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

1 in ~30% of carriers and is most often B-cell acute lymphoblastic leukemia.

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

3 e treatment of relapsed or refractory B cell acute lymphoblastic leukemia.

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

5 istance to asparaginase therapy in childhood acute lymphoblastic leukemia.

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

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

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

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

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

11 yielded remarkable outcomes in patients with acute lymphoblastic leukemia.

12 gnitive impairment in survivors of childhood acute lymphoblastic leukemia.

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

14 n of homeodomain-related oncogenes in T cell acute lymphoblastic leukemia.

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

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

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

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

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

20 e delivery of optimal treatment in childhood acute lymphoblastic leukemia.

21 Stabilized MYC, in concert with T cell acute lymphoblastic leukemia 1 (TAL1), directly activate

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

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

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

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

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

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

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

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

30 Children with acute lymphoblastic leukemia (ALL) are at increased risk

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

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

33 Patients undergoing treatment of acute lymphoblastic leukemia (ALL) are at risk for throm

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

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

36 are considered to drive relapse formation in acute lymphoblastic leukemia (ALL) by conferring purine

37 rkably improved outcomes for 90 infants with acute lymphoblastic leukemia (ALL) by providing excellen

38 meric antigen receptors (CARs) for B-lineage acute lymphoblastic leukemia (ALL) can salvage >80% of p

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

40 is required for Philadelphia-positive (Ph+) acute lymphoblastic leukemia (ALL) cell growth, whereas

41 Acute lymphoblastic leukemia (ALL) cells are sensitive t

42 s, we measured intracellular MTXPG levels in acute lymphoblastic leukemia (ALL) cells from 388 newly

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

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

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

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

47 Relapsed acute lymphoblastic leukemia (ALL) has remained challeng

48 der adolescents and young adults (AYAs) with acute lymphoblastic leukemia (ALL) have better survival

49 s with Philadelphia chromosome (Ph)-positive acute lymphoblastic leukemia (ALL) have improved with th

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

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

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

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

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

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

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

57 Acute lymphoblastic leukemia (ALL) is an aggressive bloo

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

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

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

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

62 plantation (HSCT) in pediatric patients with acute lymphoblastic leukemia (ALL) is efficacious, but l

63 Acute lymphoblastic leukemia (ALL) is the most common ca

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

65 hip of 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 treat

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

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

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

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

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

72 ed to investigate N-glycan changes of B-cell acute lymphoblastic leukemia (ALL) pediatric patients be

73 Acute lymphoblastic leukemia (ALL) persisting or relapsi

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

75 consistently associated with lower childhood acute lymphoblastic leukemia (ALL) risk.

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

77 either MLL-r acute myeloid leukemia or MLL-r acute lymphoblastic leukemia (ALL) showed dramatic reduc

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

79 paraginase is an essential drug in childhood acute lymphoblastic leukemia (ALL) therapy and is freque

80 mproved 5-year overall survival of childhood acute lymphoblastic leukemia (ALL) to 90%, but its impac

81 ed as antimicrobial prophylaxis in pediatric acute lymphoblastic leukemia (ALL) to decrease infection

82 ated mortality is common among children with acute lymphoblastic leukemia (ALL) treated in poor-resou

83 ins the main cause of MLL-rearranged (MLL-r) acute lymphoblastic leukemia (ALL) treatment failure res

84 ginase (ASNase) is an important component of acute lymphoblastic leukemia (ALL) treatment, but is oft

85 2.2 microdeletions in B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) using 5 different pat

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

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

88 ne marrow relapses of B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) will benefit from all

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

90 s survival in children with high-risk B-cell acute lymphoblastic leukemia (ALL) would also improve ou

91 nparalleled responses in relapsed/refractory acute lymphoblastic leukemia (ALL)(1-5), but toxicity, i

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

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

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

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

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

97 he most common genetic features of childhood acute lymphoblastic leukemia (ALL), but its pathogenetic

98 ancreatitis (AAP) is common in patients with acute lymphoblastic leukemia (ALL), but risk differences

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

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

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

102 In 5% of childhood acute lymphoblastic leukemia (ALL), the t(1,19) chromoso

103 ignificantly influence the susceptibility to acute lymphoblastic leukemia (ALL), thus providing compe

104 improved survival in relapsed or refractory acute lymphoblastic leukemia (ALL), was recently approve

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

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

107 , asparaginase is almost exclusively used in acute lymphoblastic leukemia (ALL), which is a very rare

108 esenchymal stromal cell (MSC) niche in adult acute lymphoblastic leukemia (ALL).

