ライフサイエンスコーパス: internal tandem duplication

1 in patients without a concomitant FLT3 gene internal tandem duplication.

2 torically negative prognostic effect of FLT3 internal tandem duplication.

3 ns with short spacer sequences, such as pol3 internal tandem duplications.

4 es, including the subgroup positive for FLT3 internal tandem duplications.

5 nt inhibitor of Fms tyrosine kinase-3 (FLT3) internal tandem duplication, a validated therapeutic tar

6 ug screening, we find that treatment of FLT3 internal tandem duplication AML cells with quizartinib,

7 Mutations, including a large internal tandem duplication and a deletion, were identif

8 consolidation within the cytogenetic or FLT3-internal tandem duplication and NPM1 gene mutation subgr

9 balanced for age, karyotypic risk, and FLT3-internal tandem duplication and NPM1 gene mutations.

10 n multivariate analysis, which included FLT3 internal tandem duplication and NPM1 mutation status, th

11 set of additional mutations, including FLT3-internal tandem duplication and other events contributin

12 Four prognostic biomarkers-the internal tandem duplication and point mutations in the F

13 There were data on FLT3 internal tandem duplications and NPM1 mutations (n = 592

14 pendently validated driver fusions including internal tandem duplications and other non-canonical eve

15 an-FLT3 inhibitor, is effective against both internal tandem duplications and resistance-conferring t

16 to abnormal transcripts, including two from internal tandem duplications and two fusion transcripts

17 ermediate-risk and normal cytogenetics, FLT3 internal tandem duplication, and NPM1, PTPN11, and IDH2

18 sions, including chromosomal translocations, internal tandem duplications, and mutations, have been d

19 effective against cells expressing the Flt3 internal tandem duplication, BCR-ABL, MN1, and an shRNA

20 ls and, together with a concurrent FLT3-ITD (internal tandem duplication), confers resistance to the

21 ibit Ba/F3 cells stably transduced with FLT3-internal tandem duplications containing a G697R mutation

22 te risk genotype NPM1 wild-type/FLT3 without internal-tandem duplications (EFS, 18% +/- 5 vs 40% +/-

23 A saturation mutagenesis screen of FLT3-internal tandem duplication failed to recover any resist

24 y, we determined significant iHR activity in internal tandem duplication FLT3 (FLT3-ITD) and JAK2V617

25 Fetal liver tyrosine kinase 3 internal tandem duplication (FLT3 ITD) mutations are the

26 ssifier with the prognostically adverse FLT3 internal tandem duplication (FLT3 ITD) potentially expla

27 Ascorbate depletion cooperated with Flt3 internal tandem duplication (Flt3(ITD)) leukaemic mutati

28 The FLT3 Internal Tandem Duplication (FLT3(ITD)) mutation is comm

29 for patients with FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) acute myeloid leu

30 Of 1075 patients tested, 822 had FLT3 internal tandem duplication (FLT3-ITD) and/or NPM1 mutat

31 ng in poor molecular risk patients with FLT3-internal tandem duplication (FLT3-ITD) and/or NPM1 wild-

32 at methylation of fms-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) at arginines 972

33 kaemia (AML) with FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) have limited trea

34 Risk associated to FLT3 internal tandem duplication (FLT3-ITD) in patients with

35 FLT3 internal tandem duplication (FLT3-ITD) is an activating

36 myeloid leukemia (AML) that harbors the FLT3-internal tandem duplication (FLT3-ITD) mutation.

37 g the most common type of FLT3 mutation, the internal tandem duplication (FLT3-ITD) mutation.

38 FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) mutations in acut

39 In FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD)(+)-cells protein,

40 a (AML) have a constitutively activated FLT3-internal tandem duplication (FLT3-ITD), and these patien

41 The mutational status of TP53, FLT3 internal tandem duplication (FLT3-ITD), NRAS, and KRAS c

42 In Fms-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD)-negative AML, BTK

43 Patients with relapsed or refractory FLT3 internal tandem duplication (FLT3-ITD)-positive acute my

44 In Fms-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD)-positive AML, BTK

45 uding BCR-ABL and FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD).

