ライフサイエンスコーパス: T-ALL

1 T-ALL cell lines treated with perphenazine exhibited rap

2 T-ALL is an heterogeneous disease, which presents intrin

3 T-ALL NOTCH1 mutations result in ligand-independent and

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

5 ximately 6%, assessed within a cohort of 196 T-ALL patients (64 adults and 132 children).

6 Eleven (6%) of 196 T-ALL patients enrolled in the French Group for Research

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

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

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

10 A total of 111 patients with T-ALL/LBL (68% T-ALL; 32% T-LBL) with adequate immunophenotype data wer

11 Our data identify a T-ALL niche and suggest targeting CXCL12/CXCR4 signaling

12 suppression of normal hematopoiesis using a T-ALL mouse model and human T-ALL xenografts.

13 lonal T-ALL cells was sufficient to abrogate T-ALL progression in leukemic mice, whereas late-stage m

14 oid leukemia with normal karyotype and acute T-ALL samples.

15 notype of immunophenotypically defined adult T-ALL is similar to the pediatric equivalent, with high

16 t the small molecule inhibitor GSKJ4 affects T-ALL growth, by targeting JMJD3 activity.

17 g-like small molecules with activity against T-ALL.

18 le-agent PR-104 was more efficacious against T-ALL xenografts compared with a combination regimen of

19 enotypically defined subgroup of T-cell ALL (T-ALL) associated with high rates of intrinsic treatment

20 ntly greater efficacy against T-lineage ALL (T-ALL) than B-cell-precursor ALL (BCP-ALL) xenografts.

21 4 and TCF3-HLF ALL, and in some T-cell ALLs (T-ALLs), predicting in vivo activity as a single agent a

22 Yet, although T-ALL infiltration and progression are independent of th

23 cell acute lymphoblastic leukemia (B-ALL and T-ALL, respectively), but not acute myeloid leukemia (AM

24 Cell models of AML, CML, and T-ALL were potently affected by KDM1A inhibition, and ce

25 on of T-ALL cells isolated from patients and T-ALL cells in a murine leukemia model; however, IRAK1/4

26 compared with thymic and peripheral T cells, T-ALL cells from patients have elevated levels of IRAK1

27 d not previously been described in childhood T-ALL (for example, CCND3, CTCF, MYB, SMARCA4, ZFP36L2 a

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

29 BRD4 binds enhancers near critical T-ALL genes, including MYC and BCL2.

30 ted ALL, PTPN2 mutations in TLX1 deregulated T-ALL, and PIK3R1/PTEN mutations in TAL1 deregulated ALL

31 ras(G12D) mice transduced with Myc developed T-ALLs that were GSI-insensitive and lacked Notch1 mutat

32 Patients with newly diagnosed T-ALL/LBL who received frontline chemotherapy between th

33 e capacity to cooperate with Notch1 to drive T-ALL.

34 cessed miRNAs are essential for Notch-driven T-ALL is currently unknown.

35 development and maintenance of Notch-driven T-ALL was dependent on Dicer1 function.

36 T-cell lineage did not develop Notch-driven T-ALL.

37 tumor-associated DCs supply signals driving T-ALL growth, and implicate tumor-associated DCs and the

38 ed lncRNA, LUNAR1, is required for efficient T-ALL growth in vitro and in vivo due to its ability to

39 athway in ETP-ALL blasts relative to non-ETP T-ALL.

40 y and poor prognosis associated with the ETP T-ALL group, there is an urgent need of new tailored the

41 ed that UTX escapes X-inactivation in female T-ALL lymphoblasts and normal T cells.

42 P4L might represent a promising approach for T-ALL treatment.

43 aling as a powerful therapeutic approach for T-ALL.

44 umor growth, suggesting a vascular niche for T-ALL.

45 Improving therapies for T-ALL requires the development of strategies to target p

46 develop personalized epigenetic therapy for T-ALL patients.

47 xploited as an additional target therapy for T-ALL.

48 epigenetic' drugs are not currently used for T-ALL treatment.

49 KRAS(G12D) T-ALLs do not show constitutive GTP loading of Ras.

50 cts of anti-NOTCH1 therapy in mice harboring T-ALL.