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

110 5 who received CD19-directed CAR/T cells for acute lymphoblastic leukemia (ALL).

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

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

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

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

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

116 rapy for acute myeloid leukemia and relapsed acute lymphoblastic leukemia (ALL).

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

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

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

120 otherapy continues to limit the prognosis of acute lymphoblastic leukemia (ALL).

121 ificant antileukemic activity in B-precursor acute lymphoblastic leukemia (ALL).

122 ification may be beneficial to patients with acute lymphoblastic leukemia (ALL).

123 ncies, including Burkitt's lymphoma (BL) and Acute Lymphoblastic Leukemia (ALL).

124 therapy among children and adolescents with acute lymphoblastic leukemia (ALL).

125 psed or chemotherapy refractory (r/r) B-cell acute lymphoblastic leukemia (ALL).

126 ostchemotherapy vaccination of children with acute lymphoblastic leukemia (ALL).

127 ged as an important therapeutic strategy for acute lymphoblastic leukemia (ALL).

128 B-cell acute lymphoblastic leukemia (ALL; B-ALL) is the most co

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

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

131 ulator drugs SMAC mimetics sensitized B-cell acute lymphoblastic leukemia and diffuse large B-cell ly

132 fractory hematologic malignancies, primarily acute lymphoblastic leukemia and diffuse large B-cell ly

133 a nucleobase analog used in the treatment of acute lymphoblastic leukemia and inflammatory bowel diso

134 p-helix transcription factor that promotes T acute lymphoblastic leukemia and is required for HSC spe

135 Acute Lymphoblastic Leukemia and Lymphoma.

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

137 bits Notch signaling in primary human T cell acute lymphoblastic leukemia and other Notch-dependent h

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

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

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

141 o-scapulo-humeral muscular dystrophy (FSHD), acute lymphoblastic leukemia, and sarcomas.

142 arcoma, acute myeloid leukemia, and relapsed acute lymphoblastic leukemia, and their prognostic impac

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

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

145 Erwinia asparaginase treatment of pediatric acute lymphoblastic leukemia are individualized with the

146 an activating mutation of NSD2 discovered in acute lymphoblastic leukemia are significantly associate

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

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

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

150 B-cell acute lymphoblastic leukemia (B-ALL) accounts for nearly

151 treatment options for chemoresistant B cell acute lymphoblastic leukemia (B-ALL) and acute myeloid l

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

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

154 nd Notch4 support survival of primary B-cell acute lymphoblastic leukemia (B-ALL) cells, suggesting a

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

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

157 The prerequisite to prevent childhood B-cell acute lymphoblastic leukemia (B-ALL) is to decipher its

158 arly results of a phase I/II trial in B cell acute lymphoblastic leukemia (B-ALL) patients relapsed a

159 A subset of B cell acute lymphoblastic leukemia (B-ALL) patients will relap

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

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

162 ing oncogenic lesion in patients with B cell acute lymphoblastic leukemia (B-ALL), making B-ALL an ex

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

164 ng adult (AYA) relapsed or refractory B-cell acute lymphoblastic leukemia (B-ALL).

165 progression can be extended to human B-cell acute lymphoblastic leukemia (B-ALL).

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

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

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

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

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

171 a significant proportion of childhood B-cell acute lymphoblastic leukemia (B-ALL).

172 he risk of immune escape in pediatric B-cell acute lymphoblastic leukemia (B-ALL).

173 in patients with relapsed/refractory B-cell acute lymphoblastic leukemia (B-ALL).

174 therapies as front-line treatment for B cell acute lymphoblastic leukemia (B-ALL).

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

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

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

178 icrodeletions at 13q12.2 in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) eliminate the bou

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

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

181 oli asparaginase (L-ASP) in the treatment of acute lymphoblastic leukemia because of its longer half-

182 Children's Oncology Group trials for B-cell acute lymphoblastic leukemia between 2004 and 2011 (Nati

183 signatures with CD10-ve B-progenitor infant acute lymphoblastic leukemia blast cells.

