ライフサイエンスコーパス: B-ALL

1 tration, both hallmarks of infant t(4;11)(+) B-ALL.

2 Examination of an extended cohort of 1,164 B-ALL cases identified 30 cases with MEF2D rearrangement

3 MLL-Af4 induces a B ALL distinct from MLL-AF9 through differential genomic

4 EP-2 cells suggesting that CTCF could play a B-ALL cell line specific role in maintaining MYC express

5 We found that primary human BCR-ABL1(+) B-ALL cells could be induced to reprogram into macrophag

6 liminates the leukemogenicity of BCR-ABL1(+) B-ALL cells, and suggesting a previously unidentified th

7 CD14(+) monocytes/macrophages in BCR-ABL1(+) B-ALL patient samples that possess the BCR-ABL1(+) trans

8 ll acute lymphoblastic leukemia (BCR-ABL1(+) B-ALL) is an aggressive hematopoietic neoplasm character

9 agnosis is predictive of pediatric and adult B-ALL patient survival.

10 ls expand and persist in pediatric and adult B-ALL patients relapsed after HSCT.

11 singly, AID genetic deletion does not affect B-ALL development in Pax5-haploinsufficient mice prone t

12 t provides superior in vivo activity against B-ALL compared with single-expressing CART or pooled com

13 immunotherapy, demonstrating potency against B-ALL comparable to that of CD19-CAR at biologically act

14 al of mice challenged with highly aggressive B-ALL.

15 e most frequent somatic aneuploidy among all B-ALLs.

16 identify patients with precursor B-cell ALL (B-ALL) at very low risk (VLR) of relapse and treated the

17 24/358 (6.7%) relapsed childhood B cell ALL (B-ALL) cases.

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

19 o identify new risk variants for B-cell ALL (B-ALL) we conducted a meta-analysis with four GWAS (geno

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

21 ts of ALL, including hypodiploid B-cell ALL (B-ALL), for which effective alternative therapies to cur

22 a (ALL) is a recently identified B-cell ALL (B-ALL)subtype with poor outcome that exhibits a gene exp

23 , HNRNPUL1 and SS18) in 22 B progenitor ALL (B-ALL) cases with a distinct gene expression profile, th

24 G levels (T cell ALL [T-ALL] and B cell ALL [B-ALL] with the TCF3-PBX1 or ETV6-RUNX1 fusions), and 2

25 B-cell acute lymphoblastic leukemia (ALL; B-ALL) is the most common pediatric cancer, and high hyp

26 ions, particularly for preventing T-ALL (and B-ALL) relapse.

27 In retroviral mouse models of CML and B-ALL, coexpression of IkappaBalphaSR attenuated leukemo

28 genetic strategy and mouse models of CML and B-ALL, we show here that GAB2 is essential for myeloid a

29 actor of c-Myc, significantly delayed T- and B-ALL/lymphoma in mice and interfered with the oncogenic

30 links between chromosome 21 triplication and B-ALL remain undefined.

31 motes both B cell proliferation in vitro and B-ALL in vivo.

32 wal in vitro, maturation defects in vivo and B-ALL with either the BCR-ABL fusion protein or CRLF2 wi

33 ylation (H3K27me3) in progenitor B cells and B-ALLs, and 'bivalent' genes with both H3K27me3 and H3K4

34 ic event in lymphoid lineage cancers such as B-ALL, lymphoma and multiple myeloma.

35 vival, and demonstrate monocyte abundance at B-ALL diagnosis is predictive of pediatric and adult B-A

36 ransformed mouse pre-B cells and human pre-B B-ALL cells that involves the negative regulation of FOX

37 BL-transformed murine B-1 progenitors can be B-ALL cells of origin and demonstrate that they initiate

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

39 ating cells and CD19-negative blasts in bulk B-ALL at baseline and at relapse after CART19 administra

40 ng 5 of 5 patients with CD19(dim) or CD19(-) B-ALL.

