ライフサイエンスコーパス: tandem duplication

1 mutations had AML-M0 subtype and MLL-partial tandem duplication.

2 ge part to expansion of a few subfamilies by tandem duplication.

3 the genome duplication by genomically local tandem duplication.

4 nts without a concomitant FLT3 gene internal tandem duplication.

5 ate genome-wide rates of large deletions and tandem duplications.

6 ding the subgroup positive for FLT3 internal tandem duplications.

7 lts in a unique specificity, generating only tandem duplications.

8 000 additional SVs, including insertions and tandem duplications.

9 are mostly derived from whole genome and/or tandem duplications.

10 s associated with loss of heterozygosity and tandem duplications.

11 ally and that most amplifications are due to tandem duplications.

12 ranchiostoma was observed, largely driven by tandem duplications.

13 which can detect partial, large and complex tandem duplications.

14 A gamma locus tandem duplication (5'-gamma(1)-gamma(2)-3') triggered g

15 gements include 5 interstitial deletions, 14 tandem duplications, 7 terminal deletions and 13 complex

16 These expansions are largely due to tandem duplication, a possible adaptation mechanism enab

17 tor of Fms tyrosine kinase-3 (FLT3) internal tandem duplication, a validated therapeutic target in hu

18 We identified 33 hotspots of large (>100 kb) tandem duplications, a mutational signature associated w

19 ngle-copy gene in transgenic Drosophila This tandem duplication also exhibits greater activity than t

20 ologous recombination sites for a 113,260-bp tandem duplication and an inversion.

21 e first CaML, and the gene family evolved by tandem duplication and divergence.

22 fuse astrocytoma grade II demonstrated MYBL1 tandem duplication and few other events.

23 tion within the cytogenetic or FLT3-internal tandem duplication and NPM1 gene mutation subgroups.

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

25 riate analysis, which included FLT3 internal tandem duplication and NPM1 mutation status, the presenc

26 Four prognostic biomarkers-the internal tandem duplication and point mutations in the FLT3 gene,

27 s suggest a link between stress response and tandem duplication and provide an explanation for why a

28 It appears that tandem duplication and random inactivation of duplicate

29 to C. briggsae is due to multiple rounds of tandem duplication and translocation of individual genes

30 0% of the interstitial deletions, 46% of the tandem duplications and 50% of the CGRs, indicating that

31 s underlying phenotypic variation, including tandem duplications and a transposable element insertion

32 with known mechanisms of duplication such as tandem duplications and breakage/fusion/bridge (B/F/B) c

33 There were data on FLT3 internal tandem duplications and NPM1 mutations (n = 592), CEBPA

34 the last two million years by at least three tandem duplications and one retrotransposition event.

35 redicting insertions, deletions, inversions, tandem duplications and translocations at base-pair reso

36 Genome structural variations, including tandem duplications and translocations of genes, interru

37 air events after minimal repair included MLL tandem duplications and translocations, with minor popul

38 mal transcripts, including two from internal tandem duplications and two fusion transcripts created b

39 rrangement junctions for a large deletion, a tandem duplication, and a translocation.

40 -risk and normal cytogenetics, FLT3 internal tandem duplication, and NPM1, PTPN11, and IDH2 mutations

41 e from a process of genome-wide duplication, tandem duplication, and segmental duplication followed b

42 yntenic gene families are prone to deletion, tandem duplication, and transposition.

43 , 26% are insertions of unlinked DNA, 9% are tandem duplications, and 6% are inversions.

44 olved in chromosomal translocations, partial tandem duplications, and amplifications, all of which re

45 NPM1, CEBPA, and WT1 mutations, MLL partial tandem duplications, and BAALC and ERG expression.

46 dem and mixed-lineage leukemia (MLL) partial-tandem duplications, and clinically significant chromoso

47 resulted from both amplification, largely by tandem duplications, and contraction by gene losses.

48 cluding chromosomal translocations, internal tandem duplications, and mutations, have been described

49 ant majority of illegitimate events were MLL tandem duplications, and several deletions, inversions,

50 We found that tandem duplications appear to be early events in tumor e

51 1, Lcn12, and Lcn13, that evolved by in situ tandem duplication are present on the same locus.

