemia (ALL) could not be distinguished,

68 -negative relapsed or refractory (r/r) acute lymphoblastic leukemia (ALL) eventually resulting in con

69 Survivors of childhood acute lymphoblastic leukemia (ALL) exhibit increased rates of

70 Outcome of childhood acute lymphoblastic leukemia (ALL) improved greatly by intensi

71 omes is an uncommon genetic feature of acute lymphoblastic leukemia (ALL) in both children and adults

72 eral susceptibility loci for childhood acute lymphoblastic leukemia (ALL) in populations of European

73 nosis of Philadelphia-positive (Ph(+)) acute lymphoblastic leukemia (ALL) in the elderly has improved

74 Ph-like acute lymphoblastic leukemia (ALL) is a genetically defined hi

75 Philadelphia chromosome-like (Ph-like) acute lymphoblastic leukemia (ALL) is a high-risk subtype char

76 Philadelphia chromosome (Ph)-like acute lymphoblastic leukemia (ALL) is a high-risk subtype of A

77 ose Philadelphia chromosome (Ph) -like acute lymphoblastic leukemia (ALL) is a high-risk subtype of c

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

79 Purpose Early thymic precursor (ETP) acute lymphoblastic leukemia (ALL) is an immunophenotypically

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

81 ring maintenance therapy for childhood acute lymphoblastic leukemia (ALL) is critical for sustaining

82 TCF3-HLF-positive acute lymphoblastic leukemia (ALL) is currently incurable.

83 Acute lymphoblastic leukemia (ALL) is the most common childhoo

84 Acute lymphoblastic leukemia (ALL) is the most common childhoo

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

86 Patients with B-lineage acute lymphoblastic leukemia (ALL) may also have the CD20 anti

87 a higher BMI at diagnosis of pediatric acute lymphoblastic leukemia (ALL) or acute myeloid leukemia (

88 A total of 68 survivors of childhood acute lymphoblastic leukemia (ALL) or brain tumor (BT) with id

89 Increased understanding of pediatric acute lymphoblastic leukemia (ALL) pathobiology has led to dra

90 t active transcriptional profiles from acute lymphoblastic leukemia (ALL) patients acquired here reve

91 The outcome for pediatric acute lymphoblastic leukemia (ALL) patients who relapse is dis

92 isease (MRD) in B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) patients with a sensitivity

93 Acute lymphoblastic leukemia (ALL) persisting or relapsing fol

94 nt and young adult (AYA) patients with acute lymphoblastic leukemia (ALL) poses unique challenges and

95 iladelphia chromosome-positive (Ph(+)) acute lymphoblastic leukemia (ALL) remains undefined.

96 ncept data by profiling 60 drugs on 68 acute lymphoblastic leukemia (ALL) samples mostly from resista

97 by generating a model of t(4;11) pro-B acute lymphoblastic leukemia (ALL) that fully recapitulates th

98 aluated the efficacy of pediatric-like acute lymphoblastic leukemia (ALL) therapy in adults with lymp

99 Induction therapy for childhood acute lymphoblastic leukemia (ALL) traditionally includes pred

100 Survivors of childhood acute lymphoblastic leukemia (ALL) treated with CNS-directed c

101 c position (SEP) and risk of childhood acute lymphoblastic leukemia (ALL) were investigated using dat

102 hromosome-positive (Ph(+)) B-precursor acute lymphoblastic leukemia (ALL) who progress after failure

103 Infant acute lymphoblastic leukemia (ALL) with MLL rearrangements (ML

104 ing induction therapy in patients with acute lymphoblastic leukemia (ALL) with relapse and mortality

105 ensitivity of many high-risk childhood acute lymphoblastic leukemia (ALL) xenografts to navitoclax.

