ライフサイエンスコーパス: neuroblastoma

1 and guide clinical trials for children with neuroblastoma.

2 bination therapy for patients with high-risk neuroblastoma.

3 YCN amplification drives one in six cases of neuroblastoma.

4 cally engineered murine model of MYCN-driven neuroblastoma.

5 nd to offer a new strategy for patients with neuroblastoma.

6 evelop ganglioneuroma without progression to neuroblastoma.

7 level and find a chromaffin cell identity of neuroblastoma.

8 noninvasive lesion detection modalities for neuroblastoma.

9 ght allow for effective treatment options in neuroblastoma.

10 improve outcomes for patients with high-risk neuroblastoma.

11 r therapy in preclinical models of high-risk neuroblastoma.

12 evated immune marker expression in high-risk neuroblastoma.

13 ally exclusive across all ages and stages in neuroblastoma.

14 vity of CPC and inhibit tumor progression in neuroblastoma.

15 nhibition in the treatment of MYCN-amplified neuroblastoma.

16 GFbeta-dependent immune escape mechanisms in neuroblastoma.

17 vivin in different types of cancer including neuroblastoma.

18 ure was built to assess their implication in neuroblastoma.

19 epresentative of all patients with high-risk neuroblastoma.

20 tumours, including lymphoma, lung cancer and neuroblastoma.

21 therapy in pre-clinical models of high-risk neuroblastoma.

22 ldhood cancers as lymphoma, Wilms tumor, and neuroblastoma.

23 lexity of PRMT1 as a biological regulator of neuroblastoma.

24 livering precision medicine to children with neuroblastoma.

25 a chromatin-binding enzyme overexpressed in neuroblastoma.

26 nce the therapeutic effects on p53-deficient neuroblastoma.

27 c driver in a range of human cancers such as neuroblastoma.

28 ctivity in patients with relapsed/refractory neuroblastoma.

29 trates to previously published data on human neuroblastoma.

30 rogression (CILP) in patients with high-risk neuroblastoma.

31 SMARCA4, a putative predisposition gene for neuroblastoma.

32 re transcription factors implicated in human neuroblastoma.

33 eatment strategy for patients with high-risk neuroblastoma.

34 s, including 88% of osteosarcomas and 98% of neuroblastomas.

35 l therapeutic strategy in RAS-hyperactivated neuroblastomas.

36 The 30-year incidence was highest in neuroblastoma (10.7%; 95% CI, 3.8% to 21.7%) and hepatob

37 herapeutic radiopharmaceutical for high-risk neuroblastoma, (131)I-metaiodobenzylguanidine, is ineffe

38 of 56 pediatric primary tumors, including 24 neuroblastomas, 24 Wilms tumors, and 8 rhabdomyosarcomas

39 ha3beta4 nAChRs transiently transfected into neuroblastoma-2a cells.

40 on cancers involved were osteosarcoma (53%), neuroblastoma (37%), prostate (17%) and reproductive (10

41 these, 116 patients (52%) had metastatic CNS neuroblastoma, 57 (25%) had medulloblastoma, and 51 (23%

42 atients (16.4%) had ocular manifestations of neuroblastoma, 58 at presentation and 29 during the dise

43 ion factors poses a therapeutic challenge in neuroblastoma, a pediatric cancer in which MYCN amplific

44 andscape of extrachromosomal circular DNA in neuroblastoma, a tumor arising in childhood from primiti

45 In neuroblastoma, amplification of the MYCN oncogene and in

46 ciated genomic changes-including 17q gain in neuroblastoma and 17q23 amplification in breast cancer-m

47 Dr-TrkA induced apoptosis in neuroblastoma and glioblastoma, but not in other cell ty

48 g the TRIM37 gene is frequently amplified in neuroblastoma and in breast cancer(5-8), rendering these

49 suppressive miR-186 that is downregulated in neuroblastoma and in TGFbeta-treated NK cells represses

50 regulated kinases 1/2 (ERK1/2) signaling in neuroblastoma and neural crest-derived cells.

51 havbeta3 receptors that are overexpressed in neuroblastoma and other neuroendocrine tumors.

