ライフサイエンスコーパス: ALL

1 OH)(2)VD(3)) increased the number of BCR-ABL ALL cells only when co-cultured with bone marrow stroma.

2 osing effects on mouse survival from BCR-ABL ALL.

3 derstanding and treatment of this aggressive ALL relapse subtype.

4 ntly affecting infant and paediatric AML and ALL patients.

5 profiling of the E2A-PBX1 cistrome in pre-B ALL cells and reveals a previously unappreciated pathway

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

7 ome alterations for the development of pre-B ALL.

8 nosis is predictive of pediatric and adult B-ALL patient survival.

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

10 entify patients with precursor B-cell ALL (B-ALL) at very low risk (VLR) of relapse and treated them

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

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

13 tor of c-Myc, significantly delayed T- and B-ALL/lymphoma in mice and interfered with the oncogenic t

14 val, and demonstrate monocyte abundance at B-ALL diagnosis is predictive of pediatric and adult B-ALL

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

16 ssociated with novel subtypes of childhood B-ALL, have prognostic significance.

17 oncogenic event affiliated with childhood B-ALL, the mitotic and chromosomal defects associated with

18 cations of CNV and aneuploidy in childhood B-ALL.

19 egulated gene seen at relapse in childhood B-ALL.

20 ing single-cell approaches, we demonstrate B-ALL bone marrow immune microenvironment remodeling upon

21 sk B-cell acute lymphoblastic leukemia (HR B-ALL) or NCI standard-risk B-ALL with defined minimal res

22 ot improve 5-year DFS for children with HR B-ALL.

23 We show that human B-ALL blasts alter a vascularized microenvironment promoti

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

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

26 mechanisms in driving clonal evolution in B-ALL and identifies novel pathways associated with drug r

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

28 Oncogenic lesions in B-ALL frequently mimic signalling through cytokine recepto

29 over a role for non-classical monocytes in B-ALL survival, and demonstrate monocyte abundance at B-AL

30 hildhood cancers and current challenges in B-ALL treatment include resistance, relapse and late-onset

31 se 1,148 patient-derived B-cell leukaemia (B-ALL) samples, and find that individual mutations do not

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

33 hough B-cell acute lymphoblastic leukemia (B-ALL) is the most common malignancy in children and while

34 al in B cell acute lymphoblastic leukemia (B-ALL) patients relapsed after allogeneic hematopoietic st

35 et of B cell acute lymphoblastic leukemia (B-ALL) patients will relapse and succumb to therapy-resist

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

37 dhood B-cell acute lymphoblastic leukemia (B-ALL).

38 atric B-cell acute lymphoblastic leukemia (B-ALL).

39 ctory B-cell acute lymphoblastic leukemia (B-ALL).

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

41 ute lymphoblastic leukemia (B-ALL), making B-ALL an excellent model for studying the role of aneuploi

42 ave tremendously improved the treatment of B-ALL and other B-cell malignancies, they are not yet avai

43 ronment identifies extrinsic regulators of B-ALL survival supporting new immune-based therapeutic app

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

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

46 ne marrow mononuclear cells from pediatric B-ALL patients, cultured ex vivo, with Plk1-targeting siRN

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

48 arrow mononuclear cells from ten pediatric B-ALL patients.

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

50 ifies the most common subtype of pediatric B-ALL.

51 based therapeutic approaches for high-risk B-ALL treatment.

52 c leukemia (HR B-ALL) or NCI standard-risk B-ALL with defined minimal residual disease thresholds dur

53 e bone marrow microenvironment may support B-ALL progression and treatment evasion.

54 Our profiling of the B-ALL immune microenvironment identifies extrinsic regulat

55 neuploidy and discuss its contributions to B-ALL initiation and progression.

56 unorubicin, treatment of patients with VLR B-ALL consisted of a combination of agents with relatively

57 ne 2015, 101 were classified as having VLR B-ALL.

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

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

60 highly enriched in the high-hyperdiploid BCP ALL subtype (frequency 3.9% vs 0.5% in other BCP ALL) an

61 ize the role of FLT3 as a driver gene in BCP ALL.

62 subtype (frequency 3.9% vs 0.5% in other BCP ALL) and in cases that subsequently relapsed.

