ライフサイエンスコーパス: lymphoblastic leukemia

1 % of carriers and is most often B-cell acute lymphoblastic leukemia.

2 unique functions of Tal1 and Lyl1 in T acute lymphoblastic leukemia.

3 tment of relapsed or refractory B cell acute lymphoblastic leukemia.

4 important risk factors for outcome in acute lymphoblastic leukemia.

5 e to asparaginase therapy in childhood acute lymphoblastic leukemia.

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

7 ific T cell engager, blinatumomab, for acute lymphoblastic leukemia.

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

9 somatic structural DNA alterations in acute lymphoblastic leukemia.

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

11 al malignancies, including acute and chronic lymphoblastic leukemia.

12 d remarkable outcomes in patients with acute lymphoblastic leukemia.

13 e impairment in survivors of childhood acute lymphoblastic leukemia.

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

15 omeodomain-related oncogenes in T cell acute lymphoblastic leukemia.

16 tors for pancreatitis in patients with acute lymphoblastic leukemia.

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

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

19 es of isolated nuclei from patients of acute lymphoblastic leukemia.

20 very of optimal treatment in childhood acute lymphoblastic leukemia.

21 ancy with its closely related family member, lymphoblastic leukemia 1 (Lyl1) might explain this obser

22 Stabilized MYC, in concert with T cell acute lymphoblastic leukemia 1 (TAL1), directly activates AURK

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

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

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

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

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

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

29 (DS) have a 20-fold increased risk of acute lymphoblastic leukemia (ALL) and distinct somatic featur

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

31 Children with acute lymphoblastic leukemia (ALL) are at increased risk of de

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

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

34 Patients undergoing treatment of acute lymphoblastic leukemia (ALL) are at risk for thrombosis,

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

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

37 nsidered to drive relapse formation in acute lymphoblastic leukemia (ALL) by conferring purine analog

38 improved outcomes for 90 infants with acute lymphoblastic leukemia (ALL) by providing excellent supp

39 antigen receptors (CARs) for B-lineage acute lymphoblastic leukemia (ALL) can salvage >80% of patient

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

41 quired for Philadelphia-positive (Ph+) acute lymphoblastic leukemia (ALL) cell growth, whereas expres

42 Acute lymphoblastic leukemia (ALL) cells are sensitive to aspa

43 measured intracellular MTXPG levels in acute lymphoblastic leukemia (ALL) cells from 388 newly diagno

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

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

46 Although the cure rate for childhood acute lymphoblastic leukemia (ALL) has exceeded 80% with conte

47 Relapsed acute lymphoblastic leukemia (ALL) has remained challenging to

48 olescents and young adults (AYAs) with acute lymphoblastic leukemia (ALL) have better survival rates

49 Philadelphia chromosome (Ph)-positive acute lymphoblastic leukemia (ALL) have improved with the use

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

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

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

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

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

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

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

57 Acute lymphoblastic leukemia (ALL) is an aggressive blood canc

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

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

60 Ph(+) acute lymphoblastic leukemia (ALL) is characterized by the exp

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

62 tion (HSCT) in pediatric patients with acute lymphoblastic leukemia (ALL) is efficacious, but long-te

63 Acute lymphoblastic leukemia (ALL) is the most common cancer i

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

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

66 The poor outcomes in infant acute lymphoblastic leukemia (ALL) necessitate new treatments.

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

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

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

70 s for relapsed/refractory (r/r) B-cell acute lymphoblastic leukemia (ALL) patients.

71 investigate N-glycan changes of B-cell acute lymphoblastic leukemia (ALL) pediatric patients before a

72 Acute lymphoblastic leukemia (ALL) persisting or relapsing fol

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

74 tently associated with lower childhood acute lymphoblastic leukemia (ALL) risk.

