ライフサイエンスコーパス: gene rearrangement

1 brief period following successful Ig H chain gene rearrangement.

2 locus contraction needed for distal variable gene rearrangement.

3 lease, which are both required for IgL chain gene rearrangement.

4 s sufficient only for proximal V(H) to DJ(H) gene rearrangement.

5 first thymocytes to express the products of gene rearrangement.

6 ip between CD127 expression/signaling and Ig gene rearrangement.

7 ion of gene expression, DNA replication, and gene rearrangement.

8 rmline transcription as well as Ig lambda VJ gene rearrangement.

9 e J lambda region, and activate Ig lambda VJ gene rearrangement.

10 their specificity by secondary H or L chain gene rearrangement.

11 tes Igkappa gene expression and SHM, but not gene rearrangement.

12 mcy share an invariant Vbeta8.2-Jbeta2.3 TCR gene rearrangement.

13 ice are determined by factors other than TCR gene rearrangement.

14 oliferation that is temporally distinct from gene rearrangement.

15 R signaling to induce both proliferation and gene rearrangement.

16 and frequently associated with the EGFRvIII gene rearrangement.

17 d thymus weight loss and stimulated TCRalpha gene rearrangement.

18 de the context of normal lymphocyte receptor gene rearrangement.

19 induction of the machinery that mediates Ig gene rearrangement.

20 ents with cytogenetic data, 26 (79%) had MLL gene rearrangement.

21 cessibility conducive to subsequent targeted gene rearrangement.

22 for studying mechanisms of recombination and gene rearrangement.

23 t for the vast majority of kappa light-chain gene rearrangement.

24 are essential for effecting antigen receptor gene rearrangement.

25 fic regulation of immunoglobulin heavy chain gene rearrangement.

26 lowing successful immunoglobulin heavy chain gene rearrangement.

27 g pre-B cells for immunoglobulin light chain gene rearrangement.

28 ant loss of RAG1/2-mediated antigen receptor gene rearrangement.

29 genic DNA lesions elicited by RAG1/2-induced gene rearrangement.

30 in the germline or generated somatically by gene rearrangement.

31 of NKX3.1 as a suppressor of the pathogenic gene rearrangement.

32 in genes required for T- and B-cell receptor gene rearrangement.

33 of entrectinib, regardless of tumour type or gene rearrangement.

34 lone-specific T-cell receptor/immunoglobulin gene rearrangements.

35 nd molecular studies demonstrated clonal IgH gene rearrangements.

36 n redifferentiated after triggering Iglambda gene rearrangements.

37 revealed additional candidate mutations and gene rearrangements.

38 alysis of immunoglobulin and T-cell receptor gene rearrangements.

39 ed degenerate RT-PCR to identify clonal Tcrb gene rearrangements.

40 a key component of the T4SS and can undergo gene rearrangements.

41 tion codons (PTCs) as a result of programmed gene rearrangements.

42 such as CD3 staining, or clonal Tcrb or Igh gene rearrangements.

43 on of the first products of antigen receptor gene rearrangements.

44 ours characterized by the non-random EWS-ETS gene rearrangements.

45 kemia, including the high frequency of KMT2A gene rearrangements.

46 s a transposase that mediates immunoglobulin gene rearrangements.

47 l of a B or T cell precursor during receptor gene rearrangements.

48 te leukemias, notably those with KMT2A (MLL) gene rearrangements.

49 is necessary for selection of productive IgH gene rearrangements.

50 a diverse antibody repertoire by undergoing gene rearrangements.

51 ypermutation in 71/79 (89.8%) IGHV-IGHD-IGHJ gene rearrangements.

52 FR) gene or anaplastic lymphoma kinase (ALK) gene rearrangements.

53 as analysis of several sequential human TCR gene rearrangements.

54 42, and all had clonal T-cell receptor (TCR) gene rearrangements.

55 e formation for lineage and stage specific V gene rearrangement [2,3,4(*),5,6(*)].

56 nmutated immunoglobulin heavy chain variable gene rearrangement, 58% with del(17p) by fluorescence in

57 on was particularly high in samples with MLL gene rearrangements (82%, n = 11; P = .0005), high hyper

58 s from highly expressed ROS1 gene instead of gene rearrangement, a phenomenon distinct from other can

59 e fusions, 57% of which are cryptic adjacent gene rearrangements (AGRs).

