ライフサイエンスコーパス: ARMS

1 ARMS can physically associate with TrkA and p75 neurotro

2 ARMS cells were more invasive than ERMS cells and adopte

3 ARMS expresses the product of a genomic translocation th

4 ARMS is characterized by a chromosomal translocation gen

5 ARMS is characterized by a t(2;13) chromosomal transloca

6 ARMS is rapidly tyrosine phosphorylated after binding of

7 ARMS PCR primers were developed to recognize polymorphis

8 ARMS symptom severity and transition to psychosis appear

9 ARMS with local invasion (T2) had a higher rate of metas

10 ARMS-PCR efficiently identified mutations in individuals

11 ARMS-PCR's limits of detection for mutations M184V, T215

12 ARMS/Kidins220 undergoes multiple tyrosine phosphorylati

13 atures of this ARMS subset, we identified 23 ARMS cases in which PAX3-FKHR and PAX7-FKHR transcripts

14 unique cancer-specific molecules to achieve ARMS-specific expression of therapeutic genes, we have s

15 reatment with small interference RNA against ARMS substantially reduce neurotrophin-elicited signalin

16 Embryonal (ERMS) and alveolar (ARMS) are the two major RMS subtypes that are distinct i

17 cal subtypes, embryonal (ERMS) and alveolar (ARMS).

18 btypes of rhabdomyosarcoma include alveolar (ARMS) and embryonal (ERMS) tumors.

19 rs in vivo, argue for syncytial muscle as an ARMS tissue of origin, and demonstrate that Drosophila p

20 ulator gene using SERRS active primers in an ARMS assay.

21 uency, suggesting that skeletal muscle is an ARMS tissue of origin.

22 risk of developing psychosis who require an ARMS assessment and specialized care.

23 ound that the fusion RNA profile of RH30, an ARMS cell line, is most similar to the myogenesis time p

24 first episode patients and subjects with an ARMS (ANOVA; F = 8.16, P = 0.01).

25 brain responses from 16 individuals with an ARMS, 10 patients with first episode schizophrenia and 1

26 number spectrum for the more common ERMS and ARMS and revealed corresponding methylation signatures.

27 elationship between PAX3-FKHR expression and ARMS histogenesis in primary tumors and cell culture sys

28 resent the association between PAX3-FKHR and ARMS, and we investigated this link by examining the eff

29 g and T-ARMS-PCR for genotyping of MICA, and ARMS-PCR for HLA-B*51.

30 by PAX3-FOXO1 in mouse primary myoblasts and ARMS cell lines, contributes to PAX3-FOXO1 phenotypes, b

31 ons between transmembrane domains of Trk and ARMS.

32 ce experiments in myoblast-derived tumor and ARMS cells revealed that high PAX3-FKHR expression plays

33 augment FOXO1a activity may be effective as ARMS therapeutics.

34 re a new technology, NAPA: NaME-PrO-assisted ARMS, that overcomes the ARMS deficiency by adding a bri

35 ith a first episode of psychosis detected by ARMS services in secondary mental health services, and t

36 VDR mutations can be sensitively detected by ARMS-PCR and sequencing methods with comparable performa

37 GA and the presence of risk alleles for CFH, ARMS 2, HTRA1, C3, or TLR3.

38 sitive signals issue derived through classic ARMS-PCR and provides an ideal combination of speed, acc

39 Comparing ARMS-PCR with Sanger sequencing as a reference, we obtai

40 of At-Risk Mental States (CAARMS) to confirm ARMS.

41 205 in a variety of translocation-containing ARMS cell lines.

42 mplete regression of primary patient-derived ARMS xenografts in vivo.

43 rom the sessile and mobile fractions of each ARMS.

44 However, Tyr(1096) phosphorylation enables ARMS/Kidins220 to recruit CrkL through its SH2 domain, t

45 Moreover, endogenous ARMS protein is tyrosine phosphorylated after neurotroph

46 We established ARMS cell lines that exhibited stable expression of the

47 Here we show that PAX3-FOXO1-expressing ARMS cells are sensitive to pharmacological ataxia telan

48 gy to identify the target genes critical for ARMS tumorigenesis.

