ライフサイエンスコーパス: lymphoblastic leukemia

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

2 important risk factors for outcome in acute lymphoblastic leukemia.

3 e to asparaginase therapy in childhood acute lymphoblastic leukemia.

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

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

6 tors for pancreatitis in patients with acute lymphoblastic leukemia.

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

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

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

10 2 are common in early T-cell precursor acute lymphoblastic leukemia.

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

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

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

14 potentially curable neoplasms such as acute lymphoblastic leukemia.

15 shed component of induction therapy of acute lymphoblastic leukemia.

16 K1 and JAK3 are recurrently mutated in acute lymphoblastic leukemia.

17 yeloproliferative neoplasms and B cell acute lymphoblastic leukemia.

18 phase 1 trial for treatment of B cell acute lymphoblastic leukemia.

19 somatic structural DNA alterations in acute lymphoblastic leukemia.

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

21 al malignancies, including acute and chronic lymphoblastic leukemia.

22 d remarkable outcomes in patients with acute lymphoblastic leukemia.

23 acute leukemias (including four T-cell acute lymphoblastic leukemias), 12 developed Hodgkin lymphoma

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

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

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

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

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

29 002 and 2007 (including 2,275 cases of acute lymphoblastic leukemia (ALL) and 418 cases of acute myel

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

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

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

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

34 mon genetic rearrangement in childhood acute lymphoblastic leukemia (ALL) and gives rise to the TEL-A

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

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

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

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

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

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

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

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

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

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

45 3 mimetic drugs may be useful to treat acute lymphoblastic leukemia (ALL) but the sensitivity of prim

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

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

48 Childhood acute lymphoblastic leukemia (ALL) can often be traced to a pr

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

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

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

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

53 n P-glycoprotein overexpressing T-cell acute lymphoblastic leukemia (ALL) cells, which escaped a ther

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

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

56 With cure rates of childhood acute lymphoblastic leukemia (ALL) exceeding 85%, there is a n

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

58 transplantation (HCT) of patients with acute lymphoblastic leukemia (ALL) identifies patients at high

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

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

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

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

63 lete response (CR) rate in adults with acute lymphoblastic leukemia (ALL) is 80% to 90%, and the cure

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

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

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

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

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

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

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

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

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

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

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

75 Acute lymphoblastic leukemia (ALL) is the commonest childhood

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

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

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

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

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

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

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

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

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

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

86 Acute lymphoblastic leukemia (ALL) persisting or relapsing fol

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

88 Relapsed and refractory acute lymphoblastic leukemia (ALL) remains difficult to treat,

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

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

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

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

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

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

95 Acute lymphoblastic leukemia (ALL) typically originates from p

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

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

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

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

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

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

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

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

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

105 e universally used in the treatment of acute lymphoblastic leukemia (ALL), and resistance to glucocor

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

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

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

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

110 d fitness among survivors of childhood acute lymphoblastic leukemia (ALL), especially those treated w

111 or IKAROS, are a hallmark of high-risk acute lymphoblastic leukemia (ALL), however the role of IKZF1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 ion chemotherapy regimens in pediatric acute lymphoblastic leukemia (ALL).

127 sone response in pediatric B-precursor acute lymphoblastic leukemia (ALL).

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

129 ansformation in mouse models for pre-B acute lymphoblastic leukemia (ALL).

130 nd two occurrences of B cell-precursor acute lymphoblastic leukemia (ALL).

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

132 s the mainstay of curative therapy for acute lymphoblastic leukemia (ALL).

133 s with relapsed/refractory B-precursor acute lymphoblastic leukemia (ALL).

134 leotide [TGN] levels) in children with acute lymphoblastic leukemia (ALL).

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

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

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

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

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

140 Asparaginase is used to treat acute lymphoblastic leukemia (ALL); however, hypersensitivity

141 4 disease categories: AML (n = 5310); acute lymphoblastic leukemia (ALL, n = 1883); chronic myeloid

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

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

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

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

146 etions in ribosomal proteins in T-cell acute lymphoblastic leukemia and solid tumors, further extendi

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

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

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

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

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

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

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

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

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

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

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

158 lopment are a hallmark of B-progenitor acute lymphoblastic leukemia (B-ALL) and most commonly involve

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

160 role of CD9 in the dissemination of B acute lymphoblastic leukemia (B-ALL) cells, by stably downregu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 cluding the high-risk subset of B cell acute lymphoblastic leukemias (B-ALLs) with CRLF2 rearrangemen

180 condary genetic events in human B-cell acute lymphoblastic leukemias (B-ALLs), illustrating the oncog

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

182 % to 30% of pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) could not be classified

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

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

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

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

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

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

189 Patients with B cell precursor acute lymphoblastic leukemia (BPL) respond well to chemotherap

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

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

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

193 6-RUNX1 is associated with childhood acute B-lymphoblastic leukemia (cALL) functioning as a first-hit

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

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

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

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

198 Acute lymphoblastic leukemia developed in 2 of the 29 patients

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 /T cell, angioimmunoblastic, and precursor T-lymphoblastic leukemia/lymphoma types.

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

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

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

221 B-cell NHL, HL, and acute lymphoblastic leukemia occur at a high rate and earlier

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

223 BCR-ABL(+) acute lymphoblastic leukemia patients have transient responses

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

240 4, 95% CI: 1.72, 3.18; n = 6) than for acute lymphoblastic leukemia (sRR = 1.57; 95% CI: 1.21, 2.05;

241 ize unfavorable subsets of acute myeloid and lymphoblastic leukemias, such as those with MLL and BCR/

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 T-cell immunophenotype of acute lymphoblastic leukemia (T-ALL) is an uncommon aggressive

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

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

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

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

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

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

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

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

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

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

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

271 role of the microenvironment in T cell acute lymphoblastic leukemia (T-ALL), or any acute leukemia, i

272 role Wnt signaling may play in T-cell acute lymphoblastic leukemia (T-ALL), we used a stably integra

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

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

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

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

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

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

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

280 ressed with activated NOTCH1 in T cell acute lymphoblastic leukemia (T-ALL).

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

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

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

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

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

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

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

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

289 Survivors of childhood acute lymphoblastic leukemia treated on contemporary chemother

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

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

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

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

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

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

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

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

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

299 g antitumor responses against systemic acute lymphoblastic leukemia xenografts.

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