63 precursor acute lymphoblastic leukemia (BCP-ALL) eliminate the boundary of a topologically associate

64 all MRD response groups in late relapsed BCP-ALL.

65 MTXPG levels (T cell ALL [T-ALL] and B cell ALL [B-ALL] with the TCF3-PBX1 or ETV6-RUNX1 fusions), a

66 y to identify patients with precursor B-cell ALL (B-ALL) at very low risk (VLR) of relapse and treate

67 t model of alpha6 in murine BCR-ABL1+ B-cell ALL cells and showed that alpha6-deficient ALL cells und

68 Adults with r/r B-cell ALL received CTL019 in 1 of 2 trials.

69 ap in survival between T-cell ALL and B-cell ALL, although novel treatment options for T-cell ALL are

70 ALL subtypes had lower MTXPG levels (T cell ALL [T-ALL] and B cell ALL [B-ALL] with the TCF3-PBX1 or

71 ht narrow the gap in survival between T-cell ALL and B-cell ALL, although novel treatment options for

72 although novel treatment options for T-cell ALL are limited.

73 outcomes among 6,148 survivors of childhood ALL (median age, 27.9 years; range, 5.9-61.9 years) diag

74 patient-derived xenograft model of childhood ALL, TCR-KO-CAR-T cells clearly controlled CD19+ leukemi

75 and mucositis during treatment of childhood ALL.

76 bolite drug resistance in relapsed childhood ALL.

77 ors of contemporary, standard-risk childhood ALL are comparable to the general population.

78 agnosed infections were related to childhood ALL risk in an integrated health-care system in the Unit

79 ls of coT-ALL, using both cell lines and coT-ALL patient-derived primary blasts.

80 activity in vivo in xenograft models of coT-ALL, using both cell lines and coT-ALL patient-derived p

81 In the DCOG ALL-11 protocol, polyethylene glycol-conjugated Escheric

82 l ALL cells and showed that alpha6-deficient ALL cells underwent apoptosis.

83 otrexate (HDMTX) (1 g/m2) treatment, defined ALL subtypes, and assessed genomic and epigenomic varian

84 Cytotoxicity assays on primary clinical DS-ALL samples demonstrated that, regardless of mutation st

85 On primary clinical DS-ALL samples, we show that wtRAS-activation is an obligat

86 wn syndrome acute lymphoblastic leukemia (DS-ALL) is characterized by high frequency of CRLF2-rearran

87 unified treatment target for up to 80% of DS-ALL.

88 treatment was more effective in eradicating ALL than treatment with a TKI (nilotinib) alone.

89 ildren undergoing induction chemotherapy for ALL, autologous HSCT and allogeneic HSCT.

90 ay provide alternative treatment options for ALL in general and may suppress incurable drug-resistant

91 ort alpha6 as a novel therapeutic target for ALL.

92 a cell line as a potential novel therapy for ALL patients.

93 Children treated for ALL had lower antibody levels than controls against pneu

94 g previously vaccinated children treated for ALL.

95 HyperD-ALL cells show chromatid cohesion defects and an impaire

96 defects associated with HyperD B-ALL (HyperD-ALL) remain poorly characterized.

97 that condensin complex is impaired in HyperD-ALL cells, leading to chromosome hypocondensation, loss

98 o be early pathogenic contributors in HyperD-ALL.

99 We report that HyperD-ALL blasts are low proliferative and show a delay in ear

100 cellular MTXPG levels across all subtypes if ALL.CONCLUSIONSThese findings provide insights into mech

101 In ALL patients both AURKA and AURKB showed a significant o

102 In ALL patients receiving L-ASP therapy, the use of fibrino

103 en implicated in minimal residual disease in ALL and in the migration of ALL cells to the central ner

104 ian-diagnosed early-life infections increase ALL risk, thereby raising the possibility that stronger

105 Exclusion criteria included: infant ALL, relapsed ALL, and stem cell transplant recipients.

106 of pediatric Acute Lymphoblastic Leukaemia (ALL) patients and the efficacy of two AURKA and AURKB de

107 Children with acute lymphoblastic leukemia (ALL) are at increased risk of developing invasive pneumo

108 g treatment of acute lymphoblastic leukemia (ALL) are at risk for thrombosis, caused in part by the u

109 e formation in acute lymphoblastic leukemia (ALL) by conferring purine analog resistance.

