ライフサイエンスコーパス: ALL

1 pretreatment bone marrow specimens (n = 127 ALL in comparison with 38 acute myeloid leukemia cases i

2 The study included 8,383 ALL cases diagnosed at age </=19 years in 2000-2010.

3 the SAD group and in a weaker manner MAD and ALL.

4 In a transgenic pre-B ALL mouse model, the heterozygous deletion of Pax5 incre

5 ros functions as a tumor suppressor in pre-B ALL remain poorly understood.

6 nd IKZF1 in samples from patients with pre-B ALL restored a non-permissive state and induced energy c

7 analyzed a mouse model of BCR-ABL1(+) pre-B ALL together with a new model of inducible expression of

8 r B cell acute lymphoblastic leukemia (pre-B ALL).

9 t genes in mouse and human BCR-ABL1(+) pre-B ALL, revealing novel conserved gene pathways associated

10 aros in IKZF1 mutant human BCR-ABL1(+) pre-B ALL.

11 munotherapy, demonstrating potency against B-ALL comparable to that of CD19-CAR at biologically activ

12 into Children's Oncology Group B-cell ALL (B-ALL) clinical trials.

13 Patients with newly diagnosed B-cell ALL (B-ALL) who received frontline chemotherapy at MD Anderson

14 However, in both B-ALL and AML, TRC105 synergized with reduced intensity my

15 o opposing transcriptional programs drives B-ALL and suggest that restoring the balance of these path

16 ontrol of Ikaros expression in established B-ALL in vivo.

17 y represent a novel therapeutic option for B-ALL and AML.

18 while the role of PAX5 fusion proteins in B-ALL development is largely unknown.

19 results suggest that IKZF1 alterations in B-ALL leads to induction of multiple genes associated with

20 ish the clinical activity of a CD22-CAR in B-ALL, including leukemia resistant to anti-CD19 immunothe

21 on following disease establishment, but in B-ALL, TRC105 alone was ineffective due to the shedding of

22 PAX5 is a tumor suppressor in B-ALL, while the role of PAX5 fusion proteins in B-ALL dev

23 he balance of these pathways might inhibit B-ALL.

24 e-B-ALL, and fasting effectively inhibited B-ALL growth in a human xenograft model.

25 KCbeta, NF-kappaB1 and IKAROS, to initiate B-ALL.

26 l and T cell acute lymphoblastic leukemia (B-ALL and T-ALL, respectively), but not acute myeloid leuk

27 (AML) and acute B-lymphoblastic leukemia (B-ALL).

28 CR(+) B cell acute lymphoblastic leukemia (B-ALL).

29 ll precursor acute lymphoblastic leukemia (B-ALL).

30 le in B cell acute lymphoblastic leukemia (B-ALL).

31 nostic factor in B-lymphoblastic leukemia (B-ALL).

32 ssion contributes to maintenance of murine B-ALL cells with compromised Ikaros function.

33 CD22 is also expressed in most cases of B-ALL and is usually retained following CD19 loss.

34 ll as genes that affect the sensitivity of B-ALL cells to dex.

35 integrate the transcriptional response of B-ALL to GCs with a next-generation short hairpin RNA scre

36 hibitor ibrutinib in preclinical models of B-ALL.

37 like, 31.1% had Ph(+), and 35.8% had other B-ALL subtypes (B-other).

38 ves upon FC for MRD detection in pediatric B-ALL by identifying a novel subset of patients at end of

39 e prognosis of pediatric patients with pre-B-ALL, and fasting effectively inhibited B-ALL growth in a

40 e Cdkna2a/b tumor suppressors in promoting B-ALL development.

41 synergistically kill even highly resistant B-ALL with diverse genetic backgrounds.

42 ar observations made in human PAX5-ETV6(+) B-ALLs, these data identified PAX5-ETV6 as a potent oncopr

43 Pax5-Etv6 target genes identified in these B-ALLs encode proteins implicated in pre-B-cell receptor (

44 377 bone marrow follow-up samples of 178 BCP-ALL patients.