106 a panel of 7 patient-derived pediatric acute lymphoblastic leukemia (ALL) xenografts, PR-104 showed s

107 cells, in CSF samples at diagnosis of acute lymphoblastic leukemia (ALL), a uniform CSF and risk gro

108 radiotherapy (CRT) in the treatment of acute lymphoblastic leukemia (ALL), adult survivors of childho

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

110 omponent in the treatment of pediatric acute lymphoblastic leukemia (ALL), but can induce serious adv

111 promising target for immunotherapy of acute lymphoblastic leukemia (ALL), but CD19(-) relapses remai

112 ntegral part of treatment of childhood acute lymphoblastic leukemia (ALL), but it is associated with

113 In acute lymphoblastic leukemia (ALL), central nervous system (CN

114 e (Ph)-negative B-cell precursor (BCP) acute lymphoblastic leukemia (ALL), often comprising small num

115 y performed in children with high-risk acute lymphoblastic leukemia (ALL), the influence of donor typ

116 n etiologic role in the development of acute lymphoblastic leukemia (ALL), the most common childhood

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

118 mor suppressive role for PTEN in pre-B acute lymphoblastic leukemia (ALL), we induced Cre-mediated de

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

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

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

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

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

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

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

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

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

128 e is a chemotherapy drug used to treat acute lymphoblastic leukemia (ALL).

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

130 been associated with risk of childhood acute lymphoblastic leukemia (ALL).

131 se (MRD) in 48 patients with childhood acute lymphoblastic leukemia (ALL).

132 lity in pediatric patients treated for acute lymphoblastic leukemia (ALL).

133 4 disease categories: AML (n = 5310); acute lymphoblastic leukemia (ALL, n = 1883); chronic myeloid

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

135 progression of both B cell and T cell acute lymphoblastic leukemia (B-ALL and T-ALL, respectively),

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

137 ociated with poor outcome in B lineage acute lymphoblastic leukemia (B-ALL) and occur in >70% of the

138 We treated 7 patients with B-cell acute lymphoblastic leukemia (B-ALL) harboring rearrangement o

139 relapsed and/or refractory pre-B cell acute lymphoblastic leukemia (B-ALL), but antigen loss is a fr

140 leukemia-rearranged (MLL-rearranged) B-acute lymphoblastic leukemia (B-ALL), which constitutes a subt

141 erapy is an important prognostic factor in B-lymphoblastic leukemia (B-ALL).

142 uch less effective against Ph(+)B-cell acute lymphoblastic leukemia (B-ALL).

143 tes poor prognosis in precursor B-cell acute lymphoblastic leukemia (B-ALL).

144 tients with relapsed/refractory B cell acute lymphoblastic leukemia (B-ALL).

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

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

147 ly prognostic in pediatric B-precursor acute lymphoblastic leukemia (B-ALL).

148 ng early B-cell development and B-cell acute lymphoblastic leukemia (B-ALL).

149 eradicate disease in high-risk B-cell acute lymphoblastic leukemia (B-ALL).

150 ith acute myeloid leukemia (AML) and acute B-lymphoblastic leukemia (B-ALL).

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

152 therapy for childhood B-cell precursor acute lymphoblastic leukemia (B-ALL).

153 or STAT5 has a critical role in B cell acute lymphoblastic leukemia (B-ALL).

154 B cell precursor acute lymphoblastic leukemia (BCP ALL) is the most common mali

155 % to 30% of pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) could not be classified

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

157 h relapsed/refractory B-cell precursor acute lymphoblastic leukemia (BCP-ALL).

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

159 elapsed or refractory B-cell precursor acute lymphoblastic leukemia (BCP-ALL).

160 BCR-ABL1(+) precursor B-cell acute lymphoblastic leukemia (BCR-ABL1(+) B-ALL) is an aggress

161 6-RUNX1 is associated with childhood acute B-lymphoblastic leukemia (cALL) functioning as a first-hit

162 c-inspired Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) protocol yielded a marke

163 l from the Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) show that young to middl

164 ntensified Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL)-2003/2005 trials.