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

76 MLL-r acute myeloid leukemia or MLL-r acute lymphoblastic leukemia (ALL) showed dramatic reductions

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

78 nase is an essential drug in childhood acute lymphoblastic leukemia (ALL) therapy and is frequently g

79 d 5-year overall survival of childhood acute lymphoblastic leukemia (ALL) to 90%, but its impact on l

80 antimicrobial prophylaxis in pediatric acute lymphoblastic leukemia (ALL) to decrease infections with

81 ortality is common among children with acute lymphoblastic leukemia (ALL) treated in poor-resource se

82 e main cause of MLL-rearranged (MLL-r) acute lymphoblastic leukemia (ALL) treatment failure resulting

83 (ASNase) is an important component of acute lymphoblastic leukemia (ALL) treatment, but is often dis

84 crodeletions in B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) using 5 different patient c

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

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

87 row relapses of B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) will benefit from allogenei

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

89 ival in children with high-risk B-cell acute lymphoblastic leukemia (ALL) would also improve outcomes

90 leled responses in relapsed/refractory acute lymphoblastic leukemia (ALL)(1-5), but toxicity, includi

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

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

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

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

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

96 t common genetic features of childhood acute lymphoblastic leukemia (ALL), but its pathogenetic impac

97 titis (AAP) is common in patients with acute lymphoblastic leukemia (ALL), but risk differences acros

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

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

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

101 In 5% of childhood acute lymphoblastic leukemia (ALL), the t(1,19) chromosomal tr

102 cantly influence the susceptibility to acute lymphoblastic leukemia (ALL), thus providing compelling

103 ved survival in relapsed or refractory acute lymphoblastic leukemia (ALL), was recently approved for

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

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

106 raginase is almost exclusively used in acute lymphoblastic leukemia (ALL), which is a very rare cance

107 ymal stromal cell (MSC) niche in adult acute lymphoblastic leukemia (ALL).

108 to thiopurine chemotherapy in relapsed acute lymphoblastic leukemia (ALL).

109 received CD19-directed CAR/T cells for acute lymphoblastic leukemia (ALL).

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

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

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

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

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

115 or acute myeloid leukemia and relapsed acute lymphoblastic leukemia (ALL).

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

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

118 py continues to limit the prognosis of acute lymphoblastic leukemia (ALL).

119 t antileukemic activity in B-precursor acute lymphoblastic leukemia (ALL).

120 ion may be beneficial to patients with acute lymphoblastic leukemia (ALL).

121 including Burkitt's lymphoma (BL) and Acute Lymphoblastic Leukemia (ALL).

122 py among children and adolescents with acute lymphoblastic leukemia (ALL).

123 r chemotherapy refractory (r/r) B-cell acute lymphoblastic leukemia (ALL).

124 motherapy vaccination of children with acute lymphoblastic leukemia (ALL).

125 an important therapeutic strategy for acute lymphoblastic leukemia (ALL).

126 B-cell acute lymphoblastic leukemia (ALL; B-ALL) is the most common p

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

128 MLL-AF4 are a major cause of incurable acute lymphoblastic leukemias (ALL).

129 drugs SMAC mimetics sensitized B-cell acute lymphoblastic leukemia and diffuse large B-cell lymphoma

130 ry hematologic malignancies, primarily acute lymphoblastic leukemia and diffuse large B-cell lymphoma

131 eobase analog used in the treatment of acute lymphoblastic leukemia and inflammatory bowel disorders.

132 x transcription factor that promotes T acute lymphoblastic leukemia and is required for HSC specifica

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

134 Acute Lymphoblastic Leukemia and Lymphoma.

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

136 otch signaling in primary human T cell acute lymphoblastic leukemia and other Notch-dependent human t

137 -old man was diagnosed with precursor B-cell lymphoblastic leukemia and underwent transplantation of

138 -old man was diagnosed with precursor B-cell lymphoblastic leukemia and underwent transplantation of

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

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

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

142 ulo-humeral muscular dystrophy (FSHD), acute lymphoblastic leukemia, and sarcomas.