49 ng this potential pathogenetic mechanism for ARMS tumor initiation.

50 ity downstream of ROCKII and is required for ARMS cell invasion.

51 and repression of target genes required for ARMS tumorigenesis.

52 roteins as potential therapeutic targets for ARMS treatment.

53 osures of entinostat in three PAX3::FOXO1(+) ARMS mouse models.

54 Metastatic PAX3::FOXO1(+) ARMS often responds to chemotherapies initially, only to

55 igratory behavior of cell lines derived from ARMS and ERMS biopsies using a three-dimensional spheroi

56 nografts from individual clones derived from ARMS cell lines showed all of the classical morphologica

57 e prs-9 sequences in cell lines derived from ARMS, but remained at or below baseline levels in other

58 of ATR inhibitors in patients suffering from ARMS.

59 prominently expressed in primary tumors from ARMS patients and cell cultures.

60 e that were engrafted with the KRAB-PAX3-HBD ARMS cell lines and were implanted with 4-hydroxytamoxif

61 on profile conserved between mouse and human ARMS, as well as a Pax3:Fkhr signature, including the ta

62 olecular markers and histology seen in human ARMS are exclusively produced in this model.

63 that expression of KMT1A is induced in human ARMS cancer cell lines when cultured under differentiati

64 ession and p16(INK4A) loss was seen in human ARMS tumor tissue, as both human rhabdomyosarcoma cell l

65 hat our mouse model is most similar to human ARMS when compared with other pediatric cancers.

66 nd gene expression profiles similar to human ARMS.

67 FFS rate was 31% for patients with group III ARMS/UDS at unfavorable sites with regional lymph node d

68 and secondary (CDK4) genetic alterations in ARMS.

69 Furthermore, FOXO1a induced apoptosis in ARMS by directly activating the transcription of caspase

70 yrosine (Tyr(1096)) phosphorylation event in ARMS/Kidins220 that plays a critical role in neurotrophi

71 parable to the endogenous level expressed in ARMS cells, result in growth suppression.

72 38 genes were most consistently expressed in ARMS relative to a reference cell line.

73 nction, the fusion products are expressed in ARMS tumors at higher levels than the corresponding wild

74 been previously reported to be expressed in ARMS.

75 and that restoration of FOXO1a expression in ARMS cells is sufficient to induce cell cycle arrest and

76 3-FKHR expression is a consistent feature in ARMS tumors.

77 ssion of differentiation-associated genes in ARMS cells, thereby blocking muscle differentiation.

78 To identify molecular pathways involved in ARMS aggressiveness, we first characterized the migrator

79 n potentiate the antitumor activity of IR in ARMS xenografts by suppressing a classical NF-kappaBeta

80 sults suggested that high levels of KMT1A in ARMS cells under differentiation conditions impairs MyoD

81 Specifically, RhoE expression was low in ARMS biopsies, and its overexpression in ARMS cells redu

82 ilize a common gain of function mechanism in ARMS.

83 are deregulated by the PAX3-FKHR oncogene in ARMS.

84 eam targets of the PAX3-FOXO1 oncoprotein in ARMS have been defined, the functional relevance of thes

85 because it is linked with disease outcome in ARMS patients, determine tumor behavior.

86 in ARMS biopsies, and its overexpression in ARMS cells reduced their invasion potential.

87 eover, hippocampal long-term potentiation in ARMS/Kidins220(+/-) mice was enhanced, and inhibition of

88 table expression of the PAX3-KRAB protein in ARMS cell lines resulted in loss of the ability of the c

89 ly, would prevent transition to psychosis in ARMS in a randomised, double-blind, placebo-controlled t

90 ivating protein for Rac, was up-regulated in ARMS biopsies.

91 transfected and integrated PAX3 reporters in ARMS cells.

92 Chemotherapy resistance in ARMS has previously been attributed to PAX3::FOXO1-media

93 These results in ARMS demonstrate the potential of cDNA microarray techno

94 of skeletal muscle cells as an early step in ARMS tumorigenesis.

95 s targeting G9a as a therapeutic strategy in ARMS.