46 ops driven by the FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD).

47 Using FLT3 internal tandem duplication (FLT3/ITD) as a molecular ma

48 s with acute myeloid leukemia (AML) and FLT3/internal tandem duplication (FLT3/ITD) have poor prognos

49 FLT3 internal tandem duplication (FLT3/ITD) is a common somat

50 se inhibitor (TKI) with activity against the internal tandem duplication (FLT3/ITD) mutants and the F

51 Acute myeloid leukemia with a FLT3 internal tandem duplication (FLT3/ITD) mutation is an ag

52 with acute myeloid leukemia (AML) harboring internal tandem duplication (FLT3/ITD) mutations.

53 he most potent activity to date against FLT3 internal tandem duplication (FLT3/ITD) mutations.

54 eloid leukemia (AML) with low levels of FLT3 internal tandem duplications (FLT3(ITD)) do not have a w

55 The applicability of FLT3-internal tandem duplications (FLT3-ITD) for assessing me

56 01) after adjustment for WT1 mutations, FLT3 internal tandem duplications (FLT3-ITD), and high ERG ex

57 also were assessed for the presence of FLT3 internal tandem duplications (FLT3-ITD), FLT3 tyrosine k

58 sence of NPM1 mutations (NPM1(mut)) and FLT3 internal tandem duplications (FLT3-ITD).

59 FLT3-internal tandem duplications (FLT3-ITDs) are prognostic

60 FLT3 internal tandem duplications (FLT3/ITDs) in the juxtamem

61 in the FLT3 gene (FMS-like tyrosine kinase 3-internal tandem duplication [FLT3-ITD]), causing constit

62 tated CEBPA and/or mutated NPM1 without FLT3 internal tandem duplication [FLT3-ITD]), TET2-mutated pa

63 For example, FLT3 internal tandem duplication (FLT3ITD) mutations cooperat

64 The impact of a FLT3-internal tandem duplication (FLT3ITD) on prognosis of pa

65 In functional studies, FLT3 internal tandem duplication gain or TP53 loss conferred

66 We assayed NRAS oncogene mutation and FLT3 internal tandem duplication in 447 AML patients with an

67 ow that DNMT3A loss synergizes with the FLT3 internal tandem duplication in a dose-influenced fashion

68 We found that internal tandem duplication in FLT3 (FLT3-ITD), partial

69 An internal tandem duplication in the fms-like tyrosine kin

70 nd high-risk molecular features--that is, an internal tandem duplication in the fms-related tyrosine

71 CD25 was positively correlated with internal tandem duplications in FLT3 (FLT3-ITD), DNMT3A,

72 associated with selected mutations, such as internal tandem duplications in the FLT3 gene (FLT3-ITD)

73 FLT3-ITD (internal tandem duplication) is a key driver of acute my

74 zation and an increase in intracellular FLT3/internal tandem duplication (ITD) accumulation.

75 eatment in fms-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD) acute myeloid leukemia

76 quently, some centers consider baseline FLT3-internal tandem duplication (ITD) an indication for tran

77 FLT3 internal tandem duplication (ITD) and nucleophosmin muta

78 Constitutively activating internal tandem duplication (ITD) and point mutations of

79 overexpressed or constitutively activated by internal tandem duplication (ITD) and tyrosine kinase do

80 LT3) inhibitor with high binding affinity to internal tandem duplication (ITD) and wild-type (WT) FLT

81 FLT3 internal tandem duplication (ITD) frequency was 17%, and

82 with acute myeloid leukemia (AML) and a FLT3 internal tandem duplication (ITD) have poor outcomes to

83 The FLT3 gene is mutated by an internal tandem duplication (ITD) in 20-25% of adults wi

84 Persistence of FLT3 internal tandem duplication (ITD) in adults with acute m

85 alteration in acute myeloid leukemia is the internal tandem duplication (ITD) in FLT3, the receptor

86 Recent studies have indicated that an internal tandem duplication (ITD) in the FLT3 gene may a

87 osis in acute myeloid leukemia (AML) when an internal tandem duplication (ITD) in the fms-related tyr