143 , acute myeloid leukemia, and relapsed acute lymphoblastic leukemia, and their prognostic impact is b

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

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

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

147 ia asparaginase treatment of pediatric acute lymphoblastic leukemia are individualized with therapeut

148 ivating mutation of NSD2 discovered in acute lymphoblastic leukemia are significantly associated with

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

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

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

152 B-cell acute lymphoblastic leukemia (B-ALL) accounts for nearly one f

153 ment options for chemoresistant B cell acute lymphoblastic leukemia (B-ALL) and acute myeloid leukemi

154 mia (MLL) gene occur in ~10% of B-cell acute lymphoblastic leukemia (B-ALL) and define a group of pat

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

156 ch4 support survival of primary B-cell acute lymphoblastic leukemia (B-ALL) cells, suggesting a role

157 Children and young adults with hypodiploid B-lymphoblastic leukemia (B-ALL) fare poorly and hematopoi

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

159 Although B-cell acute lymphoblastic leukemia (B-ALL) is the most common malign

160 erequisite to prevent childhood B-cell acute lymphoblastic leukemia (B-ALL) is to decipher its etiolo

161 esults of a phase I/II trial in B cell acute lymphoblastic leukemia (B-ALL) patients relapsed after a

162 A subset of B cell acute lymphoblastic leukemia (B-ALL) patients will relapse and

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

164 defining new subtypes of B-progenitor acute lymphoblastic leukemia (B-ALL), however many cases lack

165 cogenic lesion in patients with B cell acute lymphoblastic leukemia (B-ALL), making B-ALL an excellen

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

167 lt (AYA) relapsed or refractory B-cell acute lymphoblastic leukemia (B-ALL).

168 ession can be extended to human B-cell acute lymphoblastic leukemia (B-ALL).

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

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

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

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

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

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

175 ificant proportion of childhood B-cell acute lymphoblastic leukemia (B-ALL).

176 k of immune escape in pediatric B-cell acute lymphoblastic leukemia (B-ALL).

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

178 ies as front-line treatment for B cell acute lymphoblastic leukemia (B-ALL).

179 with relapsed/refractory (R/R) B-cell acute lymphoblastic leukemia (B-ALL).

180 case SUP-B15 cells representing B-cell acute lymphoblastic leukemia (B-ALL).

181 % to 30% of pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) could not be classified

182 letions at 13q12.2 in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) eliminate the boundary

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

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

185 paraginase (L-ASP) in the treatment of acute lymphoblastic leukemia because of its longer half-life a

186 ren's Oncology Group trials for B-cell acute lymphoblastic leukemia between 2004 and 2011 (National C

187 tures with CD10-ve B-progenitor infant acute lymphoblastic leukemia blast cells.

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

189 Unintentional transduction of B-cell acute lymphoblastic leukemia blasts during CART19 manufacturin

190 e an effective treatment for pediatric acute lymphoblastic leukemia but are less effective for chroni

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

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

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 We validate these findings in T cell acute lymphoblastic leukemia cell lines and patient samples an

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

197 Acute lymphoblastic leukemia developed in 2 of the 29 patients

198 Down syndrome acute lymphoblastic leukemia (DS-ALL) is characterized by high

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

200 Treatment for childhood acute lymphoblastic leukemia has evolved over the past five de

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

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

203 is and increased chemotaxis; in B-cell acute lymphoblastic leukemia, high cortactin levels correlate

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

205 ancer Institute (NCI) high-risk B-cell acute lymphoblastic leukemia (HR B-ALL) or NCI standard-risk B

206 Analysis of 13 T-lineage acute lymphoblastic leukemias identified a recurrent intronic

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

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

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

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

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

212 latory approval for products targeting acute lymphoblastic leukemia, lymphomas, and multiple myeloma

213 cy were studied in an Arf(-/-) BCR-ABL acute lymphoblastic leukemia murine model.

214 for non-Hodgkin lymphoma (n = 23) and acute lymphoblastic leukemia (n = 1), and 1 patient treated wi

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

216 HF23 (NP23) mice develop an aggressive acute lymphoblastic leukemia of B-1 lymphocyte progenitor orig

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

218 sion are commonly altered in pediatric acute lymphoblastic leukemia (PALL).

219 breaks co-localize with those found in acute lymphoblastic leukemia patients and occur at key cancer

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

221 apeutic drug administered to pediatric acute lymphoblastic leukemia patients.

