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 In fact, all 22 B-ALLs with mutant JAK2 that we analyzed overexpress CRL

4 apamycin controlled leukemia burden in all 8 B-ALL samples.

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

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

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

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

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

10 risk refractory/relapsed HER2-positive adult B-ALL population.

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

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

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

14 24/358 (6.7%) relapsed childhood B cell ALL (B-ALL) cases.

15 receptor tyrosine kinase in pre-B-cell ALL (B-ALL) cell lines and pediatric patient samples.

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

17 induction of Notch signaling in B-cell ALL (B-ALL) leads to growth arrest and apoptosis.

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

19 in 2143 children with precursor B-cell ALL (B-ALL).

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

21 type of pediatric high-risk B-precursor ALL (B-ALL) which exhibits a gene expression profile similar

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

23 lymphoblastic leukemia/lymphoma (T-ALL) and B-ALL are evolved.

24 progenitors also results in AML, T-ALL, and B-ALL, respectively.

25 on of PTEN delays the development of CML and B-ALL and prolongs survival of leukemia mice.

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

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

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

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

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

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

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

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

34 tself is required to eradicate Ph(+)/Bmi1(+) B-ALL-initiating cells and confirm their addiction to BC

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

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

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

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

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

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

41 ase activities by dasatinib affords complete B-ALL remission.

42 However, curing B-ALL and CML mice requires killing leukemic stem cells

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

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

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

46 o unrelated kindreds with autosomal dominant B-ALL.

47 attenuation of BCR-ABL reversed Bmi1-driven B-ALL development, which was accompanied by induction of

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

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

50 PB and CB CAR(+) CTLs completely eliminated B-ALL blasts over 5 days of coculture.

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

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

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

54 IL-7R-expressing B-ALL cells grew in culture in response to IL-7 and coul

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

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

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

58 tor subunit CRLF2 in a functional screen for B-ALL-derived mRNA transcripts that can substitute for I

59 tion is a promising therapeutic strategy for B-ALL as well as other conditions dependent on IL7R sign

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

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

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

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

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

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

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

67 ia to the nucleus, resulting in apoptosis in B-ALL but not T-cell ALL.

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

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

70 activation, and results in PARP1 cleavage in B-ALL.

71 gs implicate CRLF2 as an important factor in B-ALL with diagnostic, prognostic, and therapeutic impli

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

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

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

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

76 Inhibition of Mer in B-ALL cell lines decreased activation of AKT and MAPKs a

77 TEL, and BCR/ABL rearrangements, but not in B-ALL with these rearrangements or other lymphoid malign

78 observed in MPNs) or JAK2 R683G (observed in B-ALL).

79 The novel interaction of HES1 and PARP1 in B-ALL modulates the function of the HES1 transcriptional

80 reproduce this tumor suppressor phenotype in B-ALL; however, the mechanism is not yet known.

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

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

83 he key scaffold for mutant JAK2 signaling in B-ALL.

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

85 ify Mer as a potential therapeutic target in B-ALL and suggest that inhibitors of Mer may potentiate

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

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

88 oid progenitors in vitro and BCR/ABL-induced B-ALL in vivo.

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

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

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

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

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

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

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

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

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

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

99 t Ph(+) B cell acute lymphoblastic leukemia (B-ALL) and CML blast crisis.

100 ML) and B-cell acute lymphoblastic leukemia (B-ALL) and is induced by the BCR-ABL oncogene.

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

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

103 tive (Ph(+)) B-acute lymphoblastic leukemia (B-ALL) can initiate in committed B-cell progenitors.

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

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

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

107 /ABL-induced acute B-lymphoblastic leukemia (B-ALL) in mice, whereas forced expression of IRF-4 poten

108 B cell acute lymphoblastic leukemia (B-ALL) is frequently associated with mutations or chromo

109 B-precursor acute lymphoblastic leukemia (B-ALL) is the most common childhood tumor and the leadin

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

111 ts with B-cell acute lymphoblastic leukemia (B-ALL) receiving allogeneic hematopoietic stem cell (HSC

112 ecursor B-cell acute lymphoblastic leukemia (B-ALL) remains poor, in part from a lack of therapeutic

113 k B-progenitor acute lymphoblastic leukemia (B-ALL) with alteration of IKZF1, a gene expression profi

114 (MPNs), B cell acute lymphoblastic leukemia (B-ALL) with rearrangements of the cytokine receptor subu

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

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

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

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

119 f B-progenitor acute lymphoblastic leukemia (B-ALL), including Down syndrome (DS-ALL) patients, lacki

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

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

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

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

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

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

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

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

128 th B precursor acute lymphoblastic leukemia (B-ALL).