51 C-overexpressing thymocytes and used a human T-ALL cell line to screen for small molecules that syner

52 o induce apoptosis in fish, mouse, and human T-ALL cells.

53 both in NOTCH-induced mouse T-ALL and human T-ALL xenograft models.

54 opoiesis using a T-ALL mouse model and human T-ALL xenografts.

55 ed miRNA deregulated in both mouse and human T-ALL.

56 hat Ras-induced mouse T-ALL as well as human T-ALL carrying mutations in the RAS/MAPK pathway display

57 nt in vivo, supported by evidence from human T-ALL samples, highlights that future therapeutic interv

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

59 wth in vivo and that RUNX silencing in human T-ALL cells triggers apoptosis.

60 e it is induced by the TAL1 complex in human T-ALL cells.

61 1, one of the most common mutations in human T-ALL, suggesting Idh1 mutations may have the capacity t

62 sly transcribed X (UTX) chromosome, in human T-ALL.

63 T-199 as a new therapeutic strategy in human T-ALL.

64 translocations previously described in human T-ALL.

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

66 in silico gene expression analysis of human T-ALL samples we observed a significant correlation betw

67 lecular target in specific subtypes of human T-ALL that could be exploited by ABT-199.

68 reatment of this aggressive subtype of human T-ALL using our Zeb2-driven mouse model.

69 ifferent molecular genetic subtypes of human T-ALL.

70 ssion, and CXCR4 antagonism suppressed human T-ALL in primary xenografts.

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

72 rimary tumors extend recent work using human T-ALL cell lines and xenografts and suggest that the Not

73 f ZEB2 and demonstrated that mouse and human T-ALLs with increased ZEB2 levels critically depend on K

74 Finally, human T-ALLs treated with perphenazine exhibited suppressed ce

75 may be an effective therapy for relapsed/IF T-ALL patients.

76 transcriptional program related to immature T-ALL, exhibited high in vitro and in vivo sensitivity f

77 FLT3 mutations were associated with immature T-ALL, JAK3/STAT5B mutations in HOXA1 deregulated ALL, P

78 In T-ALL cell lines, pharmacological inhibition or short in

79 uggest that pharmacologic PP2A activation in T-ALL and other cancers driven by hyperphosphorylated PP

80 al trials incorporating CXCR4 antagonists in T-ALL treatment.

81 iciency led to the induction of apoptosis in T-ALL cells, whereas cell cycle progression remained una

82 of the newly identified Notch3-Pin1 axis in T-ALL aggressiveness and progression.

83 activity at low micro molar concentration in T-ALL cell lines.

84 We demonstrate that ORP4L is expressed in T-ALL but not normal T-cells and its abundance is propor

85 ly, most endogenous super-enhancers found in T-ALL cells are occupied by MYB and CBP, which suggests

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

87 ession of AKR1C3 was significantly higher in T-ALL xenografts compared with BCP-ALL, and correlated w

88 and is frequently genetically inactivated in T-ALL.

89 ugs that synergize with NOTCH1 inhibition in T-ALL.

90 he selective pressure for Notch mutations in T-ALL and response and resistance of T-ALL to Notch path

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

92 t other pathways can substitute for Notch in T-ALL.

93 result, the oncogenic activity of NOTCH1 in T-ALL is strictly dependent on MYC upregulation, which m

94 ration of the bone marrow commonly occurs in T-ALL and relapsed B-cell acute lymphoblastic leukemia p

95 xpression, SCL contributes to oncogenesis in T-ALL.

96 proliferation rate via distinct pathways in T-ALL.

97 PLCbeta3 catalyzes IP3 production in T-ALL as opposed to PLCgamma1 in normal T-cells.

98 rapeutically targeting T-cell progenitors in T-ALL while also underscoring the need to tightly regula

99 r involved in the transcriptional program in T-ALL.

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

101 signalling could promote drug resistance in T-ALL.

102 lex 2 (PRC2) has a tumour-suppressor role in T-ALL.

103 istically, inhibition of NOTCH1 signaling in T-ALL induces a metabolic shutdown, with prominent inhib

104 signalling pathway operating specifically in T-ALL cells in which ORP4L mediates G protein-coupled li

105 are key regulators of the oncogenic state in T-ALL.

106 locus is activated under a superenhancer in T-ALL cells but not in normal T cells.

