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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 FLT3 internal tandem duplication (ITD) and nucleophosmin muta

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

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

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

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

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

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

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

65 Internal tandem duplication (ITD) in the juxtamembrane p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 Internal tandem duplication (ITD) mutations in the FLT3

82 3 activating mutations have been identified: internal tandem duplication (ITD) mutations in the juxta

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

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

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

86 Internal tandem duplication (ITD) mutations of the juxta

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

88 Internal tandem duplication (ITD) mutations of the recep

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

90 Internal tandem duplication (ITD) mutations within the F

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 Internal tandem duplications (ITDs) are found in approxi

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

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

122 Internal tandem duplications (ITDs) in the FLT3 receptor

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

124 Internal tandem duplications (ITDs) in the juxtamembrane

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 , 15 (37%) had FMS-related tyrosine kinase 3 internal tandem duplication mutations (FLT3-ITD+), which

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

142 Internal tandem duplication mutations in FLT3 are common

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

144 Internal tandem duplication mutations in the Flt3 tyrosi

145 Internal tandem duplication mutations of FLT3 (FLT3/ITD

146 Internal tandem duplication mutations of the FLT3 kinase

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

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

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

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

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

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

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

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

155 Internal tandem duplication of the Fms-like tyrosine kin

156 Internal tandem duplication of the FMS-like tyrosine kin

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

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

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

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

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

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

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

164 1 years, respectively; P < .001), lower FLT3 internal tandem duplication prevalence (4% v 21%, respec

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

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

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

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

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