45 uate-redesign phases with a total of 319 BCP-ALL patients at diagnosis, two 8-color antibody tubes we

46 ive below 10 nM in B-cell precursor ALL (BCP-ALL) subsets, including MLL-AF4 and TCF3-HLF ALL, and in

47 ) relapse after CD19-directed therapy in BCP-ALL may be a result of the selection of preexisting CD19

48 precursor acute lymphoblastic leukemia (BCP-ALL) could not be classified into any of the established

49 precursor acute lymphoblastic leukemia (BCP-ALL).

50 s of 617 adult patients with Ph-negative BCP-ALL (median age, 38 years), treated in the intensified G

51 monoclonal antibody therapy in pediatric BCP-ALL, we tested an Fc-engineered CD19 antibody carrying t

52 We present 2 BCR-ABL1 fusion-positive BCP-ALL patients with CD19(-) myeloid lineage relapse after

53 les from patients with BCR-ABL1-positive BCP-ALL, we identified HSC involvement in 40% of the patient

54 2-like PDX trial using 13 MLL-rearranged BCP-ALL samples.

55 ased on their contribution in separating BCP-ALL cells from normal/regenerating BCP cells in multidim

56 as a promising targeted agent for pre-BCR(+) ALL and highlight the importance of ibrutinib effects on

57 Pre-BCR(+) ALL cells were exquisitely sensitive to ibrutinib at the

58 In pre-BCR(+) ALL, ibrutinib thwarted autonomous and induced pre-BCR s

59 ated synergistic activity against pre-BCR(+) ALL.

60 relevant targets of ibrutinib in pre-BCR(+) ALL.

61 e, standard-risk patients of trial AIEOP-BFM ALL 2000 (Combination Chemotherapy Based on Risk of Rela

62 owed with time but remain very wide for both ALL and AML.

63 The importance of VEGF produced by ALL cells in mediating leukemia-cell entry into the CNS

64 orated into Children's Oncology Group B-cell ALL (B-ALL) clinical trials.

65 Patients with newly diagnosed B-cell ALL (B-ALL) who received frontline chemotherapy at MD An

66 cells could contribute to the strong B-cell ALL association of MLL-AF4 leukemia observed in the clin

67 Survival from precursor-cell ALL was very close to that of all lymphoid leukaemias co

68 unophenotypically defined subgroup of T-cell ALL (T-ALL) associated with high rates of intrinsic trea

69 ce for the main components of complex T-cell ALL treatment regimens is described.

70 f adult patients with newly diagnosed T-cell ALL with an emphasis on the immunophenotypic and genetic

71 se inhibitors, in adult patients with T-cell ALL.

72 MLL-AF4 and TCF3-HLF ALL, and in some T-cell ALLs (T-ALLs), predicting in vivo activity as a single a

73 We treated 10 childhood ALL patient-derived xenograft models harboring various P

74 rved between C-section overall and childhood ALL risk (<15 years of age), but elective C-section was

75 CMV infection is a risk factor for childhood ALL and is more prominent in Hispanic children.

76 ake during maintenance therapy for childhood ALL should aim to simplify administration.

77 class of genomic abnormalities in childhood ALL and that recurrent translocations involving EP300 an

78 Self-report of 6MP intake in childhood ALL overestimates true intake, particularly in nonadhere

79 us (CMV) infection at diagnosis in childhood ALL, demonstrating active viral transcription in leukemi

80 The incidence rate of childhood ALL was negatively associated with SEP among Hispanics b

81 s associated with a higher risk of childhood ALL, especially at the peak ages of incidence.

82 ion (C-section) in the etiology of childhood ALL.

83 C-section was not associated with childhood ALL.

84 all, PI3K/mTOR inhibition potently decreased ALL burden in vivo; antileukemia activity was further en

85 d to enhance phagocytosis of patient-derived ALL blasts by human macrophages in vitro.

86 Patient-derived ALL cell lines COG-LL-332 and COG-LL-317 were isolated i

87 of somatic deletions in children who develop ALL.