107 reviously described as a tumor suppressor in T-ALL, is in fact a pro-oncogenic cofactor essential for

108 functions as a bona fide tumor suppressor in T-ALL.

109 hog pathway as a novel therapeutic target in T-ALL and demonstrate that hedgehog inhibitors approved

110 ies validate PI3K as a therapeutic target in T-ALL and raise the unexpected possibility that dual inh

111 ransformation and as a therapeutic target in T-ALL.

112 eveal RUNX1 as a novel therapeutic target in T-ALL.

113 oward multitargeted JAK1 and JAK3 therapy in T-ALL.

114 ine 27 (H3K27) demethylases JMJD3 and UTX in T-ALL.

115 subtype-specific epigenetic vulnerability in T-ALL by which a particular subgroup of T-ALL characteri

116 stablished that overexpression of RasGRP1 in T-ALLs results in a constitutively high GTP-loading rate

117 es below 20 nM was detected in 2 independent T-ALL cohorts, which correlated with similar cytotoxic a

118 sociated with a subtype of Notch-independent T-ALLs that bear Myc gene rearrangements and Pten mutati

119 initiation and maintenance of Notch-induced T-ALL.

120 thymocyte development and in NOTCH1-induced T-ALL.

121 depletion in a mouse model of Notch3-induced T-ALL, by reducing N3IC expression and signaling, impair

122 al integration sites in gene therapy-induced T-ALL, suggesting that such events occur at preferential

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

124 Genome-wide analysis in Jurkat T-ALL cells shows that THZ1 disproportionally affects tr

125 Loss of CXCR4 targeted key T-ALL regulators, including the MYC pathway, and decreas

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

127 human T-cell acute lymphoblastic leukaemia (T-ALL) and used intravital microscopy to monitor the pro

128 T-cell acute lymphoblastic leukaemia (T-ALL) is a haematological malignancy with a dismal over

129 ent in T-cell acute lymphoblastic leukaemia (T-ALL), and often coexist.

130 human T-cell acute lymphoblastic leukaemia (T-ALL), have exceptional sensitivity to THZ1.

131 T-cell acute lymphoblastic leukaemias (T-ALL) are aggressive malignant proliferations character

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

133 oods in T cell acute lymphoblastic leukemia (T-ALL) and found that tumor cell genomes contain recurre

134 n human T-cell acute lymphoblastic leukemia (T-ALL) and Notch inhibitors (gamma-secretase inhibitors

135 rapid onset of acute lymphoblastic leukemia (T-ALL) and progressive development of hepatocellular car

136 lignant T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoma lines in vitro and significan

137 bset of T-cell acute lymphoblastic leukemia (T-ALL) cases, we found that heterozygous somatic mutatio

138 16% of T-cell acute lymphoblastic leukemia (T-ALL) cases.

139 rt that T-cell acute lymphoblastic leukemia (T-ALL) cells are characterized by increased oxidative ph

140 Primary T-cell acute lymphoblastic leukemia (T-ALL) cells require stromal-derived signals to survive.

141 ated in T cell acute lymphoblastic leukemia (T-ALL) cells upon calcineurin inactivation, among other

142 gram in T-cell acute lymphoblastic leukemia (T-ALL) cells.

143 single T cell acute lymphoblastic leukemia (T-ALL) clones were assessed using a zebrafish transgenic

144 ed with T-cell Acute Lymphoblastic Leukemia (T-ALL) development and progression.

145 ies for T cell acute lymphoblastic leukemia (T-ALL) efficiently reduce tumor mass.

146 taneous T-cell acute lymphoblastic leukemia (T-ALL) in these animals.

147 T-cell acute lymphoblastic leukemia (T-ALL) is a heterogeneous group of hematological tumors

148 T-cell acute lymphoblastic leukemia (T-ALL) is a high-risk subtype of acute lymphoblastic leu

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

150 T cell acute lymphoblastic leukemia (T-ALL) is an aggressive cancer that is frequently associ

151 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive childhood leukemia that is cause

152 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive form of leukemia that is mainly

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

154 nophenotype of acute lymphoblastic leukemia (T-ALL) is an uncommon aggressive leukemia that can prese

155 ildhood T-cell acute lymphoblastic leukemia (T-ALL) is mainly based on minimal residual disease (MRD)