41 A total of 233 childhood B-ALL patients were enrolled into this study.

42 ozygosity for C1 as protective for childhood B-ALL supporting a model in which NK cells are involved

43 fications of CNV and aneuploidy in childhood B-ALL.

44 pregulated gene seen at relapse in childhood B-ALL.

45 viding evidence for a new model of childhood B-ALL development.

46 associated with novel subtypes of childhood B-ALL, have prognostic significance.

47 urvival ( approximately 85-90%) of childhood B-ALL, the outcome of infants with MLL-rearranged (MLL-r

48 ng oncogenic event affiliated with childhood B-ALL, the mitotic and chromosomal defects associated wi

49 lity of transcriptome sequencing to classify B-ALL and reinforce the central role of PAX5 as a checkp

50 Using CD34(+) progenitors from CML, B-ALL, and healthy individuals, we found that XPO1 expre

51 izing single-cell approaches, we demonstrate B-ALL bone marrow immune microenvironment remodeling upo

52 stically induced apoptosis in JAK2-dependent B-ALLs and further improved in vivo survival compared to

53 Stat5b-CA mice typically do not develop B-ALL (<2% penetrance); in contrast, 89% of Stat5b-CA mi

54 y in pediatric patients with newly diagnosed B-ALL.

55 The absence of MA4-driven B-ALL models further questions whether MA4 acts as a sin

56 two opposing transcriptional programs drives B-ALL and suggest that restoring the balance of these pa

57 Moreover, patient samples of IGH-DUX4 B-ALL have similar expression profile and IGH breakpoint

58 control of Ikaros expression in established B-ALL in vivo.

59 ng endogenous Pax5 expression in established B-ALL triggers immunophenotypic maturation and durable d

60 ilar observations made in human PAX5-ETV6(+) B-ALLs, these data identified PAX5-ETV6 as a potent onco

61 We herein describe novel risk loci for B-ALL at 9q21.31 (rs76925697, P = 2.11 x 10(-8)), for hi

62 may offer a new therapeutic opportunity for B-ALL.

63 may represent a novel therapeutic option for B-ALL and AML.

64 ther ongoing PAX5 deficiency is required for B-ALL maintenance.

65 ism and a potential therapeutic approach for B-ALLs with LNK mutations.

66 A metaanalysis of gene expression data from B-ALL patient specimens revealed that Aurora kinase B (A

67 risk B-cell acute lymphoblastic leukemia (HR B-ALL) or NCI standard-risk B-ALL with defined minimal r

68 not improve 5-year DFS for children with HR B-ALL.

69 These and similar findings in human B-ALL cell lines establish that Pax5 hypomorphism promot

70 ine B-ALL in vivo with two independent human B-ALL cohorts identified nine evolutionarily conserved I

71 Likewise, known drivers of human B-ALL are not preferentially targeted by AID.

72 pressed the growth of CRLF2-rearranged human B-ALL cells, abrogated JAK2 signaling, and improved surv

73 We show that human B-ALL blasts alter a vascularized microenvironment promo

74 Human B-ALLs with polysomy 21 are distinguished by their overe

75 d chromosomal defects associated with HyperD B-ALL (HyperD-ALL) remain poorly characterized.

76 Collectively, hyperdiploid B-ALL is associated with a defective condensin complex,

77 th therapeutic potential against hypodiploid B-ALL.

78 otential therapeutic strategy in hypodiploid B-ALL.

79 ient-derived xenograft models of hypodiploid B-ALL.

80 tial target for the treatment of hypodiploid B-ALL.

