ライフサイエンスコーパス: T-cell acute lymphoblastic leukemia

1 oma) and Jurkat (derived from a patient with T-cell acute lymphoblastic leukemia).

2 ve inhibitor of oncogenic Notch signaling in T cell acute lymphoblastic leukemia.

3 h1 heterodimer, such as in the human disease T cell acute lymphoblastic leukemia.

4 c expression, and the pervasive emergence of T cell acute lymphoblastic leukemia.

5 ns and other lesions characteristic of human T-cell acute lymphoblastic leukemia.

6 t, and its activation is a frequent event in T-cell acute lymphoblastic leukemia.

7 nt and its activation is a frequent event in T-cell acute lymphoblastic leukemia.

8 isexpressed in the majority of patients with T-cell acute lymphoblastic leukemia.

9 2) chromosomal translocation associated with T-cell acute lymphoblastic leukemia.

10 uent gain-of-function mutation recognized in T-cell acute lymphoblastic leukemia.

11 ll non-Hodgkin's lymphoma and the other with T-cell acute lymphoblastic leukemia.

12 e most common genetic lesion associated with T-cell acute lymphoblastic leukemia.

13 0;14) chromosomal translocation recurring in T-cell acute lymphoblastic leukemia.

14 e presence of CD45 inactivating mutations in T-cell acute lymphoblastic leukemia.

15 identify a tumor suppressor role for CD45 in T-cell acute lymphoblastic leukemia.

16 a key leukemogenetic role in the majority of T-cell acute lymphoblastic leukemias.

17 ts developed acute leukemias (including four T-cell acute lymphoblastic leukemias), 12 developed Hodg

18 the body of the scl gene, is associated with T-cell acute lymphoblastic leukemia (ALL) and T-cell lym

19 lic changes in P-glycoprotein overexpressing T-cell acute lymphoblastic leukemia (ALL) cells, which e

20 T-cell acute lymphoblastic leukemia (ALL) is a rare dise

21 ldren with acute leukemia, including 10 with T-cell acute lymphoblastic leukemia (ALL), 7 with pre-B-

22 In contrast to T-cell acute lymphoblastic leukemia (ALL), where Notch a

23 thioredoxin in samples from 28 children with T-cell acute lymphoblastic leukemia and analyzed their s

24 F1 and RUNX2 were observed in both precursor T-cell acute lymphoblastic leukemia and colorectal cance

25 ng genes EZH2, EED, and SUZ12 are present in T-cell acute lymphoblastic leukemia and in myeloid malig

26 CD45-expressing cells induces development of T-cell acute lymphoblastic leukemia and lymphoma, but no

27 tions and deletions in ribosomal proteins in T-cell acute lymphoblastic leukemia and solid tumors, fu

28 drome, is also present in about 38% of adult T-cell acute lymphoblastic leukemias and 3% of adult acu

29 blood from a febrile patient with precursor T-cell acute lymphoblastic leukemia, and after antibioti

30 ), nelarabine, demonstrated efficacy against T-cell acute lymphoblastic leukemia, and its effectivene

31 patients with acute myeloid leukemia (AML), T-cell acute lymphoblastic leukemia, and myelodysplastic

32 ic leukemia/lymphoma 11B) locus is linked to T-cell acute lymphoblastic leukemia, and the loss of het

33 -rich domains, the same two hotspots seen in T-cell acute lymphoblastic leukemias, and led to pathway

34 The biology and outcome of adult T-cell acute lymphoblastic leukemia are poorly understoo

35 utations of NOTCH1 (a well-known oncogene in T-cell acute lymphoblastic leukemia) are present in appr

36 main protein that is aberrantly expressed in T-cell acute lymphoblastic leukemia as a consequence of

37 helix (bHLH) oncoprotein that is involved in T-cell acute lymphoblastic leukemia as well as in normal

38 the leukemic progression of both B cell and T cell acute lymphoblastic leukemia (B-ALL and T-ALL, re

39 ently introduced and effective treatment for T-cell acute lymphoblastic leukemia, but how ara-G and a

40 n factor, overexpressed in as much as 60% of T cell acute lymphoblastic leukemia cases.