156 ions in T cell acute lymphoblastic leukemia (T-ALL) led to clinical testing of gamma-secretase inhibi

157 murine T-cell acute lymphoblastic leukemia (T-ALL) model, we previously showed that expression of on

158 taneous T-cell acute lymphoblastic leukemia (T-ALL) occurred in 100% of Sur-TCR-Tg mice derived from

159 diatric T-cell acute lymphoblastic leukemia (T-ALL) patients and murine models, in which RasGRP1 T-AL

160 half of T-cell acute lymphoblastic leukemia (T-ALL) patients harbor gain-of-function mutations in the

161 Pediatric T-acute lymphoblastic leukemia (T-ALL) patients often display resistance to glucocortico

162 apse of T-cell acute lymphoblastic leukemia (T-ALL) patients treated on Dutch Childhood Oncology Grou

163 bset of T-cell acute lymphoblastic leukemia (T-ALL) patients, and RUNX1 mutations are associated with

164 primary T-cell acute lymphoblastic leukemia (T-ALL) samples and pave the way toward multitargeted JAK

165 tic tools in T-acute lymphoblastic leukemia (T-ALL) using T-ALL cell lines and patient-derived sample

166 en with T-cell acute lymphoblastic leukemia (T-ALL), 20% to 30% of patients undergo induction failure

167 mmature T-cell acute lymphoblastic leukemia (T-ALL), a heterogenic subgroup of human leukemia charact

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

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

170 e human T-cell acute lymphoblastic leukemia (T-ALL), in that they predominantly exhibit activating No

171 ment in T cell acute lymphoblastic leukemia (T-ALL), or any acute leukemia, is poorly understood.

172 play in T-cell acute lymphoblastic leukemia (T-ALL), we used a stably integrated fluorescent Wnt repo

173 e of T-lineage acute lymphoblastic leukemia (T-ALL), which occurs at an incidence of approximately 6%

174 MO2) in T-cell acute lymphoblastic leukemia (T-ALL).

175 ociated with T Acute lymphoblastic Leukemia (T-ALL).

176 rget in T-cell acute lymphoblastic leukemia (T-ALL).

177 ogression of T acute lymphoblastic leukemia (T-ALL).

178 mmon in T cell acute lymphoblastic leukemia (T-ALL).

179 TCH1 in T cell acute lymphoblastic leukemia (T-ALL).

180 tion of T-cell acute lymphoblastic leukemia (T-ALL).

181 e human T-cell acute lymphoblastic leukemia (T-ALL).

182 n human T cell acute lymphoblastic leukemia (T-ALL).

183 n human T cell acute lymphoblastic leukemia (T-ALL).

184 ated in T-cell acute lymphoblastic leukemia (T-ALL).

185 vent in T-cell acute lymphoblastic leukemia (T-ALL).

186 cer and T-cell acute lymphoblastic leukemia (T-ALL).

187 cluding T-cell acute lymphoblastic leukemia (T-ALL).

188 gene in T-cell acute lymphoblastic leukemia (T-ALL).

189 ng from T-cell acute lymphoblastic leukemia (T-ALL).

190 TCH1 in T-cell acute lymphoblastic leukemia (T-ALL).

191 eukemia/T-cell acute lymphoblastic leukemia [T-ALL] 1) is an essential transcription factor in normal

192 murine T-cell acute lymphoblastic leukemias (T-ALLs) deficient for Pten, our results suggest that act

193 driven T-cell acute lymphoblastic leukemias (T-ALLs) has recently been established.

194 kingly associated with TCRgammadelta lineage T-ALLs, as defined by expression of TCRgammadelta, TCRde

195 -cell acute lymphoblastic leukemia/lymphoma (T-ALL), and that loss of just one Rpl22 allele accelerat

196 high-risk T lymphoblastic leukemia/lymphoma (T-ALL/LBL) subgroup.

197 induces T-cell acute lymphoblastic lymphoma (T-ALL), a tumor type known to carry CIC mutations, albei

198 X mutations were exclusively present in male T-ALL patients and allelic expression analysis revealed

199 n oncogene in several lymphoid malignancies (T-ALL, B-chronic lymphocytic leukemia, splenic marginal

200 GF1R signaling was necessary for DC-mediated T-ALL survival.

201 Here we modeled T-ALL resistance, identifying GSI-tolerant 'persister' c

202 leukemic mice, whereas late-stage monoclonal T-ALL cells were counterselected against loss of Dicer1.