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

130 ins, in B-cell acute lymphoblastic leukemia (B-ALL).

131 in Ph+ B-cell acute lymphoblastic leukemia (B-ALL).

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

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

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

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

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

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

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

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

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

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

142 ting cells to result in B-lymphoid leukemia (B-ALL) in vivo.

143 10% of B-cell acute lymphoblastic leukemias (B-ALLs) overexpress the cytokine receptor subunit CRLF2,

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

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

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

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

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

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

150 gesting that BCR-ABL is required to maintain B-ALL and that BCR-ABL and Bmi1 cooperate toward blast t

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

152 lineage acute lymphoblastic leukemia (MRD(+) B-ALL).

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

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

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

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

157 NCT00466531 (CLL protocol) and #NCT01044069 (B-ALL protocol).

158 of CRLF2, which is overexpressed in ~ 10% of B-ALL.

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

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

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

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

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

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

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

166 The majority of B-ALL cases are aneuploid or harbor recurring structural

167 inhibitor ibrutinib in preclinical models of B-ALL.

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

169 suppression pathways in the pathogenesis of B-ALL.

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

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

172 1/2 activation, increased the sensitivity of B-ALL cells to cytotoxic agents in vitro by promoting ap

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

174 .29 x 10(-10)), especially in the subtype of B-ALL (OR = 1.39, P = 2.47 x 10(-9)).

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

176 w that JQ1 potently reduces the viability of B-ALL cell lines with high-risk cytogenetics.

177 r receptor 2 (ErbB2) is expressed in ~30% of B-ALLs, and numerous small molecule inhibitors are avail

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

179 n receptor (CAR) targeting CD19 expressed on B-ALL.

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

181 tested efficacy against CRLF2-overexpressing B-ALL.

182 CRLF2 overexpressing B-ALLs share a transcriptional signature that significan

183 Subsets of CRLF2-overexpressing B-ALLs also have a gain-of-function CRLF2 F232C mutation

184 rapamycin in xenograft models of 8 pediatric B-ALL cases with and without CRLF2 and JAK genomic lesio

185 as primary inclusion criterion for pediatric B-ALL patients in future clinical trials of ROR1-targete

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

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

188 ssociated with inferior outcome in pediatric B-ALL, particularly SR patients who require more intensi

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

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

191 imately 15% of adult and high-risk pediatric B-ALL that lack MLL, TCF3, TEL, and BCR/ABL rearrangemen

192 xpression was found in many of the pediatric B-ALL patients with multiply relapsed and refractory dis

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

194 that the molecular events that control Ph(+) B-ALL initiation and tumor suppression in the B-cell lin

195 g the pro-B cell, efficiently initiate Ph(+) B-ALL.

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

197 To clarify the role of Bcl-xL in Ph+ B-ALL, we generated 2 mouse models.

198 In the first model, Ph+ B-ALL and loss of Bcl-xL expression are coinduced; in th

199 ients with relapsed/refractory HER2-positive B-ALL.

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

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

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

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

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

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

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

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

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

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

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

211 ry lymphoblasts from pediatric T-ALL and pre-B ALL patients.

212 howing universal expression of BAFF-R by pre-B ALL cells and opens the possibility of blocking its fu

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

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

215 nt of mice injected with patient-derived pre-B ALL xenograft cells abrogated leukemia in 3 of 5 mice

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

217 s leukemia-initiating cells derived from pre-B ALL xenografts in vitro and in vivo, and hence constit

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

219 L-AML1 transgenic zebrafish models human pre-B ALL, identifies the molecular pathways associated with

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

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

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

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

224 rcomes MTI-mediated growth inhibition in pre-B ALL.

225 sor B-cell acute lymphoblastic leukemia (pre-B ALL) in NSG mice.

226 precursor acute lymphoblastic leukemia (pre-B ALL) is the most common pediatric cancer.