88 ansfected with FLT3 containing an activating internal tandem duplication (ITD) in the juxtamembrane d

89 Activating mutations in FLT3, including internal tandem duplication (ITD) in the juxtamembrane d

90 Internal tandem duplication (ITD) in the juxtamembrane p

91 Frequently, the mutation is an in-frame internal tandem duplication (ITD) in the juxtamembrane r

92 Here, we identified an internal tandem duplication (ITD) in the switch II domai

93 e Fms-like tyrosine kinase-3 receptor (FLT3) internal tandem duplication (ITD) is found in 30% of acu

94 Concurrent presence of FLT3-internal tandem duplication (ITD) is observed in 25% of

95 Constitutive activation of FLT3 by internal tandem duplication (ITD) is one of the most com

96 We hypothesized that FLT3/internal tandem duplication (ITD) leukemia cells exhibit

97 nvestigate the role of constitutively active internal tandem duplication (ITD) mutants of the Fms-lik

98 iated with poor outcomes; however, only FLT3-internal tandem duplication (ITD) mutation and adverse k

99 Clinical evidence has shown that FLT3 internal tandem duplication (ITD) mutation confers poor

100 eport we investigated the mechanism by which internal tandem duplication (ITD) mutation of FLT3 signa

101 FMS-like tyrosine kinase-3 (FLT3)-internal tandem duplication (ITD) mutation was detected

102 ation in the tyrosine kinase domain (TKD) or internal tandem duplication (ITD) mutation with either a

103 was 71 years and 73% of patients had an FLT3-internal tandem duplication (ITD) mutation.

104 Because of the correlation between FLT3 internal tandem duplication (ITD) mutations and poor pro

105 FLT3 kinase internal tandem duplication (ITD) mutations are common i

106 artial tandem duplication (PTD) and the FLT3 internal tandem duplication (ITD) mutations associate wi

107 Activating internal tandem duplication (ITD) mutations in FLT3 (FLT

108 t acute myeloid leukemia (AML) patients with internal tandem duplication (ITD) mutations in FLT3.

109 Internal tandem duplication (ITD) mutations in the FLT3

110 3 activating mutations have been identified: internal tandem duplication (ITD) mutations in the juxta

111 FLT3 mutations in acute myeloid leukemia are internal tandem duplication (ITD) mutations in the juxta

112 tion of FMS-like tyrosine kinase 3 (FLT3) by internal tandem duplication (ITD) mutations is one of th

113 h acute myeloid leukaemia (AML) positive for internal tandem duplication (ITD) mutations of FLT3 have

114 The internal tandem duplication (ITD) mutations of the FMS-l

115 Internal tandem duplication (ITD) mutations of the juxta

116 Constitutively activating internal tandem duplication (ITD) mutations of the recep

117 Internal tandem duplication (ITD) mutations of the recep

118 FLT3 internal tandem duplication (ITD) mutations result in co

119 3 years in patients with both NPM1 and FLT3 internal tandem duplication (ITD) mutations was 69% (95%

120 Internal tandem duplication (ITD) mutations within the F

121 id leukemia (AML) patients and, at least for internal tandem duplication (ITD) mutations, are associa

122 acute myeloid leukemia (AML) containing FLT3 internal tandem duplication (ITD) mutations.

123 In acute myeloid leukemia (AML), internal tandem duplication (ITD) of FLT3 at the juxtame

124 Internal tandem duplication (ITD) of fms-like tyrosine k

125 Internal tandem duplication (ITD) of the fms-related tyr

126 Somatic mutations of FLT3 involving internal tandem duplication (ITD) of the juxtamembrane d

127 eloid leukemia (AML) patients have either an internal tandem duplication (ITD) of the juxtamembrane r

128 LT3 is constitutively activated either by an internal tandem duplication (ITD) or by a point mutation

129 e myeloid leukemia (AML)-related mutant FLT3 internal tandem duplication (ITD) protein.