52 oximately 10-kilobase microhomology-mediated tandem duplications are abundant in the genomes of BRCA1

53 Tandem duplications are among the most common mutation e

54 l mapping of Danio rerio genes indicate that tandem duplications are an unlikely mechanism for genera

55 rearrangement architectures are present, but tandem duplications are particularly common in some canc

56 , as observed in humans, tandem or partially tandem duplications are the dominant form of insertion (

57 ct, RAPTR-SV showed superior sensitivity for tandem duplications, as it identified 2-fold more duplic

58 riking similarity to the common BRAF fusion, tandem duplication at 3p25 was observed, which produces

59 , but not BRCA2, suppresses the formation of tandem duplications at a site-specific chromosomal repli

60 e against cells expressing the Flt3 internal tandem duplication, BCR-ABL, MN1, and an shRNA against p

61 mplate switching, the latter forming complex tandem duplication breakpoints.

62 ogether with a concurrent FLT3-ITD (internal tandem duplication), confers resistance to the FLT3 prot

63 3 cells stably transduced with FLT3-internal tandem duplications containing a G697R mutation that con

64 y a single gene insertion/deletion and local tandem duplications differing between the regions.

65 five representative BCG strains of the four tandem duplication (DU) groups.

66 ) that occurred first and a subsequent large tandem duplication, dupIS186, bearing the genes acrAB an

67 enotype NPM1 wild-type/FLT3 without internal-tandem duplications (EFS, 18% +/- 5 vs 40% +/- 7; Cox P

68 A tandem duplication event, located on chromosome 17 in a

69 , duplC-ATLs, which arose from segmental and tandem duplication events in Brassicaceae.

70 Tandem duplication events in the last common ancestor ap

71 all genomes, as well as evidence for recent tandem duplication events in the zebrafish, indicating t

72 entification of 22 duplicated blocks and six tandem duplication events.

73 the total gene content in plants arose from tandem duplications events, which often result in paralo

74 monophyletic groups of SCNA genes, and that tandem duplications expanded the number of genes in two

75 Tandem duplications explain most of the rest.

76 turation mutagenesis screen of FLT3-internal tandem duplication failed to recover any resistant colon

77 ermined significant iHR activity in internal tandem duplication FLT3 (FLT3-ITD) and JAK2V617F-mutated

78 ith the prognostically adverse FLT3 internal tandem duplication (FLT3 ITD) potentially explained the

79 bate depletion cooperated with Flt3 internal tandem duplication (Flt3(ITD)) leukaemic mutations to ac

80 The FLT3 Internal Tandem Duplication (FLT3(ITD)) mutation is common in adu

81 r molecular risk patients with FLT3-internal tandem duplication (FLT3-ITD) and/or NPM1 wild-type, whe

82 Risk associated to FLT3 internal tandem duplication (FLT3-ITD) in patients with acute mye

83 FLT3 internal tandem duplication (FLT3-ITD) is an activating mutation

84 eukemia (AML) that harbors the FLT3-internal tandem duplication (FLT3-ITD) mutation.

85 t common type of FLT3 mutation, the internal tandem duplication (FLT3-ITD) mutation.

86 FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) mutations in acute myeloid

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

88 ave a constitutively activated FLT3-internal tandem duplication (FLT3-ITD), and these patients exhibi

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

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

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

92 Using FLT3 internal tandem duplication (FLT3/ITD) as a molecular marker, we

93 ute myeloid leukemia (AML) and FLT3/internal tandem duplication (FLT3/ITD) have poor prognosis if tre

94 FLT3 internal tandem duplication (FLT3/ITD) is a common somatic mutati

95 tor (TKI) with activity against the internal tandem duplication (FLT3/ITD) mutants and the FLT3/D835

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

97 te myeloid leukemia (AML) harboring internal tandem duplication (FLT3/ITD) mutations.

98 otent activity to date against FLT3 internal tandem duplication (FLT3/ITD) mutations.

99 kemia (AML) with low levels of FLT3 internal tandem duplications (FLT3(ITD)) do not have a worse prog

100 adjustment for WT1 mutations, FLT3 internal tandem duplications (FLT3-ITD), and high ERG expression;

101 e assessed for the presence of FLT3 internal tandem duplications (FLT3-ITD), FLT3 tyrosine kinase dom

102 NPM1 mutations (NPM1(mut)) and FLT3 internal tandem duplications (FLT3-ITD).

103 FLT3 internal tandem duplications (FLT3/ITDs) in the juxtamembrane dom

104 T3 gene (FMS-like tyrosine kinase 3-internal tandem duplication [FLT3-ITD]), causing constitutive kin

105 PA and/or mutated NPM1 without FLT3 internal tandem duplication [FLT3-ITD]), TET2-mutated patients ha

106 The impact of a FLT3-internal tandem duplication (FLT3ITD) on prognosis of patients wi

107 that this family expanded from segmental and tandem duplications following a tetraploidization event.