60 lso demonstrate a simple protocol to use the gene rearrangement algorithm to improve gene tree parsim

61 MRD) by real-time PCR directed to TCR and Ig gene rearrangements allows a refined evaluation of respo

62 ing wild-type p53 due to a point mutation or gene rearrangement also failed to senesce in response to

63 erived from purified lymphocytes, as well as gene rearrangement analysis, we found that committed som

64 the role of promoters in regulating variable gene rearrangement and allelic exclusion, we constructed

65 For infants with the MLL gene rearrangement and an appropriate donor, HSCT was th

66 itional ablation of TRIM28 impaired TCRalpha gene rearrangement and compromised the development of al

67 f syntenic conservation and species-specific gene rearrangement and duplication and gives an insight

68 d diagnostic method for the detection of ALK gene rearrangement and expression and particularly the m

69 Upon productive VH-DJH gene rearrangement and expression of a mu heavy chain, h

70 ncides with the onset of endogenous TCRalpha gene rearrangement and expression.

71 arranged gene transcription, lower levels of gene rearrangement and histone H3 acetylation, and marke

72 -B cells are greatly impaired in distal V(H) gene rearrangement and Igh locus compaction, and we demo

73 d pre-TCR checkpoint with failure of TCRbeta gene rearrangement and increased apoptosis, resulting in

74 k events, the second is dominated by somatic gene rearrangement and mutation and cell selection, and

75 revious studies (rRNA, ftsZ) indicating that gene rearrangement and operon fragmentation are common i

76 its catalytic activities, is required for Ig gene rearrangement and production of B cell receptors (B

77 antigen receptors instead promote continued gene rearrangement and receptor editing.

78 ells are a common and natural product of TCR gene rearrangement and thymocyte development.

79 iously shown to impair T cell receptor (TCR) gene rearrangement and to cause a partial block in CD4(+

80 on yeast, such patterns result from directed gene rearrangements and chromosomally inherited epigenet

81 ly specific V(D)J recombinase TCRbeta immune gene rearrangements and coding joint processing at RSS i

82 e pre-BCR from inducing additional Igl chain gene rearrangements and driving pre-B cells with RAG DSB

83 Thus, despite several gene rearrangements and duplications, these data indicat

84 ctice has led to identification of recurrent gene rearrangements and fusions in a variety of tumors.

85 e succumbed to lymphoid tumors containing Ig gene rearrangements and immunophenotypes characteristic

86 ertion of complete cassettes of genes and of gene rearrangements and insertions of DNA within genes,

87 Immunoglobulin (Ig) gene rearrangements and oncogenic translocations are rou

88 algorithm designed to fully characterize Ig gene rearrangements and oncogenic translocations from sh

89 view the data currently available on both Ig gene rearrangements and protein patterns seen in myeloma

90 pe of Notch-independent T-ALLs that bear Myc gene rearrangements and Pten mutations.

91 IgVH gene rearrangements and selection of the IgH repertoire

92 e cancers with mutant SPOP lacked ETS family gene rearrangements and showed a distinct pattern of gen

93 induce specific signatures of immunoglobulin gene rearrangements and that pathogen exposure can poten

94 Studies of gene rearrangements and the consequent oncogenic fusion

95 which shared the same H and L chain germline gene rearrangements and then diversified by numerous som

96 Cases of ALL with MLL gene rearrangements and those with high hyperdiploidy (>

97 nitive series of tumors with NUT and/or BRD4 gene rearrangements and to determine distinct clinicopat

98 d on immunoglobulin/T-cell receptor (Ig/TCR) gene rearrangements and with quantification of IKZF1 del

99 ination of blood smears, and T cell receptor gene rearrangements), and performed muscle immunohistoch

100 a B-1 progenitor immunophenotype, clonal Igh gene rearrangement, and Bcor indel mutation, whereas con

101 CD8 coreceptors, underwent antigen receptor gene rearrangement, and demonstrated functional maturity

102 The latter involves RAG re-expression, TCR gene rearrangement, and expression of a novel TCR.

103 P53 upregulation, BRAF-KIAA gene rearrangement, and IDH1R132H mutation typically ass

104 nation of immunoglobulin and T cell receptor gene rearrangements, and initial studies using these met

105 , including RBM15-MKL1, CBFA2T3-GLIS2, KMT2A gene rearrangements, and NUP98-KDM5A.

