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

9 ARMS-PCR efficiently identified mutations in individuals

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

11 ARMS/Kidins220 undergoes multiple tyrosine phosphorylati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

28 ons between transmembrane domains of Trk and ARMS.

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

30 augment FOXO1a activity may be effective as ARMS therapeutics.

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

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

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

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

35 205 in a variety of translocation-containing ARMS cell lines.

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

37 Moreover, endogenous ARMS protein is tyrosine phosphorylated after neurotroph

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

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

40 ng this potential pathogenetic mechanism for ARMS tumor initiation.

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

42 and repression of target genes required for ARMS tumorigenesis.

43 roteins as potential therapeutic targets for ARMS treatment.

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

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

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

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

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

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

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

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

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

53 nd gene expression profiles similar to human ARMS.

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

55 and secondary (CDK4) genetic alterations in ARMS.

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

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

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

59 38 genes were most consistently expressed in ARMS relative to a reference cell line.

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

61 been previously reported to be expressed in ARMS.

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

63 3-FKHR expression is a consistent feature in ARMS tumors.

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

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

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

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

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

69 ilize a common gain of function mechanism in ARMS.

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

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

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

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

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

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

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

77 transfected and integrated PAX3 reporters in ARMS cells.

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

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

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

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

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

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

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

85 1 (KLC1) as a binding partner for Kidins220/ARMS by a yeast two-hybrid screen.

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

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

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

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

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

91 Most ARMS are associated with chromosomal translocations that

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

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

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

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

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

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

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

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

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

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

102 roteins may contribute to the development of ARMS.

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

104 signaling pathways leads to the formation of ARMS.

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

106 le-specific oligonucleotide hybridization of ARMS PCR products.

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

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

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

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

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

112 cular, myogenic, and histologic phenotype of ARMS.

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

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

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

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

117 evelopment of therapies for the treatment of ARMS.

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

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

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

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

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

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

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

125 ogram of transcriptional repression prevents ARMS cells from differentiating.

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

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

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

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

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

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

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

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

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

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

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

137 0-kilodalton membrane tetraspanning protein, ARMS/Kidins220, which is rapidly tyrosine phosphorylated

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

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

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

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

142 tic antitumor activity against Rh30 and Rh41 ARMS xenografts.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 Alveolar rhabdomyosarcomas (ARMS) escape terminal differentiation despite exhibiting

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

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

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

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

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

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

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

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

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

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

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

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

177 he amplificatory refraction mutation system (ARMS) PCR.

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

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

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

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

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

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

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

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

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

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

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

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

190 The ARMS designation accounted only for a small proportion o

191 The ARMS protein consists of 1715 amino acids containing fou

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

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

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

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

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

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

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

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

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

201 3 DNA binding domain, failed to suppress the ARMS malignant phenotype.

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

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

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

205 nal differentiation, thereby contributing to ARMS formation.

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

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

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

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

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

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

212 Whereas ARMS tumors typically contain translocations generating

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

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

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

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

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

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