88 ohort study of patients with newly diagnosed ALL, comparing prospectively collected infection-related

89 treated with CTL019 in 2 different diseases (ALL and CLL).

90 In particular, we described a distinct ALL subtype with a characteristic gene expression signat

91 on abrogates the poor prognosis of adult ETP-ALL.

92 cols was not inferior to that of the non-ETP-ALL group (5-year overall survival: ETP, 59.6%; 95% CI,

93 ), the overall prognosis for adults with ETP-ALL treated using the GRAALL protocols was not inferior

94 s with T-ALL, including 47 patients with ETP-ALL, treated in the GRAALL (Group for Research on Adult

95 t in a large proportion of patients with ETP-ALL.

96 vestigation of CMV as an etiologic agent for ALL is warranted.

97 ildren undergoing induction chemotherapy for ALL.

98 id and higher frequency in ETV6-RUNX1 fusion ALL.

99 risk allele is preferentially retained in HD-ALL blasts consistent with inherited genetic variation c

100 perdiploid acute lymphoblastic leukaemia (HD-ALL) being the most common subgroup of paediatric ALL, i

101 l mechanism underlying hereditary risk of HD-ALL at 10q21.2.

102 morphism rs7090445 highly associated with HD-ALL (P=1.54 x 10(-38)), and residing in a predicted enha

103 ALL) subsets, including MLL-AF4 and TCF3-HLF ALL, and in some T-cell ALLs (T-ALLs), predicting in viv

104 copy number of 8 genes frequently deleted in ALL (CDKN2A, ETV6, IKZF1, PAX5, RB1, BTG1, PAR1 region,

105 gher prevalence of in utero CMV infection in ALL cases (n = 268) than healthy controls (n = 270) (odd

106 The importance of these lesions in ALL has, until now, remained unclear.

107 ukemogenesis and treatment responsiveness in ALL.

108 ovide a concise review of genomic studies in ALL and discuss the role of genomic testing in clinical

109 Clinical studies in ALL identified via searches of PubMed, MEDLINE, and clin

110 tions in vitro, it could successfully induce ALL in NSG mice.

111 Gedatolisib also inhibited ALL proliferation in ABL/platelet-derived growth factor

112 JAK-mutant models more effectively inhibited ALL proliferation than either inhibitor alone (P < .001)

113 Ibrutinib inhibited ALL cell migration toward CXCL12 and beneath marrow stro

114 aintenance of ALL, and that fasting inhibits ALL development by upregulation of LEPR and its downstre

115 recursor-cell acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemia (AML).

116 or paediatric Acute Lymphoblastic Leukaemia (ALL) treatment for more than 40 years.

117 of pre-B-cell acute lymphoblastic leukaemia (ALL).

118 uld drive both acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).

119 ractory B-cell acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL), including t

120 with pediatric acute lymphoblastic leukemia (ALL) and to identify genetic abnormalities that drive di

121 s of childhood acute lymphoblastic leukemia (ALL) are at risk for neurocognitive deficits that are as

122 CD19-positive acute lymphoblastic leukemia (ALL) blasts, was approved for use in patients with relap

123 ATR-inhibited acute lymphoblastic leukemia (ALL) cells reveals substantial remaining de novo and sal

124 tic feature of acute lymphoblastic leukemia (ALL) in both children and adults.

125 like (Ph-like) acute lymphoblastic leukemia (ALL) is a high-risk subtype characterized by genomic alt

126 T-cell acute lymphoblastic leukemia (ALL) is a rare disease in adults with inferior survival

127 recursor (ETP) acute lymphoblastic leukemia (ALL) is an immunophenotypically defined subgroup of T-ce

128 Acute lymphoblastic leukemia (ALL) is the most common childhood cancer, and despite cu

129 k of childhood acute lymphoblastic leukemia (ALL) is uncertain.