41 man glucocorticoid receptor (GR) gene in the T-cell acute lymphoblastic leukemia cell line, CEM-C7, a

42 eries of methotrexate-resistant MOLT-3 human T-cell acute lymphoblastic leukemia cell lines that show

43 Overexpression of cleaved Notch-1 in T-cell acute lymphoblastic leukemia cells activates NF-k

44 NOTCH1, which is frequently mutated in T cell acute lymphoblastic leukemia, has been an elusive

45 e describe the induction of clonally derived T cell acute lymphoblastic leukemia in transgenic zebraf

46 In contrast, FLT3-ITD induced a T-cell acute lymphoblastic leukemia in BMT mice receivin

47 product is expressed in a high percentage of T-cell acute lymphoblastic leukemias in the pediatric ag

48 nvolvement by a chromosomal rearrangement in T-cell acute lymphoblastic leukemia, is required for hem

49 region of Notch1 most frequently mutated in T-cell acute lymphoblastic leukemia lymphoma (T-ALL).

50 in addition to acute myeloid leukemia (AML), T cell acute lymphoblastic leukemia/lymphoma (T-ALL) and

51 TCH1 mutations are found in 50%-70% of human T cell acute lymphoblastic leukemia/lymphoma (T-ALL) cas

52 equently present in both childhood and adult T cell acute lymphoblastic leukemia/lymphoma and are det

53 p19(ARF) as potential therapeutic targets in T cell acute lymphoblastic leukemia/lymphoma and lung ad

54 light of experiments using human and murine T cell acute lymphoblastic leukemia/lymphoma cell lines

55 ce, the known involvement of NOTCH1 in human T cell acute lymphoblastic leukemia/lymphoma has been re

56 f the NOTCH1 receptor are potent inducers of T cell acute lymphoblastic leukemia/lymphoma when expres

57 NOTCH signaling in the pathogenesis of human T cell acute lymphoblastic leukemia/lymphoma, and they p

58 in T cells, double-deficient mice developed T cell acute lymphoblastic leukemia/lymphoma, which orig

59 the Notch1 receptor are very common in human T cell acute lymphoblastic leukemia/lymphoma.

60 ated forms of NOTCH1 found commonly in human T cell acute lymphoblastic leukemia/lymphoma.

61 frequent mutations involving NOTCH1 in human T cell acute lymphoblastic leukemia/lymphoma.

62 somal protein Rpl22 is a tumor suppressor in T-cell acute lymphoblastic leukemia/lymphoma (T-ALL), an

63 Children's Oncology Group trials P9404 (T-cell acute lymphoblastic leukemia/lymphoma; n = 537),

64 oblastic leukemia and in refractory-relapsed T-cell acute lymphoblastic leukemia or T-cell lymphoblas

65 died of B-cell acute lymphoblastic leukemia, T-cell acute lymphoblastic leukemia, or a myeloprolifera

66 function mutations in IL-7Ralpha from B- and T-cell acute lymphoblastic leukemia patients.

67 e associated with acute myeloid leukemia and T-cell acute lymphoblastic leukemia, respectively, where

68 whereas patients with high-risk genetics and T-cell acute lymphoblastic leukemia responded more slowl

69 proliferation of clonogenic cells among the T-cell acute lymphoblastic leukemia samples expressing r

70 with data obtained from a panel of 84 human T-cell acute lymphoblastic leukemia samples, including c

71 Finally, analysis of Myc-induced T cell acute lymphoblastic leukemia showed that cells ar

72 l transgenic mouse model of Emu-tTA/tetO-MYC T-cell acute lymphoblastic leukemia, some of the tumors

73 tumors that model distinct subtypes of human T-cell acute lymphoblastic leukemia, suggesting that eve

74 K4/6 inhibits both cell cycle entry in human T cell acute lymphoblastic leukemia (T-ALL) and disease

75 We mapped insulated neighborhoods in T cell acute lymphoblastic leukemia (T-ALL) and found th

76 berrantly expressed in 60% of cases of human T cell acute lymphoblastic leukemia (T-ALL) and initiate

77 f NOTCH1 are responsible for the majority of T cell acute lymphoblastic leukemia (T-ALL) cases.