110 0 infants with acute lymphoblastic leukemia (ALL) by providing excellent supportive care while receiv

111 positive (Ph+) acute lymphoblastic leukemia (ALL) cell growth, whereas expression of the closely rela

112 TXPG levels in acute lymphoblastic leukemia (ALL) cells from 388 newly diagnosed patients after in vi

113 for childhood acute lymphoblastic leukemia (ALL) has exceeded 80% with contemporary therapy, relapse

114 Relapsed acute lymphoblastic leukemia (ALL) has remained challenging to treat in children, with

115 (Ph)-positive acute lymphoblastic leukemia (ALL) have improved with the use of tyrosine kinase inhib

116 Ph(+) acute lymphoblastic leukemia (ALL) is characterized by the expression of an oncogenic

117 patients with acute lymphoblastic leukemia (ALL) is efficacious, but long-term side effects are conc

118 omes in infant acute lymphoblastic leukemia (ALL) necessitate new treatments.

119 y (r/r) B-cell acute lymphoblastic leukemia (ALL) patients.

120 ower childhood acute lymphoblastic leukemia (ALL) risk.

121 l of childhood acute lymphoblastic leukemia (ALL) to 90%, but its impact on long-term toxicity remain

122 s in pediatric acute lymphoblastic leukemia (ALL) to decrease infections with gram-negative bacteria.

123 children with acute lymphoblastic leukemia (ALL) treated in poor-resource settings.

124 t component of acute lymphoblastic leukemia (ALL) treatment, but is often discontinued because of tox

125 recursor (BCP) acute lymphoblastic leukemia (ALL) using 5 different patient cohorts (in total includi

126 gh-risk B-cell acute lymphoblastic leukemia (ALL) would also improve outcomes for those with standard

127 sed/refractory acute lymphoblastic leukemia (ALL)(1-5), but toxicity, including cytokine-release synd

128 patients with acute lymphoblastic leukemia (ALL), but risk differences across age groups both in rel

129 % of childhood acute lymphoblastic leukemia (ALL), the t(1,19) chromosomal translocation specifically

130 sively used in acute lymphoblastic leukemia (ALL), which is a very rare cancer in adults.

131 e prognosis of acute lymphoblastic leukemia (ALL).

132 in B-precursor acute lymphoblastic leukemia (ALL).

133 patients with acute lymphoblastic leukemia (ALL).

134 phoma (BL) and Acute Lymphoblastic Leukemia (ALL).

135 olescents with acute lymphoblastic leukemia (ALL).

136 y (r/r) B-cell acute lymphoblastic leukemia (ALL).

137 children with acute lymphoblastic leukemia (ALL).

138 c strategy for acute lymphoblastic leukemia (ALL).

139 a and relapsed acute lymphoblastic leukemia (ALL).

140 B-cell acute lymphoblastic leukemia (ALL; B-ALL) is the most common pediatric cancer, and hig

141 itized mice induced acute lymphoid leukemia (ALL) of B-1 progenitor phenotype, which has been recentl

142 Interestingly, we observed that Ph-like ALL cells have activated SRC, ERK, and PI3K signaling co

143 aling plasticity of CRLF2-rearranged Ph-like ALL following selective TKI pressure, which occurs in th

144 Ph-like ALL is driven by genetic alterations that activate const

145 ctor 2-rearranged (CRLF2-rearranged) Ph-like ALL subset.

146 peutic strategy for CRLF2-rearranged Ph-like ALL.

147 t squares-discriminant analysis of the MS/MS(ALL) lipidomic dataset, identified lipids driving the cl

148 ysis revealed that alpha6 deletion in murine ALL was associated with changes in Src signaling, includ

149 ressive malignancy that accounts for ~20% of ALL cases.

150 Cases of ALL (n = 435) diagnosed between 1994-2014 among children

151 idual disease in ALL and in the migration of ALL cells to the central nervous system.

152 only ~50% of children with first relapse of ALL survive long term, and outcomes are much worse with

153 stic regression was used to estimate risk of ALL associated with history of infections during first y

154 nce or are associated with novel subtypes of ALL, were identified.

155 n-mediated drug resistance, which depends on ALL cell adhesion to the stroma through adhesion molecul

156 tically predisposed carriers will develop pB-ALL.