227 recursor B acute lymphoblastic leukemia (pre-B ALL), inhibiting cell proliferation and inducing apopt

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

229 ated the tumor cohort according to major pre-B ALL subtypes, and methylation in CGIs, CGI shores, and

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

231 ow that TSLP stimulates proliferation of pre-B ALL cell lines.

232 a show that TSLP can promote survival of pre-B ALL cells and antagonize the effects of MTIs.

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

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

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

236 We examined the effect of TSLP on pre-B ALL cells and their response to MTIs.

237 They had a common or pre-B ALL immunophenotype, were significantly older (median

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

239 Adhesion of primary pre-B ALL cells was alpha4-dependent; alpha4 blockade sensit

240 ylation profiling enabled us to separate pre-B ALL according to major subtypes, to map epigenetic bio

241 by CpG ODN in a transplantable syngeneic pre-B ALL model.

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

243 ngle CpG-site resolution analysis of the pre-B ALL methylome beyond CpG-islands (CGI).

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

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

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

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

248 al samples of 46 childhood patients with pre-B ALL, extending single CpG-site resolution analysis of

249 AML1 (ETV6-RUNX1) fusion in precursor-B (pre-B) ALL is the most common genetic rearrangement in child

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

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

252 o cultured ALL cell lines including 697 (pre-B-ALL) and CEM-C7 (T-ALL) cells.

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 pre-B cell acute lymphoblastic leukemia (pre-B-ALL) are caused by the Philadelphia (Ph) chromosome-en

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

257 in at suppressing proliferation of mouse pre-B-ALL and human CD19+CD34+)Ph+ ALL leukemia cells treate

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

259 Using a murine model of Ph+ pre-B-ALL, we found that deletion of both Pik3r1 and Pik3r2,

260 tant T-ALL cell line, CEM-C1, and in the pre-B-ALL 697 cell line.

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

262 ghly aggressive and transplantable precursor B-ALL.

263 ells [SFCs]/10(5) T cells) and lysed primary B-ALL blasts in (51)Cr-release assays (mean, 66% +/- 5%

264 MLL-AF4+ pro-B-ALL expresses enormous levels of FLT3, occasionally be

265 candidate cooperating event in MLL-AF4+ pro-B-ALL.

266 fant acute pro-B-lymphoblastic leukemia (pro-B-ALL).

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

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

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

270 e only cytokine receptor in CRLF2-rearranged B-ALL cells significantly down-regulated by JQ1 treatmen

271 00-fold more potent against CRLF2-rearranged B-ALL cells, which correlated with JAK2 degradation and

272 ografted with primary human CRLF2-rearranged B-ALL further than an enzymatic JAK2 inhibitor.

273 ografted with primary human CRLF2-rearranged B-ALL, JQ1 suppressed c-Myc expression and STAT5 phospho

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

275 mary leukemias, including therapy-refractory B-ALL and chronic myelogenous leukemia samples, and inhi

276 Survival analysis of 2 representative B-ALL xenografts demonstrated prolonged survival with ra

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

278 on correlates with poor outcome in high-risk B-ALL patients.

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

280 ruxolitinib and rapamycin in this high-risk B-ALL subtype, for which novel treatments are urgently n

281 prove beneficial for patients with high-risk B-ALL who have recently received an HSC or CB transplant

282 rovide a new prognostic marker for high-risk B-ALL, and inhibition of CRLF2/JAK2 signaling may repres

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

284 cantly worse for patients with iAMP21 and SR B-ALL, but iAMP21 was not a statistically significant pr

285 Moreover, PTEN suppresses B-ALL development through regulating its downstream gene

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

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

288 f ALL with poor clinical outcome compared to B-ALL.

289 AK2 and CRLF2 may cooperate to contribute to B-ALL formation.

290 ag-2 can reproduce these events and leads to B-ALL apoptosis.

291 nd Spi-B, in B cells (DeltaPB mice) leads to B-ALL in mice at 100% incidence rate and with a median s

292 f PAX5 are associated with susceptibility to B-ALL, implicating PAX5 in a growing list of hematopoiet

293 of pediatric ALL patients, all of which were B-ALL, and was not limited to any particular genotype.

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

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

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

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

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

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

300 herapy-associated toxicity for patients with B-ALL.