222 ildhood leukemias are precursor B-cell acute lymphoblastic leukemias (pB-ALLs) caused by a combinatio

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

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

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

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

227 th Philadelphia chromosome-like B cell acute lymphoblastic leukemia (Ph-like B-ALL) experience high r

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

229 on in a 16-year-old female with B cell acute lymphoblastic leukemia, post CAR T cell treatment; (ii)

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

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

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

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

234 ute childhood leukemia, generally, and acute lymphoblastic leukemia, specifically.

235 treatment, up to 10% of children with acute lymphoblastic leukemia still experience relapse.

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

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

238 ecurrent RPL10-R98S mutation in T-cell acute lymphoblastic leukemia (T-ALL) and RPS15 mutations in ch

239 T-cell acute lymphoblastic leukemia (T-ALL) and T-cell acute lymphobl

240 ts with relapsed and refractory T-cell acute lymphoblastic leukemia (T-ALL) but has not been fully ev

241 he 3D chromatin architecture in T cell acute lymphoblastic leukemia (T-ALL) by using primary human le

242 lysis of sequence data from 419 T-cell acute lymphoblastic leukemia (T-ALL) cases demonstrated a sign

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

244 d the growth of Notch-dependent T cell acute lymphoblastic leukemia (T-ALL) cell lines and bound dire

245 cells, LMO2-positive DLBCLs and T cell acute lymphoblastic leukemia (T-ALL) cells exhibit a high sens

246 ors that promote cancer growth, T-cell acute lymphoblastic leukemia (T-ALL) cells require exogenous c

247 ling mediates DEX resistance in T cell acute lymphoblastic leukemia (T-ALL) cells, and that this coul

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

249 ifferentially encoded in Jurkat T-cell acute lymphoblastic leukemia (T-ALL) cells.

250 Relapsed/refractory T-cell acute lymphoblastic leukemia (T-ALL) has a dismal outcome, and

251 nes and the in vivo myc-induced T cell acute lymphoblastic leukemia (T-ALL) in a zebrafish model.

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

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

254 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematolo

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

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

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

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

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

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

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

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

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

264 and is frequently activated in T-cell acute lymphoblastic leukemia (T-ALL) patients.

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

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

267 nt of therapy for patients with T cell acute lymphoblastic leukemia (T-ALL), and although resistance

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 ed mutational features of human T cell acute lymphoblastic leukemia (T-ALL), containing mutations in

271 ssociated with a severe form of T-cell acute lymphoblastic leukemia (T-ALL), designated early T-cell

272 ermissive to the development of T cell acute lymphoblastic leukemia (T-ALL), similar to the human dis

273 MYC plays an essential role in T cell acute lymphoblastic leukemia (T-ALL), yet the mechanisms under

274 criptional loops in a subset of T-cell acute lymphoblastic leukemia (T-ALL).

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

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

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

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

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

280 cute myeloid leukemia (AML) and T-cell acute lymphoblastic leukemia (T-ALL).

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

282 is found to be associated with T-cell acute lymphoblastic leukemia, T-ALL, though its contribution t

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

284 In Philadelphia chromosome-positive acute lymphoblastic leukemia, the introduction of increasingly

285 Soon after HSCT performed for acute lymphoblastic leukemia, the patient developed a TMA due

286 Survivors of childhood acute lymphoblastic leukemia treated on contemporary chemother

287 h relapsed/refractory pediatric B cell acute lymphoblastic leukemia treated with CAT CAR T cells achi

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

289 factors for reactions in a front-line acute lymphoblastic leukemia trial and assess the usefulness o

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

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

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

293 as a tumor suppressor in hypodiploid B-acute lymphoblastic leukemia, we found that IKZF2 is required

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 Patients with B-cell acute lymphoblastic leukemia who experience relapse after or a

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

298 of the disease or in BCR-ABL1-positive acute lymphoblastic leukemia, with relapse driven by both BCR-

299 In a patient acute lymphoblastic leukemia xenograft model of CRS and neuroi

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