165 Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph(+) ALL) is currently treated

166 with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph(+) ALL) undergoing maintenanc

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

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

169 iladelphia chromosome (Ph)-like B-cell acute lymphoblastic leukemia (Ph-like ALL) is associated with

170 nt of Philadelphia chromosome-negative acute lymphoblastic leukemia (Ph-neg ALL) do not appear to req

171 llmark of BCR-ABL1(+) precursor B cell acute lymphoblastic leukemia (pre-B ALL).

172 d biology of infant and childhood PreB acute lymphoblastic leukemia (PreB-ALL), initiated by distinct

173 R = 2.07; 95% CI: 1.34, 3.20) than for acute lymphoblastic leukemia (sRR = 1.49; 95% CI: 1.07, 2.08)

174 4, 95% CI: 1.72, 3.18; n = 6) than for acute lymphoblastic leukemia (sRR = 1.57; 95% CI: 1.21, 2.05;

175 pped insulated neighborhoods in T cell acute lymphoblastic leukemia (T-ALL) and found that tumor cell

176 mutations are frequent in human T-cell acute lymphoblastic leukemia (T-ALL) and Notch inhibitors (gam

177 This causes rapid onset of acute lymphoblastic leukemia (T-ALL) and progressive developme

178 effectively eliminate malignant T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoma lines

179 ase is mutated in 10% to 16% of T-cell acute lymphoblastic leukemia (T-ALL) cases.

180 Here, we report that T-cell acute lymphoblastic leukemia (T-ALL) cells are characterized b

181 Primary T-cell acute lymphoblastic leukemia (T-ALL) cells require stromal-der

182 ration has been demonstrated in T cell acute lymphoblastic leukemia (T-ALL) cells upon calcineurin in

183 rant transcriptional program in T-cell acute lymphoblastic leukemia (T-ALL) cells.

184 ch signaling is associated with T-cell Acute Lymphoblastic Leukemia (T-ALL) development and progressi

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

186 he development of a spontaneous T-cell acute lymphoblastic leukemia (T-ALL) in these animals.

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

188 T-cell acute lymphoblastic leukemia (T-ALL) is a highly proliferative

189 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive childhoo

190 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignan

191 isk stratification in childhood T-cell acute lymphoblastic leukemia (T-ALL) is mainly based on minima

192 ecently implicated in pediatric T-cell acute lymphoblastic leukemia (T-ALL) patients and murine model

193 More than half of T-cell acute lymphoblastic leukemia (T-ALL) patients harbor gain-of-f

194 Pediatric T-acute lymphoblastic leukemia (T-ALL) patients often display re

195 actor is mutated in a subset of T-cell acute lymphoblastic leukemia (T-ALL) patients, and RUNX1 mutat

196 al of siRNNs as therapeutic tools in T-acute lymphoblastic leukemia (T-ALL) using T-ALL cell lines an

197 an oncogenic driver of immature T-cell acute lymphoblastic leukemia (T-ALL), a heterogenic subgroup o

198 uppressors, are hallmarks of T-lineage acute lymphoblastic leukemia (T-ALL), but detailed genome-wide

199 tors compared with wild type in T cell acute lymphoblastic leukemia (T-ALL), but its administration i

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

201 f function mutations, including T-cell acute lymphoblastic leukemia (T-ALL).

202 f LMO2, a prominent oncogene in T-cell acute lymphoblastic leukemia (T-ALL).

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

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

205 plified by LIM-only 2 (LMO2) in T-cell acute lymphoblastic leukemia (T-ALL).

206 utants of Notch1 NRR associated with T Acute lymphoblastic Leukemia (T-ALL).

207 hway functions in the progression of T acute lymphoblastic leukemia (T-ALL).

208 tations in NOTCH1 are common in T cell acute lymphoblastic leukemia (T-ALL).

209 river and therapeutic target in T-cell acute lymphoblastic leukemia (T-ALL).