106 polymerase chain reaction analysis of Ig/TCR gene rearrangements, and patients were assigned to a gen

107 e examples of how whole-genome duplications, gene rearrangements, and substrate promiscuity potentiat

108 tions; crizotinib for those with ALK or ROS1 gene rearrangement; and following first-line recommendat

109 These findings demonstrate that AR gene rearrangements are a unique resistance mechanism by

110 rogrammed cell death due to nonproductive Ig gene rearrangements are cleared from the bone marrow by

111 Although some gene rearrangements are diagnostic of particular sarcoma

112 Stereotyped V gene rearrangements are enriched among CD5(+) B cells, p

113 Thymocytes undergoing TCRbeta gene rearrangements are maintained in a low or nonprolif

114 d, using all 13 mt protein-coding genes, and gene rearrangements are mapped onto the phylogeny.

115 Anaplastic lymphoma kinase (ALK) gene rearrangements are oncogenic drivers of non-small-c

116 overed that anaplastic lymphoma kinase (ALK) gene rearrangements are present in a small subset of non

117 Taken together, Alu-mediated BRCA1 gene rearrangements are responsible for generating hypom

118 Breast cancer cell lines harboring Notch gene rearrangements are uniquely sensitive to inhibition

119 Immunoglobulin (Ig) gene rearrangements are used to define clonality of susp

120 Thripinae clade but do not appear to promote gene rearrangement as previously proposed.

121 ut also prevents the aberrant immunoglobulin gene rearrangements associated with RAD18 deficiency, re

122 at E-protein activity regulates secondary Ig gene rearrangement at the immature B cell stage and cont

123 It positively induces gene rearrangements at immunoglobulin heavy chain gene l

124 involving Variant Surface Glycoprotein (VSG) gene rearrangements at subtelomeres.

125 e used long-template inverse PCR to focus on gene rearrangements at the MLL locus.

126 differ from the mouse are the status of TCR gene rearrangements at the nonexpressed loci, the timing

127 This modeling revealed that these AR gene rearrangements blocked full-length AR synthesis, bu

128 , and lambda) and immunoglobulin heavy-chain gene rearrangement by reverse-transcriptase-polymerase-c

129 ing, we show that PI3K signaling inhibits Ig gene rearrangement by suppressing the expression of the

130 Ikaros promoted heavy-chain gene rearrangements by inducing expression of the recomb

131 es direct repeats in regions where potential gene rearrangements can occur suggests a mechanism for t

132 lpha repertoire that is the product of early gene rearrangements can preferentially populate distinct

133 Gene rearrangement (catalyzed by the RAG1/2 recombinase)

134 without an EGFR-sensitizing mutation or ALK gene rearrangement, combination cytotoxic chemotherapy i

135 size, lower codon bias, and a higher rate of gene rearrangement compared to a reference euchromatic d

136 lated from the cell surface, and light chain gene rearrangement continues in an attempt to edit the a

137 Throughout life, these gene rearrangements continuously generate B cell reperto

138 corporating TRAV8-1/TRAJ9 and TRBV19/TRBJ2-3 gene rearrangements, contributes to the development of d

139 out-of-frame mRNAs derived from unproductive gene rearrangements, cytoplasmic pre-mRNAs, endogenous r

140 ALK gene rearrangement defines a new molecular subtype of no

141 Identification of distinct classes of ETS gene rearrangements demonstrates that dormant oncogenes

142 pecimen examined harboured both ERG and ETV1 gene rearrangements demonstrating that the observed comp

143 ibodies and T cell receptors is generated by gene rearrangement dependent on RAG1 and RAG2, enzymes p

144 Immunoglobulin gene rearrangements document the monoclonality of the tu

145 karos, which mediates proximal V(H) to DJ(H) gene rearrangement downstream of FoxO1 and cooperates wi

146 hondrial genomes are marked by high rates of gene rearrangement, duplications of the control region a

147 ms underlying the formation and selection of gene rearrangements during cancer cell evolution.

148 population of thymocytes undergoes TCRalpha gene rearrangement early in development, before the doub

149 lent pandemic H1N1 vaccination, we sequenced gene rearrangements encoding the immunoglobulin heavy ch

150 as limited evidence for correlations between gene rearrangement events and species ecology or lineage

151 en together, modular domain distribution and gene rearrangement events related to these respiratory e

152 ntitative RT-PCR assessment of different TCR gene rearrangement events revealed lower levels in MHC-I

153 domains, which are generated by separate VDJ gene rearrangement events.