96 is a potent and specific tumor suppressor in ARMS, suggesting that agents that restore or augment FOX

97 (but not short-term) tumor cell survival in ARMS.

98 ependency factor and a therapeutic target in ARMS.

99 Cnr1 as a novel tractable target to inhibit ARMS invasion and metastasis.

100 In addition, Kidins220/ARMS and kinesin-1 were shown to colocalize in nerve gro

101 The interaction between Kidins220/ARMS and the kinesin-1 motor complex was confirmed by gl

102 he formation and transport of EGFP-Kidins220/ARMS carriers to the tips of growing neurites, leaving o

103 1 (KLC1) as a binding partner for Kidins220/ARMS by a yeast two-hybrid screen.

104 ified de novo nonsense variants in KIDINS220/ARMS in three unrelated patients with spastic paraplegia

105 the binding to a short sequence of Kidins220/ARMS, termed KLC-interacting motif (KIM), which is suffi

106 rin repeat-rich membrane spanning (Kidins220/ARMS) is a conserved membrane protein mainly expressed i

107 Our results suggest that Kidins220/ARMS-positive carriers undergo a kinesin-1-dependent tra

108 Using Kidins220/ARMS and KLC1 mutants, we mapped the regions responsible

109 ally recruited to and dominated the mesocosm ARMS.

110 rly summer and winter months within mesocosm ARMS shifted significantly as the initially recruited sh

111 Thus, metastatic ARMS represents a significantly unmet clinical need.

112 Most ARMS are associated with chromosomal translocations that

113 Most ARMS tumors express the PAX3-FKHR or PAX7-FKHR (PAX-FKHR

114 nal positively charged arginine-rich motifs (ARMS) of the CPs with the negatively charged phosphate b

115 Amplification refractory mutation (ARMS) SNP assays were modified by converting the SNP-det

116 ARMS-CrkL interaction with dominant-negative ARMS mutants, or treatment with small interference RNA a

117 ession profile distinct from fusion-negative ARMS and from the other rhabdomyosarcoma variants.

118 siontranscripts are not detectable in 20% of ARMS cases.

119 However, up to 25% of ARMS tumors are fusion negative, making it unclear wheth

120 In summary, our analysis of ARMS cases without characteristic PAX3-FKHR or PAX7-FKHR

121 ent PAX-FKHR determine class and behavior of ARMS, we used oligonucleotide microarray expression prof

122 A reassembled complex of ARMS/Kidins220 and CrkL, an upstream component of the C3

123 roteins may contribute to the development of ARMS.

124 l of the classical morphological features of ARMS suggesting divergence in vivo from precursor cells

125 signaling pathways leads to the formation of ARMS.

126 usion RNA, which is considered a hallmark of ARMS, was recently found during normal muscle cell diffe

127 le-specific oligonucleotide hybridization of ARMS PCR products.

128 ticity events and suggest that the levels of ARMS/Kidins220 can be regulated by neuronal activity and

129 However, a main limitation of ARMS-PCR is the false positive results obtained due to n

130 e expression profiles and patterns of LOH of ARMS cases lacking P-F translocations are indistinguisha

131 er gain was detected in the vast majority of ARMS (88%), compared with 52% of ERMS (P < .001).

132 ously developed a conditional mouse model of ARMS by faithfully recapitulating the genetic mutations

133 t suppressor of the transformed phenotype of ARMS cells, probably via competition with the endogenous

134 cular, myogenic, and histologic phenotype of ARMS.

135 Moreover, the invasive potential of ARMS cells depended on ROCK activity, which is regulated

136 The activity-dependent proteolysis of ARMS/Kidins220 was found to occur through calpain, a cal

137 inhibitor treatment increases sensitivity of ARMS cells to PARP1 inhibition in vitro, and combined tr

138 The amino acid sequence of ARMS is highly conserved from nematode to human, suggest

139 characteristic clefts and alveolar spaces of ARMS, however, were not seen.

140 To improve the analytical specificity of ARMS, we present here a new technology, NAPA: NaME-PrO-a

141 evelopment of therapies for the treatment of ARMS.

142 ential of G9a inhibitors in the treatment of ARMS.