81 Children and young adults with hypodiploid B-ALL continue to fare poorly and do not seem to benefit

82 f children and young adults with hypodiploid B-ALL who were enrolled in recent Children's Oncology Gr

83 se results suggest that IKZF1 alterations in B-ALL leads to induction of multiple genes associated wi

84 /or analysis of genes known to be altered in B-ALL were performed in patients with BCR-ABL1-likeALL w

85 sion following disease establishment, but in B-ALL, TRC105 alone was ineffective due to the shedding

86 blish the clinical activity of a CD22-CAR in B-ALL, including leukemia resistant to anti-CD19 immunot

87 childhood cancers and current challenges in B-ALL treatment include resistance, relapse and late-ons

88 e of potentiating drug-induced cell death in B-ALL cells by upregulating intracellular levels of reac

89 ic mechanisms in driving clonal evolution in B-ALL and identifies novel pathways associated with drug

90 strongly induced aberrant BCL6 expression in B-ALL cells, germline MLL was required to up-regulate Bc

91 cant Notch receptor and ligand expression in B-ALL primary cells and cell lines.

92 these genes and associated pathways have in B-ALL.

93 m are EMP1, which was recently implicated in B-ALL proliferation and prednisolone resistance, and the

94 o improve the efficacy of JAK2 inhibition in B-ALL, we developed the type II inhibitor CHZ868, which

95 Our data suggest that targeting NF-kappaB in B-ALL increases the risk of RAG-dependent genomic instab

96 Oncogenic lesions in B-ALL frequently mimic signalling through cytokine recep

97 e depleting leukemia-associated monocytes in B-ALL animal models prolongs disease remission in vivo.

98 ncover a role for non-classical monocytes in B-ALL survival, and demonstrate monocyte abundance at B-

99 s to define the role of the Notch pathway in B-ALL chemosensitivity.

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

101 B-cell transformation and drug resistance in B-ALL.

102 Notably, even brief Pax5 restoration in B-ALL cells causes rapid cell cycle exit and disables th

103 provide evidence that CDK8 has a key role in B-ALL.

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

105 and the expression of RAG1, RAG2, and TdT in B-ALL patients.

106 tivator of transcription 5 (STAT5) to induce B-ALL.

107 deficiency also attenuated BCR-ABL1-induced B-ALL, but only the SHP2 binding site was required.

108 e, we revisit the biology of t(4;11)+ infant B-ALL with an emphasis on its origin, genetics, and dise

109 The genetic hallmark of most infant B-ALL is chromosomal rearrangements of the mixed-lineage

110 Among MLL-r infant B-ALL, t(4;11)+ patients harboring the fusion MLL-AF4 (M

111 the balance of these pathways might inhibit B-ALL.

112 pre-B-ALL, and fasting effectively inhibited B-ALL growth in a human xenograft model.

113 vitro and in vivo, and were able to initiate B-ALL in transplant recipients.

114 PKCbeta, NF-kappaB1 and IKAROS, to initiate B-ALL.

115 lyse 1,148 patient-derived B-cell leukaemia (B-ALL) samples, and find that individual mutations do no

116 ell and T cell acute lymphoblastic leukemia (B-ALL and T-ALL, respectively), but not acute myeloid le

117 Infant B-cell acute lymphoblastic leukemia (B-ALL) accounts for 10% of childhood ALL.

118 B-cell acute lymphoblastic leukemia (B-ALL) accounts for nearly one fifth of all childhood ca

119 sistant B cell acute lymphoblastic leukemia (B-ALL) and acute myeloid leukemia (AML).

120 ~10% of B-cell acute lymphoblastic leukemia (B-ALL) and define a group of patients with dismal outcom

121 f B-progenitor acute lymphoblastic leukemia (B-ALL) and most commonly involve PAX5, encoding the DNA-

122 e in B lineage acute lymphoblastic leukemia (B-ALL) and occur in >70% of the high-risk BCR-ABL1(+) (P

123 emination of B acute lymphoblastic leukemia (B-ALL) cells, by stably downregulating CD9 in REH and NA

124 primary B-cell acute lymphoblastic leukemia (B-ALL) cells, suggesting a role for Notch signaling in d

125 cell precursor acute lymphoblastic leukemia (B-ALL) exceeds 90% with risk-adapted therapy.