203 Moreover, T-ALL driven by UTX inactivation exhibits collateral sen

204 vivo models for CNS leukemia caused by mouse T-ALL and human xenografts of ALL cells, we demonstrate

205 L leukemic cells both in NOTCH-induced mouse T-ALL and human T-ALL xenograft models.

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

207 reover, genetic targeting of Cxcr4 in murine T-ALL after disease onset led to rapid, sustained diseas

208 c tumor microenvironments in multiple murine T-ALL models and primary patient samples, we discovered

209 Although our murine T-ALL model relies on transduction of HSCs, we were unab

210 ilar effects were observed in primary murine T-ALL blasts.

211 xplanation of why progression of JAK3-mutant T-ALL cases can be associated with the accumulation of a

212 y, we observed that one third of JAK3-mutant T-ALL cases harbor 2 JAK3 mutations, some of which are m

213 Rare persisters are already present in naive T-ALL populations, and the reversibility of their phenot

214 nce in TAL1-positive (but not TAL1-negative) T-ALL.

215 ransformed human T-ALL cell lines and NOTCH1 T-ALL mouse models.

216 the hedgehog pathway is activated in 20% of T-ALL samples.

217 ling, which is activated in more than 65% of T-ALL patients by activating mutations in the NOTCH1 gen

218 signaling cues in controlling the ability of T-ALL to home, survive, and proliferate, thus offering t

219 bioenergetics, cell death and abrogation of T-ALL engraftment in vivo.

220 or CXCR4 is essential to the LIC activity of T-ALL leukemic cells both in NOTCH-induced mouse T-ALL a

221 This novel, dynamic analysis of T-ALL interactions with the bone marrow microenvironment

222 sion profiling allowed the classification of T-ALL into defined molecular subgroups that mostly refle

223 data show that JAK3 mutations are drivers of T-ALL and require the cytokine receptor complex for tran

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

225 ew, we provide an update on our knowledge of T-ALL pathogenesis, the opportunities for the introducti

226 ential for the initiation and maintenance of T-ALL, as it controls important oncogenic gene targets b

227 ere protective in a mouse xenograft model of T-ALL.

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

229 ase progression in xenograft mouse models of T-ALL.

230 ing our understanding of the pathogenesis of T-ALL, and the discovery of activating mutations of NOTC

231 bitor, dramatically impeded proliferation of T-ALL cells isolated from patients and T-ALL cells in a

232 ism essential to the migratory properties of T-ALL cells.

233 ions in T-ALL and response and resistance of T-ALL to Notch pathway inhibitors.

234 In the past decade, systematic screening of T-ALL genomes by high-resolution copy-number arrays and

235 y in T-ALL by which a particular subgroup of T-ALL characterized by expression of the oncogenic trans

236 antly associated with the TAL/LMO subtype of T-ALL (P = .018) and trisomies 6 (P < .001) and 7 (P < .

237 mia (ALL) is a recently described subtype of T-ALL characterized by a unique immunophenotype and geno

238 genes and pathways, and stage or subtype of T-ALL.

239 inhibition results in efficient targeting of T-ALL-initiating cells.

240 Although advances in the treatment of T-ALL have lagged behind those of B-cell ALL, it is hope

241 d as therapeutic target for the treatment of T-ALL.

242 of JAK1/JAK3 inhibitors for the treatment of T-ALL.

243 tive therapeutic target for the treatment of T-ALL.

244 n inhibitor combinations in the treatment of T-ALL.

245 lin-like growth factor I receptor (Igf1r) on T-ALL cells, with concomitant expression of their ligand

246 e regimens with those of patients with other T-ALL/LBL immunophenotypic subtypes.

247 (siRNNs) targeting Plk1, can enter pediatric T-ALL patient cells without a transfection reagent and i

248 bits the growth of relapsed and IF pediatric T-ALL samples in vitro.

249 es and overcoming GC resistance in pediatric T-ALL patients.

250 ons affecting a few exons in 8% of pediatric T-ALL patients.