78 ired cell migration has been demonstrated in T cell acute lymphoblastic leukemia (T-ALL) cells upon c

79 issue, functional differences between single T cell acute lymphoblastic leukemia (T-ALL) clones were

80 and ZFP36L2 during thymopoiesis developed a T cell acute lymphoblastic leukemia (T-ALL) dependent on

81 Current chemotherapies for T cell acute lymphoblastic leukemia (T-ALL) efficiently

82 Very rare cases of human T cell acute lymphoblastic leukemia (T-ALL) harbor chrom

83 T cell acute lymphoblastic leukemia (T-ALL) is an aggres

84 T cell acute lymphoblastic leukemia (T-ALL) is an immatu

85 tification of activating NOTCH1 mutations in T cell acute lymphoblastic leukemia (T-ALL) led to clini

86 regulate the survival and chemoresistance of T cell acute lymphoblastic leukemia (T-ALL) still are po

87 Myc zebrafish line that develops GFP-labeled T cell acute lymphoblastic leukemia (T-ALL), allowing vi

88 resents an important oncogenic mechanism for T cell acute lymphoblastic leukemia (T-ALL), an aggressi

89 NOTCH1 receptors compared with wild type in T cell acute lymphoblastic leukemia (T-ALL), but its adm

90 ntly expressed in over 40% of cases of human T cell acute lymphoblastic leukemia (T-ALL), emphasizing

91 Using an established mouse model of T cell acute lymphoblastic leukemia (T-ALL), here we rep

92 ctor is overexpressed in most human cases of T cell acute lymphoblastic leukemia (T-ALL), often downs

93 The role of the microenvironment in T cell acute lymphoblastic leukemia (T-ALL), or any acut

94 To clarify the basis for GSI resistance in T cell acute lymphoblastic leukemia (T-ALL), we studied

95 tes occurs in the majority of cases of human T cell acute lymphoblastic leukemia (T-ALL), yet experim

96 frequently misexpressed and translocated in T cell acute lymphoblastic leukemia (T-ALL).

97 e because of its role as the main trigger of T cell acute lymphoblastic leukemia (T-ALL).

98 n-1) has a major role in the pathogenesis of T cell acute lymphoblastic leukemia (T-ALL).

99 s been associated with human cancers such as T cell acute lymphoblastic leukemia (T-ALL).

100 ncogenic protein Notch homolog-1 (NOTCH1) in T cell acute lymphoblastic leukemia (T-ALL).

101 tch1 (ICN1) are frequently observed in human T cell acute lymphoblastic leukemia (T-ALL).

102 B oncogene is frequently duplicated in human T cell acute lymphoblastic leukemia (T-ALL).

103 quent gain-of-function mutation in pediatric T cell acute lymphoblastic leukemia (T-ALL).

104 mechanism by which the Tal1 oncogene causes T cell acute lymphoblastic leukemia (T-ALL).

105 Activating mutations in NOTCH1 are common in T cell acute lymphoblastic leukemia (T-ALL).

106 uently co-expressed with activated NOTCH1 in T cell acute lymphoblastic leukemia (T-ALL).

107 nstream targets of oncogenic Notch1 in human T cell acute lymphoblastic leukemia (T-ALL).

108 recurrent chromosomal duplications in human T cell acute lymphoblastic leukemia (T-ALL).

109 s are prevalent in various tumors, including T cell acute lymphoblastic leukemia (T-ALL).

110 is a major driver of therapeutic failure in T cell acute lymphoblastic leukemia (T-ALL).

111 gressive T cell malignancy, resembling human T cell acute lymphoblastic leukemia (T-ALL).

112 3-kinase (PI3K)/Akt activation is common in T cell acute lymphoblastic leukemia (T-ALL).