157 Here, by using murine models of pB-ALL, we show that microbiome disturbances incurred by an

158 , we found that genetic predisposition to pB-ALL (Pax5 heterozygosity or ETV6-RUNX1 fusion) shaped a

159 e modification in children predisposed to pB-ALL could become a successful prevention strategy.

160 sor B-cell acute lymphoblastic leukemias (pB-ALLs) caused by a combination of prenatal genetic predis

161 of ciprofloxacin prophylaxis in a pediatric ALL population.

162 aberration as prognostic factor in pediatric ALL and summarize emerging concepts in this field.

163 pression are important findings in pediatric ALL, and designed inhibitor, GW806742X tested in vitro w

164 change throughout the treatment of pediatric ALL.

165 lantation models using patient-derived Ph(+) ALL cells.

166 orm with anti-IL7R antibody eliminates Ph(+) ALL cells including those with resistance to commonly us

167 uced transformation and development of Ph(+) ALL.

168 rential degradation of CDK6 over CDK4 in Ph+ ALL cells, and markedly suppress S-phase cells concomita

169 CDK6 are, in part, kinase-independent in Ph+ ALL.

170 tegy to exploit the "CDK6 dependence" of Ph+ ALL and, perhaps, of other hematologic malignancies.

171 Moreover, they suggest that treatment of Ph+ ALL with CDK6-selective PROTACs would spare a high propo

172 osine kinase inhibitor-resistant primary Ph+ ALL cells, and this effect was comparable or superior to

173 4/6 inhibitor palbociclib in suppressing Ph+ ALL in mice, suggesting that the growth-promoting effect

174 patients with newly diagnosed Philadelphia- ALL were included.

175 y in adults with newly diagnosed Ph-positive ALL (with no upper age limit).

176 grade 3 or higher in adults with Ph-positive ALL.

177 lyzed NT5C2 in 455 relapsed B-cell precursor ALL patients treated within the ALL-REZ BFM 2002 relapse

178 ations in 75 (16.5%) of 455 B-cell precursor ALL relapses.

179 a (T-ALL), designated early T-cell precursor ALL, which is characterized by the aberrant self-renewal

180 risk subtypes such as early T-cell precursor ALL.

181 ocking Ab P5G10 induces apoptosis in primary ALL cells in vitro and sensitizes primary ALL cells to c

182 ry ALL cells in vitro and sensitizes primary ALL cells to chemotherapy or tyrosine kinase inhibition

183 e demonstrate elevated PRMT1 levels in MLL-r ALL cells and show that inhibition of PRMT1 significantl

184 72/973), and its oncogenic function in MLL-r ALL cells is FLT3 methylation dependent.

185 S Food and Drug Administration (FDA) for r/r ALL (CD19CAR T-cell approval is restricted to patients <

186 Thirty-five adults with r/r ALL received CTL019 in 1 of 3 dosing cohorts.

187 We report outcomes for adults with r/r ALL treated with an optimized CTL019 dosing and CRS mana

188 scuss real-life scenarios of adults with r/r ALL, in which we selected either blinatumomab or CD19CAR

189 as extended options for the treatment of r/r ALL, prioritizing the sequence of these agents on an ind

190 out compromising efficacy in adults with r/r ALL.

191 sion criteria included: infant ALL, relapsed ALL, and stem cell transplant recipients.

192 nical effects of NT5C2 mutations in relapsed ALL, we analyzed NT5C2 in 455 relapsed B-cell precursor

193 eded 80% with contemporary therapy, relapsed ALL remains a leading cause of cancer-related death in c

194 effective therapy for children with relapsed ALL, and we present several cases highlighting contempor

195 eatment landscape for children with relapsed ALL.

196 de for patients > 4 years old with high-risk ALL undergoing allogeneic HSCT.

197 strategy for precision therapy in high-risk ALL.

198 mong contemporary survivors of standard-risk ALL, represented by 90sSR.

199 nd specific effects of IGF2BP1 on ETV6-RUNX1 ALL evidenced by both germline and somatic genomic analy

200 6-year OS rate for > 5,000 children with SR ALL enrolled in AALL0331 exceeded 95%.

201 excellent for this group of patients with SR ALL, with particularly good outcomes for those with SR-h

202 e outcomes for those with standard-risk (SR) ALL.

203 e was first implicated as an oncogene in a T-ALL mouse model expressing myristoylated (Myr) Akt2.