126 s with hypodiploid B-lymphoblastic leukemia (B-ALL) fare poorly and hematopoietic stem-cell transplan

127 ts with B-cell acute lymphoblastic leukemia (B-ALL) harboring rearrangement of the mixed lineage leuk

128 lthough B-cell acute lymphoblastic leukemia (B-ALL) is the most common malignancy in children and whi

129 ildhood B-cell acute lymphoblastic leukemia (B-ALL) is to decipher its etiology.

130 hat underlie B-acute lymphoblastic leukemia (B-ALL) occur in the fetus, at which time B-1 progenitor

131 rial in B cell acute lymphoblastic leukemia (B-ALL) patients relapsed after allogeneic hematopoietic

132 bset of B cell acute lymphoblastic leukemia (B-ALL) patients will relapse and succumb to therapy-resi

133 f B-progenitor acute lymphoblastic leukemia (B-ALL), a disease characterized by the accumulation of u

134 risk of B cell acute lymphoblastic leukemia (B-ALL), and polysomy 21 is the most frequent somatic ane

135 ory pre-B cell acute lymphoblastic leukemia (B-ALL), but antigen loss is a frequent cause of resistan

136 cell precursor acute lymphoblastic leukemia (B-ALL), but inherited mutations of PAX5 have not previou

137 f B-progenitor acute lymphoblastic leukemia (B-ALL), however many cases lack a known initiating genet

138 ts with B cell acute lymphoblastic leukemia (B-ALL), making B-ALL an excellent model for studying the

139 tric B-lineage acute lymphoblastic leukemia (B-ALL), short-term and long-term toxicities and chemores

140 -rearranged) B-acute lymphoblastic leukemia (B-ALL), which constitutes a subtype of this malignancy a

141 o human B-cell acute lymphoblastic leukemia (B-ALL).

142 ognostic factor in B-lymphoblastic leukemia (B-ALL).

143 ia (AML) and acute B-lymphoblastic leukemia (B-ALL).

144 -BCR(+) B cell acute lymphoblastic leukemia (B-ALL).

145 cell precursor acute lymphoblastic leukemia (B-ALL).

146 role in B cell acute lymphoblastic leukemia (B-ALL).

147 st Ph(+)B-cell acute lymphoblastic leukemia (B-ALL).

148 ecursor B-cell acute lymphoblastic leukemia (B-ALL).

149 ractory B cell acute lymphoblastic leukemia (B-ALL).

150 e infant pro-B-acute lymphoblastic leukemia (B-ALL).

151 genitor B-cell acute lymphoblastic leukemia (B-ALL).

152 ic B-precursor acute lymphoblastic leukemia (B-ALL).

153 ent and B-cell acute lymphoblastic leukemia (B-ALL).

154 gh-risk B-cell acute lymphoblastic leukemia (B-ALL).

155 tory B-lineage acute lymphoblastic leukemia (B-ALL).

156 ildhood B-cell acute lymphoblastic leukemia (B-ALL).

157 ecursor B cell acute lymphoblastic leukemia (B-ALL).

158 d Ph(+) B-cell acute lymphoblastic leukemia (B-ALL).

159 diatric B-cell acute lymphoblastic leukemia (B-ALL).

160 ractory B-cell acute lymphoblastic leukemia (B-ALL).

161 ent for B cell acute lymphoblastic leukemia (B-ALL).

162 y (R/R) B-cell acute lymphoblastic leukemia (B-ALL).

163 senting B-cell acute lymphoblastic leukemia (B-ALL).

164 ractory B-cell acute lymphoblastic leukemia (B-ALL).

165 iatric B-cell acute lymphoblastic leukemias (B-ALLs) using whole-genome bisulfite sequencing and high

166 set of B cell acute lymphoblastic leukemias (B-ALLs) with CRLF2 rearrangements.