130 recursor (BCP) acute lymphoblastic leukemia (ALL) patients with a sensitivity of </=10(-5), comparabl

131 60 drugs on 68 acute lymphoblastic leukemia (ALL) samples mostly from resistant disease in cocultures

132 k of childhood acute lymphoblastic leukemia (ALL) were investigated using data from population-based

133 )) B-precursor acute lymphoblastic leukemia (ALL) who progress after failure of tyrosine kinase inhib

134 patients with acute lymphoblastic leukemia (ALL) with relapse and mortality may improve the efficien

135 t diagnosis of acute lymphoblastic leukemia (ALL), a uniform CSF and risk group classification schema

136 some (Ph)-like acute lymphoblastic leukemia (ALL), also referred to as BCR-ABL1-like ALL, is a high-r

137 munotherapy of acute lymphoblastic leukemia (ALL), but CD19(-) relapses remain a major challenge in a

138 t of childhood acute lymphoblastic leukemia (ALL), but it is associated with relevant toxicity.

139 In acute lymphoblastic leukemia (ALL), central nervous system (CNS) involvement is a majo

140 recursor (BCP) acute lymphoblastic leukemia (ALL), often comprising small numbers of patients.

141 children with acute lymphoblastic leukemia (ALL), we identified 58 putative functional and predomina

142 used to treat acute lymphoblastic leukemia (ALL).

143 sed/refractory acute lymphoblastic leukemia (ALL).

144 k of childhood acute lymphoblastic leukemia (ALL).

145 with childhood acute lymphoblastic leukemia (ALL).

146 patients with acute lymphoblastic leukemia (ALL; n = 47), chronic lymphocytic leukemia (n = 24), and

147 the etiology of acute lymphocytic leukemia (ALL), and the involvement of the immune system suggests

148 mia (ALL), also referred to as BCR-ABL1-like ALL, is a high-risk subset with a gene expression profil

149 let count (HR, 7.437; P = .005), and Ph-like ALL (HR, 1.818; P = .03).

150 Additional genomic alterations in Ph-like ALL activate other kinases, including BLNK, DGKH, FGFR1,

151 d to define the genomic landscape of Ph-like ALL and how it varies across the age spectrum, associate

152 ) ALL is defined by BCR-ABL1 fusion, Ph-like ALL cases contain a variety of genomic alterations that

153 of kinase-activating alterations in Ph-like ALL has important therapeutic implications.

154 prevalence and genomic landscape of Ph-like ALL in adults and assess response to conventional chemot

155 in adults, an increased frequency of Ph-like ALL in adults of Hispanic ethnicity, significantly infer

156 Our findings show high frequency of Ph-like ALL in adults, an increased frequency of Ph-like ALL in

157 ta on the incidence and prognosis of Ph-like ALL in adults.

158 Conclusion Ph-like ALL is a highly prevalent subtype of ALL in adults and i

159 combinations of kinase inhibitors in Ph-like ALL patients are indicated.

160 etermined for Ph-like ALL versus non-Ph-like ALL patients.

161 ling pathways are active in specific Ph-like ALL subsets, and precision medicine trials have been ini

162 overall survival were determined for Ph-like ALL versus non-Ph-like ALL patients.

163 Sixty-eight percent of patients with Ph-like ALL were of Hispanic ethnicity.

164 B-cell acute lymphoblastic leukemia (Ph-like ALL) is associated with activated JAK/STAT, Abelson kina

165 rior outcomes of adult patients with Ph-like ALL, and significantly worse outcomes in the CRLF2(+) su

166 alterations in 88% of patients with Ph-like ALL, including CRLF2 rearrangements (51%), ABL class fus

167 e outcomes in the CRLF2(+) subset of Ph-like ALL.

168 viously reported to be rearranged in Ph-like ALL.

169 have been minimally investigated in Ph-like ALL.

170 AS, NF1, PTPN11) in 6% of those with Ph-like ALL.

171 of these agents in the treatment of Ph-like ALL.

172 erformed on 180 of 194 patients with Ph-like ALL.

173 Conclusion Children with high-risk B-lineage ALL who were age < 10 years at diagnosis are at risk for

174 tioning in children with high-risk B-lineage ALL.