204 lesions in many other genes to cause acute T-ALL.

205 btypes had lower MTXPG levels (T cell ALL [T-ALL] and B cell ALL [B-ALL] with the TCF3-PBX1 or ETV6-R

206 occur within 3 years of diagnosis and any T-ALL relapses are particularly difficult to salvage.

207 s for current treatment protocols for both T-ALL and T-lymphoblastic lymphoma.

208 M1 and suggests that IL7-responsive CD127+ T-ALL and T-LBL patients could benefit from PIM inhibition

209 leukemia survival in a PDX model of CD127+ T-ALL.

210 In addition, using different CD127+ T-ALL/T-LBL xenograft models, we also reveal that residual

211 Moloney-murine leukemia 1 (PIM1) in CD127+ T-ALL/T-LBL, thereby rendering these tumor cells sensitive

212 operties in xenograft (PDX) models of CD3+ T-ALL, resulting in prolonged host survival.

213 frontline Children's Oncology Group (COG) T-ALL clinical trial AALL1231, we demonstrated that one-th

214 dren and young adults with newly diagnosed T-ALL without increased toxicity.

215 expression of Dlx5 was sufficient to drive T-ALL in mice by directly activating Akt and Notch signali

216 However, in TAL1-expressing T-ALL cells, the leukemia-prone TAL1 promoter-IV specifica

217 myeloid cells provide signals critical for T-ALL growth in multiple organs in vivo and implicate tumo

218 lignancies, they are not yet available for T-ALL.

219 and less-toxic therapeutic strategies for T-ALL/T-LBL patients has largely focused on the identifica

220 Similarly, human T-ALL cell lines with activated NOTCH and AKT and elevated

221 esterol synthesis pathway in primary human T-ALL specimens.

222 key role for Ldb1, a nonproto-oncogene, in T-ALL and support a model in which Lmo2-induced T-ALL resu

223 In T-ALL cell lines overexpression of RASGRP1 increases flux

224 1 (LEF1) and potentiates Wnt signaling in T-ALL cells with low levels of Notch.

225 on is disrupted by the -31CBS inversion in T-ALL cells.

226 Our findings uncover a role for NRARP in T-ALL pathogenesis and indicate that Notch inhibition may

227 s indicate that NRARP plays a dual role in T-ALL pathogenesis, regulating both Notch and Wnt pathways

228 tor RASGRP1 is frequently overexpressed in T-ALL patients.

229 dependent of FcgammaR-mediated pathways in T-ALL PDXs.

230 Although NOTCH is a known driver in T-ALL, its clinical inhibition has significant limitations

231 a strong negative prognostic indicator in T-ALL, the mechanisms of GC resistance remain poorly under

232 oter IV interaction for TAL1 activation in T-ALL.

233 nteractions and TAD boundary insulation in T-ALL.

234 ignaling, could have a suppressive role in T-ALL.

235 t CTCF boundary plays a pathogenic role in T-ALL.

236 e transcriptional upregulation of IL7RA in T-ALL/T-LBL patient-derived xenograft (PDX) cells, ultimat

237 ed the importance of Ldb1 for Lmo2-induced T-ALL by conditional deletion of Ldb1 in thymocytes in an

238 and support a model in which Lmo2-induced T-ALL results from failure to downregulate Ldb1/Lmo2-nucle

239 vel agents, the development of intensified T-ALL-focused protocols has resulted in significant improv

240 g in T-cell acute lymphoblastic leukaemia (T-ALL), and the involvement of BCL6 in other types of leuk

241 on in T-cell acute lymphoblastic leukemia (T-ALL) and RPS15 mutations in chronic lymphocytic leukemia

242 T-cell acute lymphoblastic leukemia (T-ALL) and T-cell acute lymphoblastic lymphoma (T-LBL) are

243 ctory T-cell acute lymphoblastic leukemia (T-ALL) but has not been fully evaluated in those with newl

244 re in T cell acute lymphoblastic leukemia (T-ALL) by using primary human leukemia specimens and exami

245 owth, T-cell acute lymphoblastic leukemia (T-ALL) cells require exogenous cells or signals to survive

246 ce in T cell acute lymphoblastic leukemia (T-ALL) cells, and that this could be effectively reversed

247 urkat T-cell acute lymphoblastic leukemia (T-ALL) cells.