108 double-stranded DNA breaks, indicating that tandem duplications form specifically at stalled forks.

109 r, implicating misrepair of these lesions in tandem duplication formation.

110 niquely required for the de novo creation of tandem duplications from noniterated sequence.

111 Tandem duplications had a similar size distribution sugg

112 In some cases, amplification and tandem duplication have occurred with genes suspected of

113 tion of synteny indicated that segmental and tandem duplications have contributed greatly to the expa

114 Notably, these tandem-duplication hotspots were enriched in breast canc

115 NMT3A loss synergizes with the FLT3 internal tandem duplication in a dose-influenced fashion to gener

116 ved in chromosomal translocations or partial tandem duplication in acute leukemia.

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

118 ndem duplication in FLT3 (FLT3-ITD), partial tandem duplication in MLL (MLL-PTD), and mutations in AS

119 ponsiveness is correlated with the degree of tandem duplication in RLK/Pelle subfamilies.

120 n ancestor of Brassicales, before undergoing tandem duplication in the ancestor of Brassicaceae.

121 individuals in this family carried a partial tandem duplication in the elastin locus.

122 An internal tandem duplication in the fms-like tyrosine kinase 3 gen

123 isk molecular features--that is, an internal tandem duplication in the fms-related tyrosine kinase 3

124 y of homologous recombination leading to MYB tandem duplication in the peripheral blood mononuclear c

125 lassical okra leaf shape allele has a 133-bp tandem duplication in the promoter, correlated with elev

126 African and Norwegian families is caused by tandem duplications in a non-coding genomic region conta

127 cause of an expansion of the F-box genes via tandem duplications in Arabidopsis and Oryza.

128 Tandem duplications in BRCA1 mutant cells arise by a rep

129 has expanded to a four-member gene family by tandem duplications in cattle; all four genes are transc

130 with 119 CNVs and found that most (83%) were tandem duplications in direct orientation.

131 CD25 was positively correlated with internal tandem duplications in FLT3 (FLT3-ITD), DNMT3A, and NPM1

132 aled rearrangements inconsistent with simple tandem duplications in four patients.

133 ion is strongly associated with 10 kilobase tandem duplications in ovarian cancer.

134 ed with selected mutations, such as internal tandem duplications in the FLT3 gene (FLT3-ITD) and muta

135 Tandem duplications in the TRIM5alpha B30.2 domain v1 re

136 ts region of P. albomaculatus consists of 53 tandem duplications (including one partial repeat), whic

137 that these genes expanded through sequential tandem duplications independently of genes from cacao an

138 changes in H3K27me3 and gene expression than tandem duplications, indicating that local chromatin con

139 Recurrent tandem duplications intersecting with a TAD boundary med

140 xtensions allowing the application of AGE to tandem duplications, inversions and complex events invol

141 Tandem duplications involving the BRAF kinase gene have

142 d an increase in intracellular FLT3/internal tandem duplication (ITD) accumulation.

143 FLT3 internal tandem duplication (ITD) and nucleophosmin mutations occ

144 on in acute myeloid leukemia is the internal tandem duplication (ITD) in FLT3, the receptor for cytok

145 e tyrosine kinase-3 receptor (FLT3) internal tandem duplication (ITD) is found in 30% of acute myeloi

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

147 Constitutive activation of FLT3 by internal tandem duplication (ITD) is one of the most common molec

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

149 inical evidence has shown that FLT3 internal tandem duplication (ITD) mutation confers poor prognosis

150 FMS-like tyrosine kinase-3 (FLT3)-internal tandem duplication (ITD) mutation was detected in 40 (93

151 the tyrosine kinase domain (TKD) or internal tandem duplication (ITD) mutation with either a high rat

152 use of the correlation between FLT3 internal tandem duplication (ITD) mutations and poor prognosis in

153 FLT3 kinase internal tandem duplication (ITD) mutations are common in acute m

154 ndem duplication (PTD) and the FLT3 internal tandem duplication (ITD) mutations associate with a poor

155 Activating internal tandem duplication (ITD) mutations in FLT3 (FLT3-ITD) ar

156 yeloid leukemia (AML) patients with internal tandem duplication (ITD) mutations in FLT3.