143 G9a significantly affected the viability of ARMS cell lines.

144 ling the surrounding climax community and on ARMS placed in unestablished mesocosms receiving unfilte

145 mega-3 appears to have beneficial effects on ARMS and mood symptom severity but it increased transiti

146 ment was monitored bimonthly over 2 years on ARMS deployed within a natural coral reef habitat resemb

147 S express muscle cell-specific markers, only ARMS cells express PAX3-FOXO1a or PAX7-FOXO1a chimeric p

148 a is not expressed in primary ARMS tumors or ARMS-derived tumor cell lines and that restoration of FO

149 are frequently found in RMSs, in particular ARMS, and are associated with disease progression and ou

150 actory mutation system and quantitative PCR (ARMS-qPCR).

151 nt strategy for t(2;13)- or t(1;13)-positive ARMS.

152 the molecular phenotype of PAX-FKHR-positive ARMS tumors and, because it is linked with disease outco

153 X-FKHR that is specific to PAX-FKHR-positive ARMS tumors.

154 ogram of transcriptional repression prevents ARMS cells from differentiating.

155 port that FOXO1a is not expressed in primary ARMS tumors or ARMS-derived tumor cell lines and that re

156 Thus, we developed Tetra-primer ARMS assays for rapid, reliable, reproducible and econom

157 primers, and tetra-primers for tetra-primer ARMS PCR), as well as DNA sequencing primers.

158 ously based on the principle of tetra-primer ARMS-PCR (also known as PCR-CTPP).

159 The modified tetra-primer ARMS-PCR assay can achieve the desired sensitivity and s

160 tudy suggests that the modified tetra-primer ARMS-PCR assay can be used for the rapid, species identi

161 First, a tetra-primer ARMS-PCR assay was designed based on a single-nucleotide

162 a single PCR reaction based on tetra-primer ARMS-PCR or PCR-CTPP, and can serve as an invaluable too

163 put for gel-based resolution of tetra-primer ARMS-PCR products.

164 Tetra-primer ARMS-PCR was combined with microplate array diagonal gel

165 method is reported here, named tetra-primer ARMS-PCR, which employs two primer pairs to amplify, res

166 hoE/ROCK/ARHGAP25 signaling pathway promotes ARMS invasive potential and identify these proteins as p

167 kyrin repeat-rich membrane-spanning protein (ARMS) as a novel interaction partner of resting and stim

168 unusual ankyrin-rich transmembrane protein (ARMS+kidins220) is closely associated with Trk receptor

169 0-kilodalton membrane tetraspanning protein, ARMS/Kidins220, which is rapidly tyrosine phosphorylated

170 In the rat, ARMS is specifically expressed in the developing nervous

171 y mutation system polymerase chain reaction (ARMS-PCR) was used for genotyping IL-10 polymorphism.

172 y mutation system-polymerase chain reaction (ARMS-PCR) was used for genotyping IL-10 polymorphisms.

173 ived species initially recruited to the reef ARMS, suggesting that despite available space, the stage

174 suggested a role for PAX-FKHR in regulating ARMS proliferation and differentiation.

175 iptional analyses of ATR inhibitor resistant ARMS cells identifies the RAS-MAPK pathway and its targe

176 tic antitumor activity against Rh30 and Rh41 ARMS xenografts.

177 comes observed in alveolar rhabdomyosarcoma (ARMS) and the adult-type pleomorphic rhabdomyosarcoma (P

178 n of RNA from the alveolar rhabdomyosarcoma (ARMS) cancer cell line, with 3.5-fold greater extraction

179 a group of seven alveolar rhabdomyosarcoma (ARMS) cell lines characterized by the presence of the PA

180 Alveolar rhabdomyosarcoma (ARMS) cells often harbor one of two unique chromosomal t

181 osarcoma known as alveolar rhabdomyosarcoma (ARMS) have a 5-year survival of <30%.