113 genes have a key role in the pathogenesis of T cell acute lymphoblastic leukemia (T-ALL).

114 n of cyclin D3 in mice bearing Notch1-driven T cell acute lymphoblastic leukemias (T-ALL) triggered t

115 Early immature T cell acute lymphoblastic leukemias (T-ALLs) account fo

116 T cell acute lymphoblastic leukemias (T-ALLs) arise from

117 ic lymphomas (T-LBL) are commonly treated on T-cell acute lymphoblastic leukemia (T-ALL) -derived pro

118 T-cell acute lymphoblastic leukemia (T-ALL) accounts for

119 t with (1) acute myeloid leukemia (AML), (2) T-cell acute lymphoblastic leukemia (T-ALL) and (3) B-ce

120 We treated 26 patients with T-cell acute lymphoblastic leukemia (T-ALL) and 13 with

121 of the most recurrent oncogenic hallmarks of T-cell acute lymphoblastic leukemia (T-ALL) and are gene

122 CH1 are frequently detected in patients with T-cell acute lymphoblastic leukemia (T-ALL) and in mouse

123 ating NOTCH1 mutations are frequent in human T-cell acute lymphoblastic leukemia (T-ALL) and Notch in

124 methylthioadenosine phosphorylase (MTAP) in T-cell acute lymphoblastic leukemia (T-ALL) and other ca

125 CAR T cells effectively eliminate malignant T-cell acute lymphoblastic leukemia (T-ALL) and T-cell l

126 s one of the most common molecular events in T-cell acute lymphoblastic leukemia (T-ALL) and, in pedi

127 tivating lesions frequently affect Notch1 in T-cell acute lymphoblastic leukemia (T-ALL) and, recentl

128 cal and cytogenetic features associated with T-cell acute lymphoblastic leukemia (T-ALL) are not pred

129 volved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly u

130 Notch1 ectodomain occur frequently in human T-cell acute lymphoblastic leukemia (T-ALL) but are rare

131 tivating mutations occur in more than 50% of T-cell acute lymphoblastic leukemia (T-ALL) cases and in

132 In a subset of T-cell acute lymphoblastic leukemia (T-ALL) cases, we fo

133 tyrosine kinase is mutated in 10% to 16% of T-cell acute lymphoblastic leukemia (T-ALL) cases.

134 Here, we report that T-cell acute lymphoblastic leukemia (T-ALL) cells are ch

135 f spontaneous apoptosis by IL-7 in precursor T-cell acute lymphoblastic leukemia (T-ALL) cells correl

136 Primary T-cell acute lymphoblastic leukemia (T-ALL) cells requir

137 In colony-forming assays, primary T-cell acute lymphoblastic leukemia (T-ALL) cells were 3

138 duces an aberrant transcriptional program in T-cell acute lymphoblastic leukemia (T-ALL) cells.

139 regulated Notch signaling is associated with T-cell Acute Lymphoblastic Leukemia (T-ALL) development

140 we report contributions of mTORC2 to thymic T-cell acute lymphoblastic leukemia (T-ALL) driven by No

141 Patients relapsing with T-cell acute lymphoblastic leukemia (T-ALL) face a disma

142 Previously, we reported that most primary T-cell acute lymphoblastic leukemia (T-ALL) harbored p16

143 y reported a significantly better outcome in T-cell acute lymphoblastic leukemia (T-ALL) harboring NO

144 We observed the development of a spontaneous T-cell acute lymphoblastic leukemia (T-ALL) in these ani

145 hypothesis in a mouse model of Notch-induced T-cell acute lymphoblastic leukemia (T-ALL) in which the

146 Frequent hallmarks of T-cell acute lymphoblastic leukemia (T-ALL) include aber

147 ently been implicated in the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL) induced by T