157 Internal tandem duplication (ITD) mutations in the FLT3 tyrosine

158 tions in acute myeloid leukemia are internal tandem duplication (ITD) mutations in the juxtamembrane

159 MS-like tyrosine kinase 3 (FLT3) by internal tandem duplication (ITD) mutations is one of the most co

160 The internal tandem duplication (ITD) mutations of the FMS-like tyros

161 Internal tandem duplication (ITD) mutations within the FMS-like t

162 ia (AML) patients and, at least for internal tandem duplication (ITD) mutations, are associated with

163 loid leukemia (AML) containing FLT3 internal tandem duplication (ITD) mutations.

164 In acute myeloid leukemia (AML), internal tandem duplication (ITD) of FLT3 at the juxtamembrane (J

165 Internal tandem duplication (ITD) of fms-like tyrosine kinase 3 (

166 Internal tandem duplication (ITD) of the fms-related tyrosine kin

167 Somatic mutations of FLT3 involving internal tandem duplication (ITD) of the juxtamembrane domain or

168 leukemia (AML)-related mutant FLT3 internal tandem duplication (ITD) protein.

169 ukemia AML patients with known FLT3 internal tandem duplication (ITD) status for FLT3/TKDs; they were

170 TRA and FLT3 TKIs to eliminate FLT3/internal tandem duplication (ITD)(+) LSCs.

171 ith normal cytogenetics [e.g., FLT3-internal tandem duplication (ITD)+].

172 harmacologic inhibition of the Flt3 internal tandem duplication (ITD), a mutated receptor tyrosine ki

173 mal karyotype, the presence of FLT3-internal tandem duplication (ITD), and a < 4-log reduction in PB-

174 cterized for BAALC expression, FLT3 internal tandem duplication (ITD), and MLL partial tandem duplica

175 The most common type, internal tandem duplication (ITD), confers poor prognosis.

176 within coding exons, referred to as internal tandem duplication (ITD), remains challenging due to ine

177 ave recently demonstrated that FLT3-internal tandem duplication (ITD), when localized to the biosynth

178 t Fms-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD), which mediate resistance to ac

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

180 the N-oxide potently inhibited FLT3-internal tandem duplication (ITD; binding constant, 70 nmol/L) an

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

182 ) and frequently co-occur with FLT3 internal tandem duplications (ITD) or, less commonly, NRAS or KRA

183 Internal tandem duplications (ITDs) are found in approximately 25

184 etal liver tyrosine kinase 3 (FLT3) internal tandem duplications (ITDs) are powerful adverse prognost

185 rt on the identification of somatic internal tandem duplications (ITDs) clustering in the C terminus

186 Internal tandem duplications (ITDs) in the FLT3 receptor tyrosine

187 emia have constitutively activating internal tandem duplications (ITDs) of the FLT3 receptor tyrosine

188 Internal tandem duplications (ITDs) of the FMS-like tyrosine kina

189 The clinical impact of FLT3-internal tandem duplications (ITDs), an adverse prognostic marker

190 ic ratio and insertion site (IS) of internal tandem duplications (ITDs), as well as concurrent gene m

191 ne-third of AML patients, mostly by internal tandem duplications (ITDs).

192 tamembrane autoregulatory domain by internal tandem duplications (ITDs).

193 rboring NPM1 mutations without FLT3-internal tandem duplications (ITDs; NPM1-positive/FLT3-ITD-negati

194 ay activation in PAs, particularly through a tandem duplication leading to an oncogenic BRAF fusion g

195 The clinical impact of MLL partial tandem duplication (MLL-PTD) was evaluated in 238 adults

196 nsferase, the mixed lineage leukemia partial tandem duplication (MLL-PTD), exhibits increased global

197 te myeloid leukemia (AML) is through partial tandem duplication (MLL-PTD); however, the mechanism by

198 ase domain mutations (FLT3-TKD), MLL partial tandem duplications (MLL-PTD), NPM1 and CEBPA mutations,

199 row that are Flt3 wild-type or Flt3 internal tandem duplication mutant.

200 consequences of an activating FLT3 internal tandem duplication mutation (FLT3-ITD), we created a tra

201 heterozygosity to homozygosity for internal tandem duplication mutation of FLT3 (FLT3 ITD).