182 R gene fusions in alveolar rhabdomyosarcoma (ARMS) indicated that the corresponding fusiontranscripts

183 Alveolar rhabdomyosarcoma (ARMS) is a devastating pediatric disease driven by expre

184 Alveolar rhabdomyosarcoma (ARMS) is a muscle-derived childhood tumor characterized

185 Alveolar rhabdomyosarcoma (ARMS) is an aggressive myogenic-type tumor and a gain-of

186 Alveolar rhabdomyosarcoma (ARMS) is an aggressive pediatric cancer with poor progno

187 Alveolar rhabdomyosarcoma (ARMS) is an aggressive pediatric muscle cancer, which ar

188 Alveolar rhabdomyosarcoma (ARMS) is an aggressive pediatric soft tissue tumor with

189 Alveolar rhabdomyosarcoma (ARMS) is consistently associated with the characteristic

190 ive muscle cancer alveolar rhabdomyosarcoma (ARMS) is one of the most common soft tissue sarcoma of c

191 Alveolar rhabdomyosarcoma (ARMS) patients harboring paired-box fusion proteins (PAX

192 cogene-expressing alveolar rhabdomyosarcoma (ARMS) remain dismal.

193 translocations of alveolar rhabdomyosarcoma (ARMS) result in chimeric PAX3-FKHR or PAX7-FKHR transcri

194 ood muscle cancer alveolar rhabdomyosarcoma (ARMS) that is driven by the chromosomal translocation pr

195 translocation in alveolar rhabdomyosarcoma (ARMS), a cancer associated with the skeletal muscle line

196 key component in alveolar rhabdomyosarcoma (ARMS), a childhood solid muscle tumor.

197 use, we selected alveolar rhabdomyosarcoma (ARMS), a myogenic pediatric cancer whose exact cell of o

198 ses of the cancer alveolar rhabdomyosarcoma (ARMS), and juxtaposes the genes encoding the PAX3 and FK

199 ong RMS subtypes, alveolar rhabdomyosarcoma (ARMS), which is characterized by the presence of the PAX

200 Alveolar rhabdomyosarcomas (ARMS) are aggressive soft-tissue sarcomas affecting chil

201 Alveolar rhabdomyosarcomas (ARMS) are highly malignant soft-tissue sarcomas that ari

202 Alveolar rhabdomyosarcomas (ARMS) escape terminal differentiation despite exhibiting

203 In contrast, alveolar rhabdomyosarcomas (ARMS) have fewer genetic lesions overall and no known re

204 ll, outcomes for patients with alveolar RMS (ARMS) or UDS were worse than for patients with ERMS.

205 as more frequently observed in alveolar RMS (ARMS) than in embryonal RMS (ERMS) (81% v 32%, respectiv

206 has a favorable prognosis, and alveolar RMS (ARMS), which has a poor outcome.

207 n subgroups, embryonal RMS and alveolar RMS (ARMS).

208 Axillary Access Registry to Monitor Safety (ARMS) was a prospective, observational multicenter regis

209 AX-FKHR expression signature that segregated ARMS patients into three risk groups with 5-year overall

210 By searching across the seven ARMS cell lines, we found that 37 of 1238 genes were mos

211 kDa)/ankyrin repeat-rich membrane spanning (ARMS) acts as a signaling platform at the plasma membran

212 ng of ankyrin repeat-rich membrane spanning (ARMS), which encodes a novel downstream target of neurot

213 The overall effect of At Risk Mental State (ARMS) services for the detection of individuals who will

214 sis in persons with an at-risk mental state (ARMS).

215 a and subjects with an At Risk Mental State (ARMS).

216 ing 51 Autonomous Reef Monitoring Structure (ARMS), a standardized non-destructive monitoring device,

217 Using Autonomous Reef Monitoring Structures (ARMS) as standardized habitats, we examine the assembly

218 The alveolar subtype (ARMS) has the poorest prognosis and represents the great

219 For the alveolar subtype (ARMS), the presence of the PAX3::FOXO1 fusion gene and/o

220 an amplification refractory mutation system (ARMS) is reported.

221 he amplificatory refraction mutation system (ARMS) PCR.

222 he amplification refractory mutation system (ARMS) was used.

223 he amplification refractory mutation system (ARMS), we have determined the parental origin of the new

224 an amplification refractory mutation system (ARMS)-PCR assay was developed and used to investigate th

225 ng amplification-refractory mutation system (ARMS)-PCR, Sanger sequencing, and longitudinal next-gene

226 he amplification refraction mutation system (ARMS)-to genotype 128 patients with type 1 Gaucher disea

227 eal-time allele-refractory mutations system (ARMS) quantitative polymerase chain reaction (qPCR).