148 The most common translocation in childhood T-cell acute lymphoblastic leukemia (T-ALL) involves the

149 T-cell acute lymphoblastic leukemia (T-ALL) is a challen

150 T-cell acute lymphoblastic leukemia (T-ALL) is a hematol

151 T-cell acute lymphoblastic leukemia (T-ALL) is a heterog

152 T-cell acute lymphoblastic leukemia (T-ALL) is a high-ri

153 T-cell acute lymphoblastic leukemia (T-ALL) is a highly

154 T-cell acute lymphoblastic leukemia (T-ALL) is an aggres

155 T-cell acute lymphoblastic leukemia (T-ALL) is an aggres

156 T-cell acute lymphoblastic leukemia (T-ALL) is an aggres

157 T-cell acute lymphoblastic leukemia (T-ALL) is an aggres

158 T-cell acute lymphoblastic leukemia (T-ALL) is an aggres

159 T-cell acute lymphoblastic leukemia (T-ALL) is an aggres

160 Adult T-cell acute lymphoblastic leukemia (T-ALL) is an aggres

161 Risk stratification in childhood T-cell acute lymphoblastic leukemia (T-ALL) is mainly ba

162 Childhood T-cell acute lymphoblastic leukemia (T-ALL) is one of th

163 chromosomal rearrangements in patients with T-cell acute lymphoblastic leukemia (T-ALL) is SCL/tal.

164 In a murine T-cell acute lymphoblastic leukemia (T-ALL) model, we pr

165 Spontaneous T-cell acute lymphoblastic leukemia (T-ALL) occurred in

166 Children with T-cell acute lymphoblastic leukemia (T-ALL) or advanced

167 ein 1), was recently implicated in pediatric T-cell acute lymphoblastic leukemia (T-ALL) patients and

168 More than half of T-cell acute lymphoblastic leukemia (T-ALL) patients har

169 For example, although 95% of pediatric T-cell acute lymphoblastic leukemia (T-ALL) patients hav

170 re an independent risk factor for relapse of T-cell acute lymphoblastic leukemia (T-ALL) patients tre

171 anscription factor is mutated in a subset of T-cell acute lymphoblastic leukemia (T-ALL) patients, an

172 ries of JAK3 mutations identified in primary T-cell acute lymphoblastic leukemia (T-ALL) samples and

173 Also, 13 T-cell acute lymphoblastic leukemia (T-ALL) samples were

174 1 mutations are found in 50% to 60% of human T-cell acute lymphoblastic leukemia (T-ALL) samples.

175 ute for gamma-secretase inhibitors (GSIs) in T-cell acute lymphoblastic leukemia (T-ALL) therapy, we

176 ugh prognosis has improved for children with T-cell acute lymphoblastic leukemia (T-ALL), 20% to 30%

177 that ZEB2 is an oncogenic driver of immature T-cell acute lymphoblastic leukemia (T-ALL), a heterogen

178 Here we show that in T-cell acute lymphoblastic leukemia (T-ALL), a small set

179 ts with acute myeloid leukemia (AML), 4 of 7 T-cell acute lymphoblastic leukemia (T-ALL), and 11 of 1

180 We recently found that in T-cell acute lymphoblastic leukemia (T-ALL), both the p1

181 These tumors resemble human T-cell acute lymphoblastic leukemia (T-ALL), in that the

182 n factor that is frequently overexpressed in T-cell acute lymphoblastic leukemia (T-ALL), including e

183 esis are often misexpressed in the thymus in T-cell acute lymphoblastic leukemia (T-ALL), leading to

184 It is frequently misregulated in T-cell acute lymphoblastic leukemia (T-ALL), often due t

185 ) or partial remission (n=5) was achieved in T-cell acute lymphoblastic leukemia (T-ALL), T-lymphoid

186 T-cell acute lymphoblastic leukemia (T-ALL), unlike othe

187 n domain of NOTCH1 occur frequently in human T-cell acute lymphoblastic leukemia (T-ALL), we assessed

188 contribution of the PTEN-PI3K-AKT pathway to T-cell acute lymphoblastic leukemia (T-ALL), we examined

189 ooperating genetic events in LMO2-associated T-cell acute lymphoblastic leukemia (T-ALL), we investig

190 urther unravel the molecular pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL), we performe

191 address what role Wnt signaling may play in T-cell acute lymphoblastic leukemia (T-ALL), we used a s

192 ogenitors are susceptible to Notch1-mediated T-cell acute lymphoblastic leukemia (T-ALL).