202 hat possess an M5 subtype with FLT3-internal tandem duplication mutation.

203 Parental cell lines carry the FLT3-ITD (tandem duplication) mutation and are highly responsive t

204 etic abnormalities and/or FLT3-ITD (internal tandem duplication) mutation, or with secondary AML bene

205 ) had FMS-related tyrosine kinase 3 internal tandem duplication mutations (FLT3-ITD+), which were dif

206 (AML) patients with activating FLT3 internal tandem duplication mutations at the time of acquired res

207 Internal tandem duplication mutations in FLT3 are common in acute

208 (CDK1) pathway is also affected by internal tandem duplication mutations in FLT3.

209 Internal tandem duplication mutations in the Flt3 tyrosine kinase

210 Internal tandem duplication mutations of FLT3 (FLT3/ITD mutations

211 Internal tandem duplication mutations of the FLT3 kinase (FLT3/IT

212 te myeloid leukemia (AML) harboring internal tandem duplication mutations of the FLT3 receptor (FLT3/

213 taurtinib and control: 74% had FLT3-internal tandem duplication mutations, 23% FLT3-tyrosine kinase d

214 s with normal karyotype and no FLT3 internal tandem duplication (n = 148), the 3-year RFS rates in th

215 lecular low-risk (NPM1-mutated/FLT3-internal tandem duplication-negative) IDH1-mutated patients had s

216 gh frequency of diverse and novel 50-bp unit tandem duplications not found in chicken or mammals.

217 roved the predictive value of Flt-3 internal tandem duplication/NPM-1 status, with inferior survival

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

219 We conclude that Alu-mediated MYB tandem duplication occurs at low frequency during normal

220 diversification appears to have occurred by tandem duplication of a multigene cassette that was not

221 ndle domains, each of which derived from the tandem duplication of a primitive helix-strand-helix uni

222 Some clusters also emerged by tandem duplication of a single microRNA.

223 The alpha(D)-globin gene originated via tandem duplication of an embryonic alpha-like globin gen

224 of eukaryotic SWEETs may not have evolved by tandem duplication of an open reading frame, but rather

225 We also show that tandem duplication of an unrelated synthetic reporter ge

226 22Rv1 cells was linked to a 35-kb intragenic tandem duplication of AR exon 3 and flanking sequences.

227 quences confirmed the occurrence of a simple tandem duplication of defensin7 with sequence identity a

228 yses indicate that CvAOX has 10 exons with a tandem duplication of exon 10, and 3' alternative splici

229 In addition, tandem duplication of genes in an OG tends to be highly

230 The partial tandem duplication of MLL (MLL-PTD) is found in 5% to 10

231 A unique tandem duplication of Rca gene occurred in a common gras

232 Evidence is presented that the tandem duplication of related genes acts as a driving ev

233 A naturally occurring tandem duplication of the Alcohol dehydrogenase (Adh) ge

234 e expansion in the mosquito is the result of tandem duplication of the fibrinogen domain.

235 nce have been discovered, including internal tandem duplication of the FLT3 gene, mutations in the NP

236 Internal tandem duplication of the FMS-like tyrosine kinase (FLT3

237 Internal tandem duplication of the Fms-like tyrosine kinase-3 rec

238 sis of the sdhA and sdhB genes suggested the tandem duplication of the genes in conserved and may be

239 f the FLT3 gene occur because of an internal tandem duplication of the juxta-membrane domain (FLT3/IT

240 n insertion in the promoter in addition to a tandem duplication of the kn1 locus.

241 T3 gene, mutations in the NPM1 gene, partial tandem duplication of the MLL gene, high expression of t

242 nd point mutations in the FLT3 gene, partial tandem duplication of the MLL gene, mutations of the CEB

243 s a silencing protein was facilitated by the tandem duplication of the OIR domain in the Sir1 family,

244 agment at its endogenous locus to generate a tandem duplication of the region.

245 is highly efficient integration results in a tandem duplication of the target locus, which is then re

246 ns, suggesting that tRNase Z(L) arose from a tandem duplication of tRNase Z(S) followed by interdepen

247 gian families, we identified two overlapping tandem duplications of 7.67 kb (South Africans) and 15.9

248 at MFS transporters evolved from a series of tandem duplications of an ancestral 3-TM unit.

249 proliferation induced by oncogenic internal tandem duplications of Flt3.