175 patients with systemic (ALS) and localized (ALL) amyloidosis and to assess for associations between

176 therapy has improved clinical outcome, most ALL patients relapse following treatment with TKI due to

177 atopoietic subpopulations; 12% to 83% of non-ALL B lymphocytes, T cells, and/or myeloid cells harbore

178 Leveraging the addiction of ALL to folic acid, we conjugated folate to an alcohol de

179 At the peak ages of ALL incidence (2-4 years), C-section was associated with

180 gedatolisib resulted in near eradication of ALL in cytokine receptor-like factor 2 (CRLF2)/JAK-mutan

181 ntial for the development and maintenance of ALL, and that fasting inhibits ALL development by upregu

182 Thus, we identified a mechanism of ALL-cell entry into the CNS, which by targeting VEGF sig

183 ciated with a significantly elevated risk of ALL (odds ratio (OR) = 1.17, 95% confidence interval (CI

184 on was associated with an 11% higher risk of ALL (OR = 1.11, 95% CI: 1.01, 1.22) compared with vagina

185 Ph-like ALL is a highly prevalent subtype of ALL in adults and is associated with poor outcome.

186 EBF1-PDGFRB, in almost one third of B-other ALL cases.

187 L (10.1%; 39 of 386 T-ALL cases) and B-other ALL, that is, lacking established chromosomal abnormalit

188 being the most common subgroup of paediatric ALL, its aetiology remains unknown.

189 -RUNX1 conferred a low risk of developing pB-ALL after exposure to common pathogens, corroborating th

190 cursor B-cell acute lymphocytic leukemia (pB-ALL), the underlying genetic basis for development of fu

191 ) and postnatal infections for human-like pB-ALL.

192 Murine and human ETV6-RUNX1 pB-ALL revealed recurrent genomic alterations, with a relev

193 /2 expression, known for human ETV6-RUNX1 pB-ALL.

194 ion of an ETV6-RUNX1 preleukemic clone to pB-ALL after infection exposure and offer the possibility o

195 laxis during induction therapy for pediatric ALL and the first to include a broad-spectrum fluoroquin

196 S) and preinfusion tumor burden in pediatric ALL.

197 d CDK6 were highly correlated in adult Ph(+) ALL (P = 0.00008).

198 Although Ph(+) ALL is defined by BCR-ABL1 fusion, Ph-like ALL cases con

199 dowed with antileukemia activity, from Ph(+) ALL patients and healthy donors.

200 onsistent with their essential role in Ph(+) ALL, pharmacologic inhibition of CDK6 and BCL2 markedly

201 peutic approaches with BCR-ABL CTLs in Ph(+) ALL.

202 positive acute lymphoblastic leukemia (Ph(+) ALL) is currently treated with BCR-ABL1 tyrosine kinase

203 positive acute lymphoblastic leukemia (Ph(+) ALL) undergoing maintenance tyrosine-kinase inhibitor tr

204 Moreover, Ph(+) ALL cells exhibited a specific requirement for CDK6 but

205 ion, colony formation, and survival of Ph(+) ALL cells ex vivo and in mice.

206 ategy to target the MYB "addiction" of Ph(+) ALL.Significance: MYB blockade can suppress Philadelphia

207 le of controlling treatment-refractory Ph(+) ALL in vivo, and support the development of adoptive imm

208 n patients with relapsed or refractory Ph(+) ALL.

209 Newly developed TKI can target Ph(+) ALL cells with BCR-ABL1-dependent resistance; however, o

210 el phase II study enrolled adults with Ph(+) ALL who had relapsed after or were refractory to at leas

211 We treated 3 patients with Ph(+) ALL with autologous or allogeneic (p190)BCR-ABL-specific

212 ant overlap with that of Ph-positive (Ph(+)) ALL and is suggestive of activated kinase signaling.

213 consistent with previous experience in Ph(-) ALL.

214 iological heterogeneity of BCR-ABL1-positive ALL may impact the patient outcomes and optimal treatmen

215 relapses in patients with BCR-ABL1-positive ALL.