193 at has been linked to human cancers, notably T-cell acute lymphoblastic leukemia (T-ALL).

194 eam signaling, have been identified in human T-cell acute lymphoblastic leukemia (T-ALL).

195 uired for the proliferation of a subgroup of T-cell acute lymphoblastic leukemia (T-ALL).

196 on(s) in Notch1 is a common genetic event in T-cell acute lymphoblastic leukemia (T-ALL).

197 Notch gain of function mutations, including T-cell acute lymphoblastic leukemia (T-ALL).

198 gene is aberrantly expressed in a subset of T-cell acute lymphoblastic leukemia (T-ALL).

199 c mutations of LMO2, a prominent oncogene in T-cell acute lymphoblastic leukemia (T-ALL).

200 ation is a common genetic event in pediatric T-cell acute lymphoblastic leukemia (T-ALL).

201 olecules may provide efficient therapies for T-cell acute lymphoblastic leukemia (T-ALL).

202 in the cure rate of patients suffering from T-cell acute lymphoblastic leukemia (T-ALL).

203 by chromosomaltranslocation in patients with T-cell acute lymphoblastic leukemia (T-ALL).

204 e most frequent gain-of-function mutation in T-cell acute lymphoblastic leukemia (T-ALL).

205 uent gain-of-function mutation recognized in T-cell acute lymphoblastic leukemia (T-ALL).

206 rs, the most notable example being NOTCH1 in T-cell acute lymphoblastic leukemia (T-ALL).

207 ells, as exemplified by LIM-only 2 (LMO2) in T-cell acute lymphoblastic leukemia (T-ALL).

208 is essential for Notch-mediated induction of T-cell acute lymphoblastic leukemia (T-ALL).

209 sive T-cell malignancies that resemble human T-cell acute lymphoblastic leukemia (T-ALL).

210 kine receptors and is recurrently mutated in T-cell acute lymphoblastic leukemia (T-ALL).

211 /CAN) fusion gene is a rare genetic event in T-cell acute lymphoblastic leukemia (T-ALL).

212 several cancers including breast cancer and T-cell acute lymphoblastic leukemia (T-ALL).

213 r oncogenic driver and therapeutic target in T-cell acute lymphoblastic leukemia (T-ALL).

214 ed NAP1L1/12q21 as another MLLT10 partner in T-cell acute lymphoblastic leukemia (T-ALL).

215 apy regimen in children with newly diagnosed T-cell acute lymphoblastic leukemia (T-ALL).

216 mission in adult zebrafish with cMYC-induced T-cell acute lymphoblastic leukemia (T-ALL).

217 onent of the molecular pathogenesis of human T-cell acute lymphoblastic leukemia (T-ALL); however, on

218 signaling is deregulated in the majority of T-cell acute lymphoblastic leukemias (T-ALL) as a result

219 tions of the MTAP gene were found in primary T-cell acute lymphoblastic leukemias (T-ALL).

220 anslocations were previously found in murine T-cell acute lymphoblastic leukemias (T-ALLs) deficient

221 ndividual microRNAs (miRNAs) in Notch-driven T-cell acute lymphoblastic leukemias (T-ALLs) has recent

222 Here, Myc-induced T-cell acute lymphoblastic leukemias (T-ALLs) have been

223 utations in NOTCH1 occur in more than 50% of T-cell acute lymphoblastic leukemias (T-ALLs).

224 n is abnormally expressed in the majority of T-cell acute lymphoblastic leukemias (T-ALLs).

225 may provide a mechanism for the induction of T-cell-acute lymphoblastic leukemia (T-ALL) that does no

226 SCL/TAL1 (stem cell leukemia/T-cell acute lymphoblastic leukemia [T-ALL] 1) is an ess

227 Analysis of 15 cases of T-cell acute lymphoblastic leukemia with spectral karyot