167 human B-cell acute lymphoblastic leukemias (B-ALLs), illustrating the oncogenic potential of the RAG

168 B cell acute lymphoblastic leukemia (Ph-like B-ALL) experience high relapse rates despite best-availa

169 ar gene expression profiles to human Ph-like B-ALLs, supporting use of this model for preclinical and

170 Tp53-/-Lnk-/- B-ALLs displayed similar gene expression profiles to hum

171 s, suggesting that KRAS activation in MA4(+) B-ALL is important for tumor maintenance rather than ini

172 acute lymphoblastic leukemia (B-ALL), making B-ALL an excellent model for studying the role of aneupl

173 of patients with relapsed and refractory MLL-B-ALL who receive CD19 CAR-T-cell therapy.

174 anying dynamic Ikaros perturbation in murine B-ALL in vivo with two independent human B-ALL cohorts i

175 ression contributes to maintenance of murine B-ALL cells with compromised Ikaros function.

176 proved survival in mice with human or murine B-ALL.

177 ial therapeutic strategies for Ikaros-mutant B-ALL.

178 B-progenitor ALL that comprises up to 7% of B-ALL.

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

180 h signaling enhances the chemosensitivity of B-ALL cells, suggesting Notch inhibition as a potential

181 development and promotes the development of B-ALL with biallelic Pax5 alteration in vivo.

182 n and may be important in the development of B-ALL.

183 T2/Onc transposon had been mobilized died of B-ALL by 3 months of age.

184 though PAX5 mutation is a critical driver of B-ALL development in mice and humans, it remains unclear

185 CXCR4-mediated migration and engraftment of B-ALL cells in the bone marrow or testis, through RAC1 a

186 hallmark genetic and phenotypic features of B-ALL and suggest that engaging the latent differentiati

187 In NOG-mouse-based xenograft models of B-ALL, co-administration of the Notch inhibitor GSI-XII

188 inhibitor ibrutinib in preclinical models of B-ALL.

189 a developmental perspective on the origin of B-ALL and indicate B cell lineage as a factor influencin

190 suppression pathways in the pathogenesis of B-ALL.

191 ging the latent differentiation potential of B-ALL cells may provide new therapeutic entry points.

192 vironment identifies extrinsic regulators of B-ALL survival supporting new immune-based therapeutic a

193 ly integrate the transcriptional response of B-ALL to GCs with a next-generation short hairpin RNA sc

194 well as genes that affect the sensitivity of B-ALL cells to dex.

195 .29 x 10(-10)), especially in the subtype of B-ALL (OR = 1.39, P = 2.47 x 10(-9)).

196 IGF2BP3 was required for the survival of B-ALL cell lines, as knockdown led to decreased prolifer

197 We then analyzed in vitro cell survival of B-ALL cells treated with conventional chemotherapeutic a

198 ult cases, we describe a revised taxonomy of B-ALL incorporating 23 subtypes defined by chromosomal r

199 have tremendously improved the treatment of B-ALL and other B-cell malignancies, they are not yet av

200 Epigenetic alteration of B-ALLs occurred in two tracks: de novo methylation of sm

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

202 tested efficacy against CRLF2-overexpressing B-ALL.

203 bone marrow mononuclear cells from pediatric B-ALL patients, cultured ex vivo, with Plk1-targeting si

204 et Plk1 mRNA in primary cells from pediatric B-ALL patients.

205 e endogenous CTCF locus in a human pediatric B-ALL cell line, SEM, and an immortal erythroid precurso

206 a potential therapeutic target in pediatric B-ALL and selective targeting of Plk1 can be achieved by

207 roves upon FC for MRD detection in pediatric B-ALL by identifying a novel subset of patients at end o

208 gens with restricted expression in pediatric B-ALL may offer the potential to reduce toxicities and p

209 nd Plk4 is significantly higher in pediatric B-ALL patients compared to healthy donors.

210 target for mAb-based therapies in pediatric B-ALL.