130 example, as point mutations of Asp835 or as internal tandem duplication (ITD) sequences in the juxta

131 ocytic leukemia AML patients with known FLT3 internal tandem duplication (ITD) status for FLT3/TKDs;

132 Although FLT3-internal tandem duplication (ITD) was an adverse risk fa

133 e Flt-3 and a constitutively activated Flt-3/internal tandem duplication (ITD) with IC(50) values of

134 mbining ATRA and FLT3 TKIs to eliminate FLT3/internal tandem duplication (ITD)(+) LSCs.

135 er risk with normal cytogenetics [e.g., FLT3-internal tandem duplication (ITD)+].

136 nd that pharmacologic inhibition of the Flt3 internal tandem duplication (ITD), a mutated receptor ty

137 an abnormal karyotype, the presence of FLT3-internal tandem duplication (ITD), and a < 4-log reducti

138 ere characterized for BAALC expression, FLT3 internal tandem duplication (ITD), and MLL partial tande

139 The most common type, internal tandem duplication (ITD), confers poor prognosi

140 lication within coding exons, referred to as internal tandem duplication (ITD), remains challenging d

141 We have recently demonstrated that FLT3-internal tandem duplication (ITD), when localized to the

142 by mutant Fms-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD), which mediate resista

143 , overexpression of constitutively activated internal tandem duplication (ITD)-Flt3 mutants in Ba/F3

144 FLT3-KO in LSCs from FLT3-internal tandem duplication (ITD)-mutated but not FLT3-w

145 togenetically normal, and 11 (15%) had FLT-3 internal tandem duplication (ITD).

146 n vitro, the N-oxide potently inhibited FLT3-internal tandem duplication (ITD; binding constant, 70 n

147 and EFS (P = .004) after adjusting for FLT3 internal tandem duplication (ITD; P < .001).

148 ions have been identified, often as in-frame internal tandem duplications (ITD) at the juxtamembrane

149 emia (AML) and frequently co-occur with FLT3 internal tandem duplications (ITD) or, less commonly, NR

150 ns of clonal evolution in patients with FLT3-internal tandem duplications (ITD)-positive AML who were

151 oring oncogenic tyrosine kinases (OTKs: FLT3(internal tandem duplication [ITD]), JAK2(V617F), BCR-ABL

152 ts (14.1%) had FLT3 mutations (FLT3mut; with internal tandem duplications [ITD], tyrosine kinase doma

153 s, 36 had FLT3 mutations (FLT3-MUs), 24 with internal tandem duplications (ITDs) and 12 with activati

154 Internal tandem duplications (ITDs) are found in approxi

155 Fetal liver tyrosine kinase 3 (FLT3) internal tandem duplications (ITDs) are powerful adverse

156 e we report on the identification of somatic internal tandem duplications (ITDs) clustering in the C

157 acute myeloid leukemia (AML) harboring FLT3 internal tandem duplications (ITDs) have poor outcomes,

158 Internal tandem duplications (ITDs) in the FLT3 receptor

159 FLT3 is constitutively activated by internal tandem duplications (ITDs) in the juxtamembrane

160 Internal tandem duplications (ITDs) in the juxtamembrane

161 About 30 to 35% of patients have either internal tandem duplications (ITDs) in the juxtamembrane

162 s in a subset of patients harboring atypical internal tandem duplications (ITDs) in the tyrosine kina

163 loid leukemia have constitutively activating internal tandem duplications (ITDs) of the FLT3 receptor

164 Internal tandem duplications (ITDs) of the FMS-like tyro

165 FLT3 mutations, either internal tandem duplications (ITDs) or aspartate residue

166 ut one of the FLT3 (46 of 47) mutations were internal tandem duplications (ITDs) within exons 11 and

167 The clinical impact of FLT3-internal tandem duplications (ITDs), an adverse prognost

168 of allelic ratio and insertion site (IS) of internal tandem duplications (ITDs), as well as concurre

169 f the juxtamembrane autoregulatory domain by internal tandem duplications (ITDs).

170 imately one-third of AML patients, mostly by internal tandem duplications (ITDs).

171 (AML) harboring NPM1 mutations without FLT3-internal tandem duplications (ITDs; NPM1-positive/FLT3-I

172 ow-level MRD before alloSCT, those with FLT3 internal tandem duplications(ITDs) had significantly poo

173 bone marrow that are Flt3 wild-type or Flt3 internal tandem duplication mutant.