216 Patients with ETV6-RUNX1-positive ALL and patients 1 to 6 years of age performed equally w

217 ighly active below 10 nM in B-cell precursor ALL (BCP-ALL) subsets, including MLL-AF4 and TCF3-HLF AL

218 with relapsed or refractory B-cell precursor ALL on the basis of single-group trials that showed effi

219 lts with heavily pretreated B-cell precursor ALL, in a 2:1 ratio, to receive either blinatumomab or s

220 We found that primary ALL cells transplanted onto nonobese diabetic/severe com

221 a-cell entry into the CNS using a primograft ALL mouse model.

222 mixed-lineage leukemia gene (MLL)-rearranged ALL were established in NOD.Cg-Prkdc(scid) Il2rg(tm1Wjl)

223 nsferases EP300 and CREBBP ZNF384-rearranged ALL showed significant up-regulation of CLCF1 and BTLA e

224 rials have been initiated for this high-risk ALL subset.

225 rs (MAD), and users of all three substances (ALL).

226 T-ALL NOTCH1 mutations result in ligand-independent and su

227 ic (6 of 160) and 5.5% of adult (9 of 163) T-ALL patient samples.

228 Using integrated genomic analysis of 264 T-ALL cases, we identified 106 putative driver genes, half

229 most frequently in T-ALL (10.1%; 39 of 386 T-ALL cases) and B-other ALL, that is, lacking established

230 tions were identified in PF-382 and DU.528 T-ALL cell lines in addition to 3.7% of pediatric (6 of 16

231 type of immunophenotypically defined adult T-ALL is similar to the pediatric equivalent, with high ra

232 otypically defined subgroup of T-cell ALL (T-ALL) associated with high rates of intrinsic treatment r

233 ll acute lymphoblastic leukemia (B-ALL and T-ALL, respectively), but not acute myeloid leukemia (AML)

234 not previously been described in childhood T-ALL (for example, CCND3, CTCF, MYB, SMARCA4, ZFP36L2 and

235 In childhood T-ALL, the N/F/R/P mutation profile is an independent pred

236 well-known target, Etv4 Importantly, human T-ALL also relies on ETV4 expression for maintaining its o

237 t Ras-induced mouse T-ALL as well as human T-ALL carrying mutations in the RAS/MAPK pathway display a

238 ll leukemia homeobox 1/3-transformed human T-ALL cell lines and NOTCH1 T-ALL mouse models.

239 RUNX proteins, impairs the growth of human T-ALL cell lines and primary patient samples.

240 h in vivo and that RUNX silencing in human T-ALL cells triggers apoptosis.

241 or MRD >/= 5%) occurred most frequently in T-ALL (10.1%; 39 of 386 T-ALL cases) and B-other ALL, that

242 tivity at low micro molar concentration in T-ALL cell lines.

243 ocus is activated under a superenhancer in T-ALL cells but not in normal T cells.

244 esult, the oncogenic activity of NOTCH1 in T-ALL is strictly dependent on MYC upregulation, which mak

245 Aberrant cell growth and proliferation in T-ALL lymphoblasts are sustained by activation of strong o

246 TAL1-induced regulatory circuit and MYC in T-ALL, thereby contributing to T-cell leukemogenesis.

247 ression, SCL contributes to oncogenesis in T-ALL.

248 eal RUNX1 as a novel therapeutic target in T-ALL.

249 involved in the transcriptional program in T-ALL.

250 below 20 nM was detected in 2 independent T-ALL cohorts, which correlated with similar cytotoxic act

251 Cic inactivation in mice induces T-ALL by a mechanism involving derepression of its well-kn

252 t detailed genome-wide sequencing of large T-ALL cohorts has not been carried out.

253 highly expressed in acute T-cell leukemia (T-ALL) and in a subset of peripheral T-cell lymphomas.

254 pid onset of acute lymphoblastic leukemia (T-ALL) and progressive development of hepatocellular carci

255 6% of T-cell acute lymphoblastic leukemia (T-ALL) cases.

256 am in T-cell acute lymphoblastic leukemia (T-ALL) cells.