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

211 eukemia and pediatric B-cell precursor acute lymphoblastic leukemia after allogeneic stem cell transp

212 CD8+ composition to adults with B cell acute lymphoblastic leukemia after lymphodepletion chemotherap

213 clinical studies for not only B-cell-derived lymphoblastic leukemia and lymphoma but also acute myelo

214 ng cells induces development of T-cell acute lymphoblastic leukemia and lymphoma, but not other hemat

215 ltransferase, are enriched in relapsed acute lymphoblastic leukemia and MLL-rearranged acute leukemia

216 uced late mortality among survivors of acute lymphoblastic leukemia and Wilms' tumor.

217 report that CD10, also known as common acute lymphoblastic leukemia antigen, neutral endopeptidase, o

218 B cell development, followed by B cell acute lymphoblastic leukemia at 100% incidence and with a medi

219 rs and primary, patient-derived B-cell acute lymphoblastic leukemia blasts compared with standard TCR

220 ation in human PBMCs (lymphocytes) and acute lymphoblastic leukemia CCRF-CEM cells documented signifi

221 gnant transformation because B-lineage acute lymphoblastic leukemia cells display a pronounced block

222 Inhibition of Hsp72 in acute lymphoblastic leukemia cells resulted in increased multi

223 Acute lymphoblastic leukemia developed in 2 of the 29 patients

224 dren and young adults with high-risk B-acute lymphoblastic leukemia has improved significantly, but 2

225 uch as non-Hodgkin lymphoma (B-NHL) or acute lymphoblastic leukemia have a poor prognosis.

226 The genomic lesions that characterize acute lymphoblastic leukemia in childhood include recurrent tr

227 ildren enrolled in clinical trials for acute lymphoblastic leukemia in Guatemala, Singapore and Japan

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

229 T cell therapy for relapsed/refractory acute lymphoblastic leukemia is leading to expanded use throug

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

231 ly occurs in T-ALL and relapsed B-cell acute lymphoblastic leukemia patients, and is associated with

232 nts with high-risk genetics and T-cell acute lymphoblastic leukemia responded more slowly.

233 with advanced non-Hodgkin lymphoma and acute lymphoblastic leukemia safely underwent hematopoietic st

234 inally, analysis of Myc-induced T cell acute lymphoblastic leukemia showed that cells are arrested at

235 n patients with relapsed or refractory acute lymphoblastic leukemia than does standard therapy.

236 . describe rare, non-cycling blasts in acute lymphoblastic leukemia that combine the phenotypes of do

237 ned adults with relapsed or refractory acute lymphoblastic leukemia to receive either inotuzumab ozog

238 Survivors of childhood acute lymphoblastic leukemia treated on contemporary chemother

239 nine subjects with relapsed/refractory acute lymphoblastic leukemia treated with chimeric antigen rec

240 c Myeloid Leukemia Evaluation and Ph(+)Acute Lymphoblastic Leukemia trial, including 231 patients in

241 with relapsed or refractory B-lineage acute lymphoblastic leukemia was conducted using a CD19 CAR pr

242 ir Arf-null counterparts in generating acute lymphoblastic leukemia when infused into unconditioned s

243 acute myelogenous leukemia and B-cell acute lymphoblastic leukemia whose tumors harbor point mutatio

244 g antitumor responses against systemic acute lymphoblastic leukemia xenografts.

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

246 he GRAALL (Group for Research on Adult Acute Lymphoblastic Leukemia) -2003 and -2005 studies.

247 OTCH1 (a well-known oncogene in T-cell acute lymphoblastic leukemia) are present in approximately 4-1

248 ation in Children and Adolescents with Acute Lymphoblastic Leukemia).

249 e, a key component in the treatment of acute lymphoblastic leukemia, acts by depleting asparagine fro

250 elapsed or refractory B-cell precursor acute lymphoblastic leukemia, and acute myeloid leukemia.

251 h acute myeloid leukemia (AML), T-cell acute lymphoblastic leukemia, and myelodysplastic syndromes.