248 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy resulting

249 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with a di

250 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy that accounts for ~20%

251 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy that has historically b

252 ed in T-cell acute lymphoblastic leukemia (T-ALL) patients.

253 roliferative disorder and T cell leukemia (T-ALL) when induced in the bone marrow via Mx1CRE.

254 with T cell acute lymphoblastic leukemia (T-ALL), and although resistance to GCs is a strong negativ

255 rm of T-cell acute lymphoblastic leukemia (T-ALL), designated early T-cell precursor ALL, which is ch

256 le in T cell acute lymphoblastic leukemia (T-ALL), yet the mechanisms underlying its deregulation rem

257 s a critical component of myeloid-mediated T-ALL growth and survival.

258 urvival and proliferation of primary mouse T-ALL cells in vitro.

259 AL1 expression in erythroid cells, but not T-ALL cells.

260 tiple organs in 2 distinct mouse models of T-ALL and prolongs survival.

261 f the TAL1 is associated with up to 60% of T-ALL cases and is involved in CTCF-mediated genome organi

262 signaling and delays the proliferation of T-ALL cells that display high levels of Notch1 signaling,

263 h1 signaling, it promotes the expansion of T-ALL cells with lower levels of Notch1 activity.

264 e capacity to directly support survival of T-ALL cells.

265 d have therapeutic efficacy in a subset of T-ALL patients.

266 study is important to our understanding of T-ALL.

267 ew therapeutic option for the treatment of T-ALL.

268 cytes in an Lmo2 transgenic mouse model of T-ALL.

269 ously, which is required for prevention of T-ALL.

270 rences found influenced the development of T-ALL.

271 The impact of the myeloid compartment on T-ALL growth is not dependent on suppression of antitumor

272 nsition of preleukemic thymocytes to overt T-ALL.

273 rectly support survival of primary patient T-ALL cells in vitro.

274 ed RASGRP1 expression surveys in pediatric T-ALL and generated a RoLoRiG mouse model crossed to Mx1CR

275 elate with inferior outcomes for pediatric T-ALL patients.

276 els are significantly increased in primary T-ALL cells suggesting that NRARP is not sufficient to blo

277 ells provide signals that directly support T-ALL cells.

278 mor-associated myeloid cells would support T-ALL in vivo.

279 tected at the promoters of key upregulated T-ALL driver genes (Hhex, Lyl1, and Nfe2) in preleukemic L

280 ree survival (DFS) rates for patients with T-ALL randomly assigned to nelarabine (n = 323) and no nel

281 ained during leukemogenesis in a subset of T-ALLs and is reversible with targeted inhibition of the I

282 we demonstrated that one-third of primary T-ALLs were resistant to GCs when cells were cultured in t

283 We demonstrated that in these T-ALLs and in distinct populations of normal developing th

284 A multivariable model including the ALL subtype (P = 1.1 x 10-14), the SLC19A1/(ABCC1 + ABCC

285 ll precursor ALL patients treated within the ALL-REZ BFM 2002 relapse trial using sequencing and sens

286 Three ALL subtypes had lower MTXPG levels (T cell ALL [T-ALL]

287 with ALL-10 (37% v 47%), which is similar to ALL-11 but with higher asparaginase levels during intens

288 roduction of collagens, potentially trapping ALL blasts.

289 , we describe real-life cases of adults with ALL who were treated with pediatric-inspired regimens th

290 g first year of life was not associated with ALL risk (odds ratio (OR) = 0.85, 95% confidence interva

291 his was a multicenter trial of children with ALL enrolled 4-12 months postchemotherapy completion.

292 ve immunity can be achieved in children with ALL is on completion of chemotherapy.

293 gene expression analyses from children with ALL showed that patients with higher expression of eithe

294 Children with ALL were allocated to study groups and received a single

295 Children with ALL were allocated to study groups and received a single

296 Children with ALL would benefit from systematic revaccination postchem

297 curred less in intensification compared with ALL-10 (37% v 47%), which is similar to ALL-11 but with

298 Of 454 patients with ALL treated at the Instituto de Medicina Integral Profes

299 samples from 129 children (0-18 years) with ALL were collected in a multicenter prospective study.

300 ruited by low MUAC, with or without low WLZ (ALL-MUAC).