250 Surprisingly, AMLs containing partial tandem duplications of MLL failed to cluster with MLL ch

251 We demonstrate a functional trajectory of tandem duplications of these motifs leading to monomeric

252 ability pattern characterized by hundreds of tandem duplications of up to 10 megabases (Mb) in size.

253 Here, we show that tandem duplication often results in more than double the

254 The fusion, caused by tandem duplication on 4p16.3, led to the loss of the 3'-

255 uence of duplication mechanism, particularly tandem duplication, on duplicate retention has not been

256 reakpoints; four gene fusions were formed by tandem duplications, one by two interconnected duplicati

257 K-Ras proteins containing this tandem duplication or a similar five amino acid E62_A66d

258 gh homology to each other, suggesting recent tandem duplication or transposition.

259 dent formation incidences, are predominantly tandem duplications or complex gains, exhibit breakpoint

260 site of insertion and from a distribution of tandem duplications or deletions of a portion of the MBP

261 e rearrangement signatures, characterized by tandem duplications or deletions, appear associated with

262 number gains detected by array CGH represent tandem duplications or unbalanced insertions.

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

264 nd NPM1 mutations (P < .0001), FLT3 internal tandem duplications (P < .0001), and tyrosine kinase dom

265 pe NPM1 (P < .001), absence of FLT3-internal tandem duplications (P = .002), mutated CEBPA (P = .01),

266 ion status of NPM1, CEBPA, and FLT3-internal tandem duplication, patients were classified into the fo

267 early demonstrated that species-specific and tandem duplications played important roles in expansion

268 respectively; P < .001), lower FLT3 internal tandem duplication prevalence (4% v 21%, respectively; P

269 The coexpression of the MLL partial tandem duplication (PTD) and the FLT3 internal tandem du

270 al tandem duplication (ITD), and MLL partial tandem duplication (PTD) and uniformly treated on Cancer

271 The MLL-partial tandem duplication (PTD) associates with high-risk cytog

272 nd HTRX1), consisting of an in-frame partial tandem duplication (PTD) of exons 5 through 11 in the ab

273 MLL (ALL-1) chimeric fusions and MLL partial tandem duplications (PTD) may have mechanistically disti

274 Tandem duplication repeats, which represent 26 out of th

275 gnificant after adjustment for FLT3-internal tandem duplication status.

276 ention in a single-lineage fashion following tandem duplication, suggesting that these tandem duplica

277 ally, a striking bias toward 31-bp partially tandem duplications suggests that errors in nucleotide e

278 on (CD), and to a much lesser extent that of tandem duplications (TDs), to distinguish between sun-pr

279 P) characterized by frequent and distributed tandem duplications (TDs).

280 is clear that genes in OGs that expanded via tandem duplication tend to be involved in responses to e

281 he Cit(+) trait originated in one clade by a tandem duplication that captured an aerobically expresse

282 The maize A1-b haplotype is a tandem duplication that consists of the components, alph

283 We identified a tandem duplication that duplicates exons 3-8 of CHD7 in

284 ions are organized into discrete clusters of tandem duplications that show depletion of genes and tra

285 The sequence identifies a number of tandem duplications that, by the nature of the duplicate

286 tion slippage is a plausible explanation for tandem duplications, the end homology required in such a

287 predicted protein-coding genes, 34% occur in tandem duplications, the largest proportion thus far in

288 But dispersed copies gave rise to tandem duplications through uneven expansion and gene si

289 ral genomes indicated that they expanded via tandem duplications to form extant propellers.

290 tion of whole genome duplications (WGDs) and tandem duplications to the observed diversity of genes i

291 sembly dominated, whereas subsequently, upon tandem duplication, tradeoffs between monomer stability

292 Tandem duplication was a major force in expanding B. dis

293 FLT3-internal tandem duplication was most frequent, and 29% of patient

294 After excluding patients with FLT3 internal tandem duplications, we compared treatment outcome of 16

295 erns for FMS-like tyrosine kinase 3-internal tandem duplication were also identified.

296 than newly diagnosed AML, and FLT3 internal tandem duplication were associated with relapse, their p

297 Tandem duplications were characterized by a bimodal ( ap

298 nts outside these regions, notably including tandem duplications, were also observed.

299 recision, as it recovered 66.4% of simulated tandem duplications with a precision of 99.2%.

300 Detection of tandem duplication within coding exons, referred to as i