154 In this study, we show that cells with AR gene rearrangements expressing both full-length and AR-V

155 nce and mechanisms of the selective variable gene rearrangement for T cell development are not fully

156 chain reaction analysis of antigen receptor gene rearrangements for detection of minimal residual di

157 in cell cycle control, DNA replication, and gene rearrangement found in t(15;19)-associated carcinom

158 H to DJH recombination, we hypothesized that gene rearrangement frequency might be influenced by the

159 Together, our data showed that gene rearrangements frequently occur in PCa genomes but

160 The amplification of nonproductive Ig gene rearrangements from HED-ID B cells reflects the inf

161 e sequenced T-cell receptor beta-chain (TRB) gene rearrangements from immunodominant Mamu-A 01-restri

162 n human V(D)J recombination, we amplified Ig gene rearrangements from individual peripheral B cells o

163 ng and interpreting clinically relevant rare gene rearrangements from next-generation sequencing data

164 analysis of productive and nonproductive Ig gene rearrangements from transgenic mice engineered to e

165 The regulation of T cell receptor Tcra gene rearrangement has been extensively studied.

166 ecular components that directly control V(H) gene rearrangement have been elucidated.

167 n whose leukemia cells harbored the TEL/AML1 gene rearrangement have excellent outcomes.

168 These findings show that recurrent gene rearrangements have key roles in subsets of carcino

169 or poor prednisolone response, BCR-ABL1, MLL gene rearrangements, hypodiploid less than 45 chromosome

170 nomas harboring BRAF (V600E) mutation or RET gene rearrangements (i.e., BRAF-like tumors) and induced

171 T-cell receptor-gamma chain gene rearrangement identified a clonal population in all

172 ptor gene segments and identifies all clonal gene rearrangements (ie, leukemia-specific sequences) at

173 included PCR for heavy chain immunoglobulin gene rearrangements, immunohistochemistry for EBV, in si

174 er pre-TCR signaling, and RORgammat promoted gene rearrangement in CD4+, CD8+ cells by inhibiting cel

175 of nuclear hormone receptors that undergoes gene rearrangement in human cancer.

176 ene (RAG) 1 and RAG2 together catalyze V(D)J gene rearrangement in lymphocytes as the first step in t

177 trnW-trnC in J. hyalinus, the first reported gene rearrangement in Membracoidea.

178 ) genes; however, Pax5 did not induce any Ig gene rearrangement in the absence of Ikaros.

179 Gene rearrangement in the form of an intragenic deletion

180 erived growth factor receptor-alpha (PDGFRA) gene rearrangement in these tumors is unknown.

181 features of the T-cell receptor beta (TCRB) gene rearrangements in 20 individuals with well-defined

182 6, immunoglobulin heavy chain (IGH), and MYC gene rearrangements in a large PCNSL cohort treated in a

183 of cell surface markers and immunoglobulin H gene rearrangements in an in vitro model demonstrated no

184 ciples of nuclear architecture drive typical gene rearrangements in B lymphocytes, whereas translocat

185 In addition to this, the analysis of Ig gene rearrangements in B-cell neoplasms provides informa

186 ifferent developmental stages with IgLlambda gene rearrangements in between.

187 results emphasize the key role of RAF family gene rearrangements in cancer, suggest that RAF and MEK

188 ries from T-cell receptor and immunoglobulin gene rearrangements in context of lymphoproliferative di

189 Here we show that AR gene rearrangements in CRPC tissues underlie a completel

190 We discovered intragenic AR gene rearrangements in CRPC tissues, which we modeled us

191 VDJ gene rearrangements in IHB cells contain insertions of N

192 We found intact Ig gene rearrangements in immunoglobulin heavy (IgH) and ka

193 to dengue, we examined antibody heavy-chain gene rearrangements in longitudinal peripheral blood sam

194 eveloping macronuclei, as for immunoglobulin gene rearrangements in mammals, but not during the DNA f

195 Recurrent gene rearrangements in nonsmall cell lung cancer fuse EM

196 e discovery of PDGFR activating mutations or gene rearrangements in other tumor types could reveal ad

197 e recently identified common ETS and non-ETS gene rearrangements in prostate cancer.

198 urth ETS family member involved in recurrent gene rearrangements in prostate cancer.

199 tion analyses of T-cell receptor gamma-chain gene rearrangements in six patients and cytogenetics in

200 ngements of the upstream Vgamma2 and Vgamma5 gene rearrangements in the adult.