211 involved in immunosurveillance of pediatric B-ALL via interaction of KIR with HLA-C ligands.

212 ntifies the most common subtype of pediatric B-ALL.

213 Here, we have used 54 primary pediatric B-ALL samples to characterize the cellular-molecular mec

214 marrow mononuclear cells from ten pediatric B-ALL patients.

215 a TKI-sensitive manner, in CML-BC and Ph(+) B-ALL.

216 Notably, XPO1 was also elevated in Ph(-) B-ALL.

217 ome profiling of Nalm6, an IGH-DUX4 positive B-ALL cell line.

218 Pre B-ALL is an aggressive cancer of the blood for which tre

219 Pre-B ALL originates from a committed pre-B cell or an earli

220 based xenotransplantation of non-t(4;11) pre-B ALL enabled detection of a high frequency of LICs (<1:

221 ter functional dependence of non-t(4;11) pre-B ALL on this niche-based interaction, providing a possi

222 t non-t(4;11) pre-B ALL, whereas t(4;11) pre-B ALL was successfully reconstituted without this adapta

223 ficient engraftment of adult non-t(4;11) pre-B ALL, whereas t(4;11) pre-B ALL was successfully recons

224 Studying 830 pre-B ALL cases from four clinical trials, we found that hum

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

226 get genes in mouse and human BCR-ABL1(+) pre-B ALL, revealing novel conserved gene pathways associate

227 Ikaros in IKZF1 mutant human BCR-ABL1(+) pre-B ALL.

228 for experimental modeling of human adult pre-B ALL and demonstrate the critical protumorogenic role o

229 ly induced cell death in patient-derived pre-B ALL cells and overcame conventional mechanisms of drug

230 selective cell death of patient-derived pre-B ALL cells in vitro and significantly prolonged surviva

231 lpha4 inhibition as a novel strategy for pre-B ALL.

232 all-molecule inhibition of PTEN in human pre-B ALL cells resulted in hyperactivation of AKT, activati

233 ed profiling of the E2A-PBX1 cistrome in pre-B ALL cells and reveals a previously unappreciated pathw

234 Loss of PTEN function in pre-B ALL cells was functionally equivalent to acute activat

235 karos functions as a tumor suppressor in pre-B ALL remain poorly understood.

236 t control mechanisms are circumvented in pre-B ALL.

237 c targets to overcome drug resistance in pre-B ALL.

238 sor B cell acute lymphoblastic leukemia (pre-B ALL).

239 Here, we show that most pre-B ALL primary samples and cell lines express IL-15 and c

240 sing ICG-001 leads to differentiation of pre-B ALL cells and loss of self-renewal capacity.

241 leles of Pten caused rapid cell death of pre-B ALL cells and was sufficient to clear transplant recip

242 ated deletion of Pten in mouse models of pre-B ALL.

243 ptome alterations for the development of pre-B ALL.

244 et sites of E2A-PBX1 in t(1,19)-positive pre-B ALL cells and show that, compared with normal E2A, E2A

245 ponents of its receptor and that primary pre-B ALL cells show increased growth in culture in response

246 Collectively, these studies reveal that pre-B ALL cells are uniquely vulnerable to ER stress and ide

247 In a transgenic pre-B ALL mouse model, the heterozygous deletion of Pax5 inc

248 However, whether pre-B ALL blasts directly respond to IL-15 is unknown.

249 leukemia from 40% to 80% and those with pre-B ALL from 35% to 50%.

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

251 C) biology in primary adult precursor B (pre-B) ALL to optimize disease modeling.

252 Based on 1382 pre-B-ALL patients, the ETV6-RUNX1 fusion positive patients

253 bined systemic and CNS leukemia of human pre-B-ALL.