174 e in vivo consequences of an activating FLT3 internal tandem duplication mutation (FLT3-ITD), we crea

175 ients with acute myeloid leukemia (AML) with internal tandem duplication mutation in the FMS-like tyr

176 ange from heterozygosity to homozygosity for internal tandem duplication mutation of FLT3 (FLT3 ITD).

177 outcomes for patients with AML harboring an internal tandem duplication mutation of FLT3 (FLT3-ITD)

178 L cells that possess an M5 subtype with FLT3-internal tandem duplication mutation.

179 k cytogenetic abnormalities and/or FLT3-ITD (internal tandem duplication) mutation, or with secondary

180 Based on fms-like tyrosine kinase-3-internal tandem duplication mutational status; the Delta

181 , 15 (37%) had FMS-related tyrosine kinase 3 internal tandem duplication mutations (FLT3-ITD+), which

182 leukemia (AML) patients with activating FLT3 internal tandem duplication mutations at the time of acq

183 Internal tandem duplication mutations in FLT3 are common

184 kinase 1 (CDK1) pathway is also affected by internal tandem duplication mutations in FLT3.

185 Internal tandem duplication mutations in the Flt3 tyrosi

186 Internal tandem duplication mutations of FLT3 (FLT3/ITD

187 Internal tandem duplication mutations of the FLT3 kinase

188 with acute myeloid leukemia (AML) harboring internal tandem duplication mutations of the FLT3 recept

189 tween lestaurtinib and control: 74% had FLT3-internal tandem duplication mutations, 23% FLT3-tyrosine

190 n patients with normal karyotype and no FLT3 internal tandem duplication (n = 148), the 3-year RFS ra

191 O in female, younger (<= 70 years), and FLT3 internal tandem duplication-negative patients with respe

192 ears), molecular low-risk (NPM1-mutated/FLT3-internal tandem duplication-negative) IDH1-mutated patie

193 SNP-A improved the predictive value of Flt-3 internal tandem duplication/NPM-1 status, with inferior

194 ortantly, there were no interactions by FLT3/internal tandem duplications, NPM1, or CEBPA mutation.

195 An internal tandem duplication of the Flt3 gene (Flt3/ITD)

196 significance have been discovered, including internal tandem duplication of the FLT3 gene, mutations

197 Internal tandem duplication of the Fms-like tyrosine kin

198 Internal tandem duplication of the FMS-like tyrosine kin

199 tations of the FLT3 gene occur because of an internal tandem duplication of the juxta-membrane domain

200 UT-7 cell proliferation induced by oncogenic internal tandem duplications of Flt3.

201 ing techniques we generated randomly located internal tandem duplications of random size within Staph

202 tic cell transplant, the persistence of FLT3 internal tandem duplication or NPM1 variants in the bloo

203 P < .0001), NPM1 mutations (P < .0001), FLT3 internal tandem duplications (P < .0001), and IDH1/2 mut

204 each); and NPM1 mutations (P < .0001), FLT3 internal tandem duplications (P < .0001), and tyrosine k

205 h wild-type NPM1 (P < .001), absence of FLT3-internal tandem duplications (P = .002), mutated CEBPA (

206 and mutation status of NPM1, CEBPA, and FLT3-internal tandem duplication, patients were classified in

207 ric SHP2 inhibitor SHP099 from two FLT3-ITD (internal tandem duplication)-positive AML cell lines.

208 1 years, respectively; P < .001), lower FLT3 internal tandem duplication prevalence (4% v 21%, respec

209 mained significant after adjustment for FLT3-internal tandem duplication status.

210 FLT3-internal tandem duplication was most frequent, and 29% o

211 After excluding patients with FLT3 internal tandem duplications, we compared treatment outc

212 sion patterns for FMS-like tyrosine kinase 3-internal tandem duplication were also identified.

213 ry rather than newly diagnosed AML, and FLT3 internal tandem duplication were associated with relapse

214 togenetics, NPM1 (HR, 0.57; P = .0004), FLT3 internal tandem duplications with low (HR, 1.85; P = .00