201 Analysis and interpretation of Ig and TCR gene rearrangements in the conventional, low-throughput

202 eaction (PCR) for immunoglobulin heavy-chain gene rearrangements in the first 6 months following tran

203 l syndrome occur only with missense or minor gene rearrangements in the KCNJ2 gene, resulting in a do

204 d demonstrate its application in identifying gene rearrangements in the model organism Saccharomyces

205 eloped approach that quantitatively predicts gene rearrangements in tumor-derived genetic material, w

206 at majority of FHIT and other CFS-associated gene rearrangements in tumors are submicroscopic, intral

207 ng V(H)1 gene, which is normally used in VDJ gene rearrangements in wt rabbits, is deleted, and inste

208 Eleven tumors had NUT gene rearrangements, including eight with BRD4-NUT fusio

209 -cell marker, T-cell receptor beta (TCRbeta) gene rearrangement indicated a T-cell origin.

210 Analysis of immunoglobulin gene rearrangements indicated that the lymphoma cells we

211 velopment correlated with increased TCRgamma gene rearrangement involving primarily Vgamma1.1 in Id3

212 We identified two classes of recurrent gene rearrangements involving genes encoding microtubule

213 a (AML) with mixed lineage leukemia 1 (MLL1) gene rearrangement is characterized by increased express

214 However, our analysis indicates that Igkappa gene rearrangement is normal in Ed-/- mice.

215 ogether, our results suggest that ordered Ig gene rearrangement is regulated by distinct activities o

216 Tight control of antigen-receptor gene rearrangement is required to preserve genome integr

217 , a deeper analysis of Ig and/or TCR (IG/TR) gene rearrangements is now within reach, which impacts o

218 rocessing inhibitory domain due to nfkappab2 gene rearrangements, is associated with the development

219 arly those with mixed lineage leukemia (MLL) gene rearrangements, is only 30% to 40%.

220 is generated by a unique process of somatic gene rearrangement known as V(D)J recombination.

221 ce of BCL6, DNA breaks during Ig light chain gene rearrangement lead to excessive up-regulation of Ar

222 occur through different processes, including gene rearrangements, local nucleotide changes, and the t

223 In heterogeneous cell populations, AR gene rearrangements marked individual AR-V-dependent cel

224 T and B cells share a common somatic gene rearrangement mechanism for assembling the genes th

225 ularly exciting are the discoveries of a new gene rearrangement mechanism in lampreys and a somatic d

226 ence of past RAG1 expression and had D-J IgH gene rearrangements; most of these derived from a subset

227 ce of EBF1 in regulating target genes and Ig gene rearrangements necessary for B cell lineage specifi

228 Large gene rearrangements, not detectable by standard molecula

229 TMPRSS2 gene rearrangements occur at DNA breaks formed during an

230 of the transgenic TCRalpha chain by ongoing gene rearrangement occurred in some cells irrespective o

231 as Stylonychia or Oxytricha, where extensive gene rearrangement occurs during differentiation of a so

232 Receptor editing or secondary Ig gene rearrangement occurs in immature, autoreactive B ce

233 Complete IgHC gene rearrangement occurs only in B cells in a stage-spe

234 c and E3' enhancers are required for maximal gene rearrangement of the locus, and that E3' is also re

235 unfavorable genetic characteristics (ie, MLL gene rearrangement or focal IKZF1 gene deletion in BCP-A

236 PCR and sequencing identified identical IGH gene rearrangements or BCL2 gene breakpoints in all pati

237 Validation of a gene rearrangement panel using 319 FFPE samples showed 1

238 l require a systematic examination for gross gene rearrangements, particularly in tumors with deficie

239 ight the importance of considering noncoding gene rearrangement partners, and the targetable gene fus

240 ve of six NHD13 thymi showed an unusual Tcrb gene rearrangement pattern with common, clonal DJ rearra

241 After productive VH-DJH gene rearrangement, pre-B cell receptor signaling ends B

242 rearrangements is blocked so that IgLlambda gene rearrangements predominate in early B cell developm

243 ecules that play critical roles in promoting gene rearrangements, proliferation, survival, or apoptos

244 emerging mechanism of CRPC progression is AR gene rearrangement, promoting synthesis of constitutivel

245 However, V(D)J gene rearrangements provide an opportunity to infer the

246 redictive biomarker candidates involving ETS gene rearrangements, PTEN inactivation, and androgen rec

247 of clonal immunoglobulin and T-cell receptor gene rearrangements, real-time quantitative-based detect

248 active B cells may undergo secondary L chain gene rearrangement (receptor editing) and change the spe

249 f IL-7 signals and the initiation of L chain gene rearrangement remains to be elucidated.

250 survival, how cells survive during IgL chain gene rearrangement remains unclear.