254 ing of signaling networks by E2A-PBX1 in pre-B-ALL, which results in hyperactivation of the key oncog

255 RAG1 while high expression of AID marked pre-B-ALL lacking common cytogenetic changes.

256 lls resulted in long-latency oligoclonal pre-B-ALL, which demonstrates that loss of Ikaros contribute

257 the prognosis of pediatric patients with pre-B-ALL, and fasting effectively inhibited B-ALL growth in

258 ghly aggressive and transplantable precursor B-ALL.

259 hese results suggest that infections promote B-ALL through AID-independent mechanisms, providing evid

260 tivity in precursor B-cells does not promote B-ALL.

261 es establish that Pax5 hypomorphism promotes B-ALL self-renewal by impairing a differentiation progra

262 the Cdkna2a/b tumor suppressors in promoting B-ALL development.

263 adult patients (age, 1-22.5 years) with R/R B-ALL were treated with 19-28z CAR T cells.

264 of CD19-specific CAR T-cell therapy for R/R B-ALL.

265 tcome of infants with MLL-rearranged (MLL-r) B-ALL remains dismal, with overall survival <35%.

266 cal pathogenetic mechanism in MLL-rearranged B-ALL and support IGF2BP3 and its cognate RNA-binding pa

267 imetic ABT-199 in eradicating MLL-rearranged B-ALL cells.

268 o vincristine chemotherapy in MLL-rearranged B-ALL patient samples.

269 g the central role of BCL6 in MLL-rearranged B-ALL, conditional deletion and pharmacological inhibiti

270 l target for the treatment of MLL-rearranged B-ALL.

271 We studied patients with relapsed/refractory B-ALL enrolled in a phase 1/2 clinical trial evaluating

272 f GC cytotoxicity in cell lines and relapsed B-ALL patient samples.

273 lating EHMT1-2, is overexpressed in relapsed B-ALL, suggesting it as a potential contributor to relap

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

275 immune-based approaches targeting high-risk B-ALL and AML, such as the leukemia-intrinsic (e.g., tar

276 In Children's Oncology Group high-risk B-ALL study AALL0232, we investigated MRD in subjects ra

277 e-based therapeutic approaches for high-risk B-ALL treatment.

278 al-B-cell phenotype that underlies high-risk B-ALL.

279 tic leukemia (HR B-ALL) or NCI standard-risk B-ALL with defined minimal residual disease thresholds d

280 The bone marrow microenvironment may support B-ALL progression and treatment evasion.

281 The B-ALL cell line was stained against a leukemic marker (t

282 Our profiling of the B-ALL immune microenvironment identifies extrinsic regul

283 mia (AML) that was clonally related to their B-ALL, a novel mechanism of CD19-negative immune escape.

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

285 aneuploidy and discuss its contributions to B-ALL initiation and progression.

286 ment in Pax5-haploinsufficient mice prone to B-ALL upon natural infection exposure.

287 this mechanism governs native non-transplant B-ALL development is unknown.

288 rrent model suggests that infection triggers B-ALL development through induction of activation-induce

289 June 2015, 101 were classified as having VLR B-ALL.

290 daunorubicin, treatment of patients with VLR B-ALL consisted of a combination of agents with relative

291 However, whether B-ALL can initiate in B-1 progenitors is unknown.

292 ype revealed a strong association of C2 with B-ALL in German cases (P = .0004).

293 curs in a subset of adults and children with B-ALL and confers a high risk of relapse.

294 f care for CNS prophylaxis for children with B-ALL and no overt CNS involvement remains IT MTX.

295 long-term disease-free survival in mice with B-ALL, without detectable toxicity.

296 was found in 158 (2%) of 7,793 patients with B-ALL age >/= 1 year; 74 (1.5%) of 5,057 standard-risk (

297 Patients with B-ALL selected by a combination of presenting features a

298 nd of induction than did other patients with B-ALL.

299 tegy to improve the outcome of patients with B-ALL.

300 iveness of Notch inhibitors in patients with B-ALL.Significance: Inhibition of Notch signaling enhanc