ライフサイエンスコーパス: lymphoblastic

1 here that OGG1 depletion obstructs A3 T-cell lymphoblastic acute leukemia growth in vitro and in vivo

2 panel of cancer cell lines, including acute lymphoblastic and myeloid leukemia (ALL/AML) and nonsmal

3 In cultured lymphoblastic cells, knockdown of XIST specifically alte

4 980 survivors of acute lymphoblastic leukaemia (50% women, median age at diagno

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

6 Children with acute lymphoblastic leukaemia (ALL) are at increased risk of i

7 ted genetic basis of susceptibility to acute lymphoblastic leukaemia (ALL) in children.

8 r overall survival above 90% in B-cell acute lymphoblastic leukaemia (ALL) in many study groups, whil

9 als involving patients with pre-B cell acute lymphoblastic leukaemia (ALL) or B cell lymphomas have r

10 e mRNA expression profile of pediatric Acute Lymphoblastic Leukaemia (ALL) patients and the efficacy

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

12 fe outcomes of patients with childhood acute lymphoblastic leukaemia (ALL).

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

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

15 ppropriate NOTCH1 signalling in T-cell acute lymphoblastic leukaemia (T-ALL), and the involvement of

16 nts with relapsed or refractory B-cell acute lymphoblastic leukaemia achieved overall remission after

17 Patients with B-cell acute lymphoblastic leukaemia aged at least 3 years at the tim

18 13, 228 patients with B-cell precursor acute lymphoblastic leukaemia and late bone marrow relapses we

19 7, 69 patients (67 patients had B-cell acute lymphoblastic leukaemia and two had B-cell lymphoblastic

20 nalysis were diagnosed with paediatric acute lymphoblastic leukaemia at St Jude Children's Research H

21 ith relapsed and/or refractory CD19(+) acute lymphoblastic leukaemia became the first gene therapy to

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

23 By age 30 years, survivors of acute lymphoblastic leukaemia had, on average, 5.4 (95% CI 5.1

24 th newly diagnosed, Ph-negative B-cell acute lymphoblastic leukaemia or lymphoblastic lymphoma with C

25 ty of life for survivors of paediatric acute lymphoblastic leukaemia requires continued medical surve

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

27 outcomes among survivors of childhood acute lymphoblastic leukaemia treated over time.

28 Although changes in paediatric acute lymphoblastic leukaemia treatment protocols have improve

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

30 aged 1-18 years with B-cell precursor acute lymphoblastic leukaemia who had late bone marrow relapse

31 omes of children with B-cell precursor acute lymphoblastic leukaemia who had late bone marrow relapse

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

33 Patients with B-cell precursor acute lymphoblastic leukaemia with late bone marrow relapses a

34 haematological malignancies, including acute lymphoblastic leukaemia, acute myeloid leukaemia (AML) a

35 cranial radiotherapy for children with acute lymphoblastic leukaemia, conditions now predominately in

36 In acute lymphoblastic leukaemia, MLPA has been used in research

37 nts with relapsed or refractory B-cell acute lymphoblastic leukaemia.

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

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

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

41 roves outcomes in patients with B-cell acute lymphoblastic leukaemia.

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

43 with Ph-negative CD20-positive B-cell acute lymphoblastic leukaemia.

44 Nine (27%) of 33 patients had Ph-like acute lymphoblastic leukaemia.

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

46 ome (Ph)-negative CD20-positive B-cell acute lymphoblastic leukaemia.

47 nts with relapsed or refractory B-cell acute lymphoblastic leukaemia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 % to 30% of pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) could not be classified

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 Acute Lymphoblastic Leukemia and Lymphoma.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

240 apeutic drug administered to pediatric acute lymphoblastic leukemia patients.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

272 % of carriers and is most often B-cell acute lymphoblastic leukemia.

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

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

275 important risk factors for outcome in acute lymphoblastic leukemia.

276 e to asparaginase therapy in childhood acute lymphoblastic leukemia.

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

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

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

280 somatic structural DNA alterations in acute lymphoblastic leukemia.

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

282 al malignancies, including acute and chronic lymphoblastic leukemia.

283 e impairment in survivors of childhood acute lymphoblastic leukemia.

284 d remarkable outcomes in patients with acute lymphoblastic leukemia.

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

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

287 very of optimal treatment in childhood acute lymphoblastic leukemia.

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

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

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

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

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

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

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

295 phoblastic leukemia (T-ALL) and T-cell acute lymphoblastic lymphoma (T-LBL) are aggressive hematologi

296 tients with newly diagnosed pediatric T-cell lymphoblastic lymphoma (T-LL) and gained preliminary dat

297 tive B-cell acute lymphoblastic leukaemia or lymphoblastic lymphoma with CD20 expression of at least

298 ent treatment protocols for both T-ALL and T-lymphoblastic lymphoma.

299 e lymphoblastic leukaemia and two had B-cell lymphoblastic lymphoma; median age 41 years [IQR 32-50])

300 subjected TAp63 (+/-) or p73 (+/-) mice to T lymphoblastic lymphomas (TLBLs).