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

252 Dicer1 allele did not significantly perturb T-ALL onset and tumor progression.

253 tivation of Dicer1 in early stage polyclonal T-ALL cells was sufficient to abrogate T-ALL progression

254 Moreover, primary T-ALL cases with high GLI1 messenger RNA levels, but not

255 Screening of primary T-ALL samples reveals that 2 of 40 tumors examined show

256 ibody decreased proliferation of the primary T-ALL cells and depleted leukemia initiating CD34/CD44 h

257 inhibitor GDC-0941 is active against primary T-ALLs from wild-type and Kras(G12D) mice, and addition

258 ome immature, TLX3- or HOXA-positive primary T-ALLs are highly sensitive to BCL-2 inhibition, whereas

259 Multiple resistant primary T-ALLs that emerged in vivo did not contain somatic Notc

260 insulated neighborhoods containing prominent T-ALL proto-oncogenes.

261 terations in signaling pathways that promote T-ALL growth, the identity of endogenous stromal cells a

262 demonstrate that IRAK1/4 signaling promotes T-ALL progression through stabilization of MCL1 and sugg

263 nd Akt pathways downstream of Ras in RasGRP1 T-ALL but not in normal thymocytes.

264 patients and murine models, in which RasGRP1 T-ALLs expand in response to treatment with interleukins

265 se of nelarabine for relapsed and refractory T-ALL results in responses in a substantial minority of

266 However, therapy-resistant or refractory T-ALL remains a major clinical challenge.

267 e as a novel therapy for relapsed/refractory T-ALL, and that AKR1C3 expression could be used as a bio

268 A patient with refractory T-ALL was treated with dasatinib on the basis of drug pr

269 Herein, we demonstrate that miR-21 regulates T-ALL cell survival via repression of the tumor suppress

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

271 invasion by and survival of chemo-resistant T-ALL cells.

272 re able to induce cell death in GC-resistant T-ALL cells, and remarkably, cotreatment with dexamethas

273 d signaling in PTEN-deficient, GSI-resistant T-ALL cell lines (Jurkat, CCRF-CEM, and MOLT3), suggesti

274 novative therapeutic opportunities in SCL(+) T-ALL.

275 th myristoylated AKT developed GSI-sensitive T-ALLs that acquired Notch1 mutations.

276 bition reduced MCL1 stability and sensitized T-ALL to combination therapy.

277 iffer at the functional level, and, as such, T-ALL treatments are uniformly applied across subtypes,

278 DCs support T-ALL growth both in primary thymic tumors and at second

279 y a molecular mechanism by which DCs support T-ALL growth, we first performed gene expression profili

280 s in the tumor microenvironment that support T-ALL remains unknown.

281 DCs, are necessary and sufficient to support T-ALL survival ex vivo.

282 essive mark is focally diminished in TAL1(+) T-ALLs.

283 kemic blasts from 11 patients confirmed that T-ALL cells were more sensitive than BCP-ALL to PR-104A

284 Here we demonstrate that T-ALL cells are in direct, stable contact with CXCL12-pr

285 Our results reveal that T-ALL cells do not depend on specific bone marrow microe

286 The T-ALL cell line LOUCY, which shows a transcriptional pro

287 c balance between RasGEF and RasGAP in these T-ALLs and put forth a new model in which IL-2/7/9 decre

288 needed to improve treatment outcomes in this T-ALL/LBL subset.

289 Thus, T-ALL clones spontaneously and continuously evolve to dr

290 directly activated by TAL1 and contribute to T-ALL pathogenesis are largely unknown.

291 ants developed a long-latency transplantable T-ALL-like disease, characterized by an accumulation of

292 we have uncovered many previously unreported T-ALL-specific lncRNA genes, a fraction of which are dir

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

294 h Pdgfrb and Igf1r were activated in ex vivo T-ALL cells, and coculture with tumor-associated, but no

295 However, it remains unclear whether T-ALL subtypes differ at the functional level, and, as s

296 ediatric and over 50% of adult patients with T-ALL do not achieve complete remission and relapse, our

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

298 g these pathways could benefit patients with T-ALL.

299 cantly improved the outcome of patients with T-ALL.

300 A total of 111 patients with T-ALL/LBL (68% T-ALL; 32% T-LBL) with adequate immunophe