252 those of acute myeloid leukemia and T-acute lymphoblastic leukemia, as well as the transcriptomic si

253 (CAR-19) have potent activity against acute lymphoblastic leukemia, but fewer results supporting tre

254 ell leukemia and in some children with acute lymphoblastic leukemia, but have been much less effectiv

255 urrent fusion gene in B-cell precursor acute lymphoblastic leukemia, but the function of the encoded

256 en with acute myeloid leukemia, infant acute lymphoblastic leukemia, hepatoblastoma, and malignant br

257 the most common initial diagnoses were acute lymphoblastic leukemia, Hodgkin lymphoma, and astrocytom

258 f 5,185 children and young adults with acute lymphoblastic leukemia, including 117 (2.3%) who were di

259 er hematologic malignancies, including acute lymphoblastic leukemia, natural killer/T-cell lymphoma,

260 ecipients with acute myeloid leukemia, acute lymphoblastic leukemia, or myelodysplastic syndrome, and

261 but no associations were observed for acute lymphoblastic leukemia, plasma cell neoplasms, or diffus

262 ty as a single agent, particularly for acute lymphoblastic leukemia, resulting in its US Food and Dru

263 from 6 patients with B-progenitor cell acute lymphoblastic leukemia, we demonstrate that patient-deri

264 on approach in a murine model of Ph(+) acute lymphoblastic leukemia, we indeed find that temporal and

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

266 exate for the treatment of high-risk B-acute lymphoblastic leukemia, with no increase in acute toxici

267 imited available data suggest that an "acute lymphoblastic leukemia-like" regimen followed by allogen

268 important risk factors for outcome in acute lymphoblastic leukemia.

269 d remarkable outcomes in patients with acute lymphoblastic leukemia.

270 ho underwent allo-SCT for treatment of acute lymphoblastic leukemia.

271 e to asparaginase therapy in childhood acute lymphoblastic leukemia.

272 tors for pancreatitis in patients with acute lymphoblastic leukemia.

273 of Philadelphia chromosome-negative acute B-lymphoblastic leukemia.

274 T cell therapy for relapsed/refractory acute lymphoblastic leukemia.

275 and mature B cells and 184 lncRNAs in acute lymphoblastic leukemia.

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

277 2 are common in early T-cell precursor acute lymphoblastic leukemia.

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

279 subgroup of childhood B-cell precursor acute lymphoblastic leukemia.

280 and the pervasive emergence of T cell acute lymphoblastic leukemia.

281 potentially curable neoplasms such as acute lymphoblastic leukemia.

282 somatic structural DNA alterations in acute lymphoblastic leukemia.

283 dergone liver transplants, or who have acute lymphoblastic leukemia.

284 al malignancies, including acute and chronic lymphoblastic leukemia.

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

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

287 LL/LBL) is a recently recognized high-risk T lymphoblastic leukemia/lymphoma (T-ALL/LBL) subgroup.

288 double-deficient mice developed T cell acute lymphoblastic leukemia/lymphoma, which originated at an

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

290 ted DNA methylomes of pediatric B-cell acute lymphoblastic leukemias (B-ALLs) using whole-genome bisu

291 roRNAs (miRNAs) in Notch-driven T-cell acute lymphoblastic leukemias (T-ALLs) has recently been estab

292 c cells with JAK3(V674A) led homogenously to lymphoblastic leukemias in BALB/c mice.

293 , the same two hotspots seen in T-cell acute lymphoblastic leukemias, and led to pathway activation i

294 h onset and progression of acute myeloid and lymphoblastic leukemias, and targeting the WDR5-MLL1 int

295 ns of 123 mammary tumors and 20 B-cell acute lymphoblastic leukemias, respectively.

296 ACTB mRNA expression levels in lymphoblastic lines and fibroblasts derived from affecte

297 hich progressed to TdT(+)CD20(-) precursor B-lymphoblastic lymphoma (B-LBL).

298 lastic leukemia (ALL) therapy in adults with lymphoblastic lymphoma (LL).

299 ctivation in adult mice induces T-cell acute lymphoblastic lymphoma (T-ALL), a tumor type known to ca

300 The patient's diagnosis was T-lymphoblastic lymphoma.