251 of genomic integrity during antigen receptor gene rearrangements requires (1) regulated access of the

252 ads to G1 arrest and induction of Ig L chain gene rearrangement, respectively.

253 We previously reported that gene rearrangements resulting in a hybrid MDR-1 transcri

254 in swine that IgL rearrangements precede IgH gene rearrangements, resulting in the expression of nake

255 RET gene rearrangements retaining the kinase domain are onco

256 pment involves rapid cellular proliferation, gene rearrangements, selection, and differentiation, and

257 Human leukemias carrying MLL gene rearrangements show DOT1L-mediated H3K79 methylatio

258 DNA products of baboon T-cell receptor (TCR) gene rearrangement (signal-joining TCR excision circles,

259 without activating mutations in KRAS contain gene rearrangements, so we investigated whether IOPNs ha

260 nt family of convergent antibody heavy chain gene rearrangements specific to influenza antigens.

261 We analyzed TMPRSS2-ERG gene rearrangement status by fluorescence in situ hybrid

262 Flow cytometry, gene rearrangement studies, and cytokine measurements ar

263 Continued antibody gene rearrangement, termed receptor editing, is an impor

264 i-B cell receptor Ab induces secondary V(D)J gene rearrangements, termed receptor editing.

265 Here, we survey MLL gene rearrangements that are associated with acute leuke

266 ther these copy number imbalances reflect AR gene rearrangements that could be linked to splicing dis

267 The genomic maps of IGL loci reveal multiple gene rearrangements that occurred in the evolution of te

268 BRAF gene rearrangements that were indicated in three tumors

269 In D to JH gene rearrangements, the D genes proximal to the JH locu

270 ction-based investigation of T-cell receptor gene rearrangement to detect clonality.

271 The approach takes advantage of natural Tcrb gene rearrangement to generate diversity in the length a

272 triggering germline transcription and Vkappa gene rearrangements to both Jkappa and RS elements.

273 ance mechanism that operates by secondary Ig gene rearrangements to change the specificity of autorea

274 e use of polymerase chain reaction for Bcl-2 gene rearrangements to detect molecular disease, however

275 re derived stochastically through the random gene rearrangements to produce T-cell receptors (TCR), a

276 e used high-throughput DNA sequencing of IGH gene rearrangements to study the BCR repertoires over tw

277 pients were younger, more likely to have MLL gene rearrangement, to have advanced leukemia, and to re

278 re-TCR) signaling includes proliferation and gene rearrangement, two cellular processes that are inco

279 of 20%, among the three patients with an ALK gene rearrangement, two had partial responses and the th

280 g clones revealed an absence of HA-tagged h7 gene rearrangements upon switching and acetylation of hi

281 tive for an anaplastic lymphoma kinase (ALK) gene rearrangement using fluorescence in situ hybridizat

282 er apoptotic components in etoposide-induced gene rearrangements using two methods.

283 aks (DSBs) are essential intermediates in Ig gene rearrangements: V(D)J and class switch recombinatio

284 ily gene member, initiating antigen receptor gene rearrangement via the RAG recombinase in an ancesto

285 ROS1 gene rearrangement was observed in around 1-2 % of NSCLC

286 Fluorescence in situ hybridization for BCL2 gene rearrangement was positive in all 17 cases tested.

287 Interphase FISH for IG and PAX5 gene rearrangements was performed on 17 cases of DLBCL.

288 expressing a repertoire biased to early TCR gene rearrangements, we developed a mouse model in which

289 These gene rearrangements were absent from all 126 control pan

290 tudies, etoposide-induced DNA damage and MLL gene rearrangements were demonstrated to be dependent in

291 Monoclonal T-cell receptor chain gene rearrangements were detected by polymerase chain re

292 amily of transcription factors (ETS)-related gene rearrangements were evaluated in three studies that

293 Gene rearrangements were only identified in ETS genes th

294 ther Ei or E3' significantly reduces Igkappa gene rearrangement, whereas the combined deletion of bot

295 ors arose at high incidence and displayed Ig gene rearrangement with downregulated expression of B ce

296 +)ALDH(high) B cells, sharing immunoglobulin gene rearrangements with lymph node HRS cells, were also

297 ogs, paralogs, hitchhiking genes, gene loss, gene rearrangement within an operon context, and also ho

298 Patients with ROS1 gene rearrangement without prior crizotinib may be offer

299 cell progenitors that have completed TCRbeta gene rearrangement without producing a functional TCRbet

300 AMP is effective in detecting gene rearrangements (without prior knowledge of the fusi