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

185 Unintentional transduction of B-cell acute lymphoblastic leukemia blasts during CART19 manufa

186 provide an effective treatment for pediatric acute lymphoblastic leukemia but are less effective for

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

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

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

190 We validate these findings in T cell acute lymphoblastic leukemia cell lines and patient samp

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

192 Acute lymphoblastic leukemia developed in 2 of the 29 pa

193 Down syndrome acute lymphoblastic leukemia (DS-ALL) is characterized b

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

195 Treatment for childhood acute lymphoblastic leukemia has evolved over the past f

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

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

198 rognosis and increased chemotaxis; in B-cell acute lymphoblastic leukemia, high cortactin levels corr

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

200 onal Cancer Institute (NCI) high-risk B-cell acute lymphoblastic leukemia (HR B-ALL) or NCI standard-

201 Analysis of 13 T-lineage acute lymphoblastic leukemias identified a recurrent int

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

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

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

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

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

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

208 d regulatory approval for products targeting acute lymphoblastic leukemia, lymphomas, and multiple my

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

210 cells for non-Hodgkin lymphoma (n = 23) and acute lymphoblastic leukemia (n = 1), and 1 patient trea

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

212 UP98-PHF23 (NP23) mice develop an aggressive acute lymphoblastic leukemia of B-1 lymphocyte progenito

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

214 expression are commonly altered in pediatric acute lymphoblastic leukemia (PALL).

215 these breaks co-localize with those found in acute lymphoblastic leukemia patients and occur at key c

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

217 motherapeutic drug administered to pediatric acute lymphoblastic leukemia patients.

218 of childhood leukemias are precursor B-cell acute lymphoblastic leukemias (pB-ALLs) caused by a comb

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

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

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

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

223 lts with Philadelphia chromosome-like B cell acute lymphoblastic leukemia (Ph-like B-ALL) experience

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

225 antation in a 16-year-old female with B cell acute lymphoblastic leukemia, post CAR T cell treatment;

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

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

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

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

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

231 ith acute childhood leukemia, generally, and acute lymphoblastic leukemia, specifically.

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

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

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

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

236 the recurrent RPL10-R98S mutation in T-cell acute lymphoblastic leukemia (T-ALL) and RPS15 mutations

237 T-cell acute lymphoblastic leukemia (T-ALL) and T-cell acute ly

238 patients with relapsed and refractory T-cell acute lymphoblastic leukemia (T-ALL) but has not been fu

239 gate the 3D chromatin architecture in T cell acute lymphoblastic leukemia (T-ALL) by using primary hu

240 Analysis of sequence data from 419 T-cell acute lymphoblastic leukemia (T-ALL) cases demonstrated

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

242 hibited the growth of Notch-dependent T cell acute lymphoblastic leukemia (T-ALL) cell lines and boun

243 cient cells, LMO2-positive DLBCLs and T cell acute lymphoblastic leukemia (T-ALL) cells exhibit a hig

244 ppressors that promote cancer growth, T-cell acute lymphoblastic leukemia (T-ALL) cells require exoge

245 signaling mediates DEX resistance in T cell acute lymphoblastic leukemia (T-ALL) cells, and that thi

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

247 i is differentially encoded in Jurkat T-cell acute lymphoblastic leukemia (T-ALL) cells.

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

249 Relapsed/refractory T-cell acute lymphoblastic leukemia (T-ALL) has a dismal outcom

250 ell lines and the in vivo myc-induced T cell acute lymphoblastic leukemia (T-ALL) in a zebrafish mode

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

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

253 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive he

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

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

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

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

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

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

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

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

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

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

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

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

266 omponent of therapy for patients with T cell acute lymphoblastic leukemia (T-ALL), and although resis

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 itulated mutational features of human T cell acute lymphoblastic leukemia (T-ALL), containing mutatio

270 2 is associated with a severe form of T-cell acute lymphoblastic leukemia (T-ALL), designated early T

271 o be permissive to the development of T cell acute lymphoblastic leukemia (T-ALL), similar to the hum

272 ion of MYC plays an essential role in T cell acute lymphoblastic leukemia (T-ALL), yet the mechanisms

273 transcriptional loops in a subset of T-cell acute lymphoblastic leukemia (T-ALL).

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

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

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

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

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

279 d in acute myeloid leukemia (AML) and T-cell acute lymphoblastic leukemia (T-ALL).

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

281 mplex, is found to be associated with T-cell acute lymphoblastic leukemia, T-ALL, though its contribu

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

283 In Philadelphia chromosome-positive acute lymphoblastic leukemia, the introduction of increa

284 Soon after HSCT performed for acute lymphoblastic leukemia, the patient developed a TM

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

286 Survivors of childhood acute lymphoblastic leukemia treated on contemporary che

287 ts with relapsed/refractory pediatric B cell acute lymphoblastic leukemia treated with CAT CAR T cell

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

289 y risk factors for reactions in a front-line acute lymphoblastic leukemia trial and assess the useful

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

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

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

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

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 Patients with B-cell acute lymphoblastic leukemia who experience relapse afte

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

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

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

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