228 ) (amplification-refractory mutation system, ARMS) is one of the most commonly used methods for mutat

229 controls were examined with sequencing and T-ARMS-PCR for genotyping of MICA, and ARMS-PCR for HLA-B*

230 mutation system/polymerase chain reaction (T-ARMS-PCR), 15 gingival tissue samples from patients with

231 amplification-refractory mutation system (T-ARMS) PCR for qualitative genotyping of three LHON mtDNA

232 atment of NG108-15 cells, demonstrating that ARMS is a downstream target for both neurotrophin and ep

233 ensional Euclidean space, we determined that ARMS cells show a consistent pattern of gene expression,

234 We found that ARMS tumors expressing either PAX-FKHR gene share a comm

235 Here we show that ARMS (ankyrin repeat-rich membrane spanning protein)/Kid

236 These findings suggest that ARMS acts as a major and neuronal-specific platform for

237 The ARMS designation accounted only for a small proportion o

238 The ARMS protein consists of 1715 amino acids containing fou

239 The ARMS-PCR assay was able to detect M184V, T215Y/F, K103N,

240 We hypothesize that PAX-FKHR determine the ARMS progenitor to the skeletal muscle lineage, which wh

241 ts provide an explanation for a role for the ARMS/Kidins220 protein in synaptic plasticity events and

242 ting the SNP-detecting linear primers in the ARMS assay to hairpin-shaped primers (HPs) through the a

243 diation induced NF-kappaBeta activity in the ARMS cells in vitro in a dose- and time-dependent manner

244 ost-effectiveness, and the simplicity of the ARMS-PCR assay make it a suitable tool to monitor HIVDR

245 To understand the role of the ARMS-specific PAX-FKHR proteins in myogenesis, we charac

246 Accordingly, disruption of Trk-ARMS or the ARMS-CrkL interaction with dominant-negative ARMS mutant

247 Overall, the ARMS-qPCR had frequent allele-dropout (ADO), rendering i

248 : NaME-PrO-assisted ARMS, that overcomes the ARMS deficiency by adding a brief enzymatic step that re

249 3 DNA binding domain, failed to suppress the ARMS malignant phenotype.

250 Compared with the ARMS designation, all of the International Statistical C

251 efore, the clinical heterogeneity within the ARMS category is associated with genetic heterogeneity.

252 To investigate the genetic features of this ARMS subset, we identified 23 ARMS cases in which PAX3-F

253 ) mediated HCC was then investigated through ARMS-PCR (Amplification Refractory Mutation System Polym

254 In addition to ARMS and ERMS, we identify two novel methylation subtype

255 nal differentiation, thereby contributing to ARMS formation.

256 that reduces wild-type alleles just prior to ARMS.

257 y MSCs as a progenitor that can give rise to ARMS.

258 of NR4A1 small-molecule antagonists to treat ARMS and other rhabdomyosarcomas driven by PAX3-FOXO1A.

259 Accordingly, disruption of Trk-ARMS or the ARMS-CrkL interaction with dominant-negative

260 ocation in alveolar rhabdomyosarcoma tumors (ARMS) creates an oncogenic transcriptional activator by

261 differences have been found between the two ARMS subtypes: PAX7-FKHR tumors more often occur as loca

262 objective of the present study was to verify ARMS-qPCR in a cohort of 20 PGD cycles with a diverse gr

263 Whereas ARMS tumors typically contain translocations generating

264 e fusion negative, making it unclear whether ARMS represent a single disease or multiple clinical and

265 ), caused by three false-positive calls with ARMS-PCR.

266 mortality rate remains high in patients with ARMS, because of its aggressive and metastatic nature.

267 e 5-year FFS rate was good for patients with ARMS/UDS at favorable sites with group I or II (80%) or

268 The FFS rate was poorer for patients with ARMS/UDS at unfavorable sites with group I or II (66%) o

269 tnatal muscle) can give rise to tumours with ARMS characteristics.