257 T-cell acute lymphoblastic leukemia (T-ALL) is a highly proliferative hematologic malignancy th

258 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy caused by the accumulat

259 dhood T-cell acute lymphoblastic leukemia (T-ALL) is mainly based on minimal residual disease (MRD) q

260 Pediatric T-acute lymphoblastic leukemia (T-ALL) patients often display resistance to glucocorticoid

261 et of T-cell acute lymphoblastic leukemia (T-ALL) patients, and RUNX1 mutations are associated with a

262 c tools in T-acute lymphoblastic leukemia (T-ALL) using T-ALL cell lines and patient-derived samples.

263 ature T-cell acute lymphoblastic leukemia (T-ALL), a heterogenic subgroup of human leukemia character

264 of T-lineage acute lymphoblastic leukemia (T-ALL), but detailed genome-wide sequencing of large T-ALL

265 pe in T cell acute lymphoblastic leukemia (T-ALL), but its administration is predicted to be toxic in

266 et in T-cell acute lymphoblastic leukemia (T-ALL).

267 kemia/T-cell acute lymphoblastic leukemia [T-ALL] 1) is an essential transcription factor in normal a

268 duces T-cell acute lymphoblastic lymphoma (T-ALL), a tumor type known to carry CIC mutations, albeit

269 Finally, we show that Ras-induced mouse T-ALL as well as human T-ALL carrying mutations in the RAS

270 lanation of why progression of JAK3-mutant T-ALL cases can be associated with the accumulation of add

271 nsformed human T-ALL cell lines and NOTCH1 T-ALL mouse models.

272 is required for the survival and growth of T-ALL cells, and forced expression of ARID5B in immature t

273 , we provide an update on our knowledge of T-ALL pathogenesis, the opportunities for the introduction

274 ng, which is activated in more than 65% of T-ALL patients by activating mutations in the NOTCH1 gene,

275 In mechanistic and translational models of T-ALL, we demonstrate NOTCH1 inhibition in vitro and in vi

276 ve therapeutic target for the treatment of T-ALL.

277 enes and pathways, and stage or subtype of T-ALL.

278 e protective in a mouse xenograft model of T-ALL.

279 iRNNs) targeting Plk1, can enter pediatric T-ALL patient cells without a transfection reagent and ind

280 poorer outcome than do the other pediatric T-ALL patients receiving a high-risk adapted therapy.

281 and overcoming GC resistance in pediatric T-ALL patients.

282 A patient with refractory T-ALL was treated with dasatinib on the basis of drug prof

283 Moreover, Cic inactivation renders T-ALL insensitive to MEK inhibitors in both mouse and huma

284 able to induce cell death in GC-resistant T-ALL cells, and remarkably, cotreatment with dexamethason

285 vative therapeutic opportunities in SCL(+) T-ALL.

286 rectly activated by TAL1 and contribute to T-ALL pathogenesis are largely unknown.

287 acute lymphoblastic leukemia (T-ALL) using T-ALL cell lines and patient-derived samples.

288 a large cohort of 213 adult patients with T-ALL, including 47 patients with ETP-ALL, treated in the

289 and TCF3-HLF ALL, and in some T-cell ALLs (T-ALLs), predicting in vivo activity as a single agent and

290 ZEB2 and demonstrated that mouse and human T-ALLs with increased ZEB2 levels critically depend on KDM

291 Because glucocorticoids are administered to ALL patients during all the different phases of therapy,

292 like L-asparaginases maintain their in vitro ALL killing potential.

293 children, adolescents, and young adults with ALL (N = 55).

294 iming of infection at birth in children with ALL and age, gender, and ethnicity matched controls to i

295 erreporting in a cohort of 416 children with ALL in first remission over 4 study months (1344 patient

296 hods Participants included 441 children with ALL receiving oral 6-MP for maintenance.

297 k of Relapse in Treating Young Patients With ALL) were investigated with the specific aim to reduce t

298 Patients with ALL, >/=4 prior antitumor regimens, and receipt of the h

299 meningeal infiltration seen in patients with ALL.

300 al in both pediatric and adult patients with ALL.