52 otential lead candidate for the treatment of neuroblastoma and other neuroendocrine tumors.

53 correlated with differentiated histology of neuroblastoma and predicted better survival for patients

54 LIN28B is highly expressed in neuroblastoma and promotes tumorigenesis, at least, in p

55 f RNA-sequencing data from 498 patients with neuroblastoma and revealed a differentially overexpresse

56 k occur at initiation of clonal expansion in neuroblastoma and rhabdomyosarcoma, whereas in Wilms tum

57 landscape of somatic structural variation in neuroblastoma and suggest that events leading to deregul

58 vel approach to study regulatory variants in neuroblastoma and suggest that noncoding somatic mutatio

59 dentifies HRK as a novel tumor suppressor in neuroblastoma and suggests dual MEK and YAP inhibition a

60 T/CT at the time of staging in children with neuroblastoma and to investigate its ability to assess t

61 and response to PD mimetics of human SH-SY5Y neuroblastoma and U-87MG glioblastoma cell lines culture

62 the MYCN oncogene occurs in ~25% of primary neuroblastomas and is the single most powerful biologica

63 d in multiple cancers, including colorectal, neuroblastoma, and breast tumors.

64 ation of CCL21 is an effective treatment for neuroblastoma, and may have potential for the delivery o

65 for the treatment of neuroendocrine tumors, neuroblastoma, and non-Hodgkin lymphoma, respectively.

66 ryl hydrocarbon receptor (AHR) expression in neuroblastoma, and overexpression of AHR downregulated M

67 and non-small cell lung carcinomas, glioma, neuroblastoma, and pancreatic carcinoma.

68 confirm that CPC is a therapeutic target in neuroblastoma, and targeting INCENP is a novel way to di

69 Here, we show that MYCN-amplified neuroblastomas are characterized by elevated rates of pr

70 These findings portray cases of bilateral neuroblastoma as having independent lesions mediated by

71 ry that controls the malignant cell state in neuroblastoma as well as GSK3B and L1CAM that are involv

72 ein YAP1 as an additional driver of relapsed neuroblastomas, as well as a mediator of trametinib resi

73 Methods: We enrolled children with neuroblastoma at onset.

74 of human embryos, fetal adrenal glands, and neuroblastoma at single-cell level and find a chromaffin

75 e medical records of patients diagnosed with neuroblastoma between 1989 and 2017 at a tertiary care p

76 Chromosome 17q21-ter is commonly gained in neuroblastoma, but it is unclear which gene in the regio

77 s the current standard of care for high-risk neuroblastoma, but its application to recurrent osteosar

78 to TERT overexpression and poor prognosis in neuroblastoma, but TERT-associated oncogenic signaling r

79 sion and increased susceptibility to develop neuroblastoma, but the oncogenic pathways downstream of

80 The outcome for 4S neuroblastoma can be improved with pre-emptive chemother

81 mozolomide, a reference therapy for relapsed neuroblastoma, caused long-term suppression of neuroblas

82 vation in in vitro assays with SH-SY5Y human neuroblastoma cell cultures, where Abeta42 aggregation i

83 a retinoic acid-differentiated SH-SY5Y human neuroblastoma cell line (RA-differentiated SH-SY5Y).

84 We generated a neuroblastoma cell line expressing a PAG1 fragment that

85 4(F20Cha) exhibits cytotoxicity against the neuroblastoma cell line SH-SY5Y.

86 a targeted lipidomic analysis and the mouse neuroblastoma cell line, Neuro-2a, the ToxCast(TM) chemi

87 to the staurosporine-induced apoptotic human neuroblastoma cell line, SH-SY5Y.

88 Furthermore, using an SH-SY5Y neuroblastoma cell line, we showed that both heavy metal

89 pendent accumulation of acidic vesicles in a neuroblastoma cell line.

90 In addition, we assessed TMM in neuroblastoma cell lines (n = 104) and patient-derived x

91 ssion of SHANK2 was low across human-derived neuroblastoma cell lines and high-risk neuroblastoma tum

92 ganglioside pattern on four melanoma and two neuroblastoma cell lines by high performance liquid chro

93 cells prevented apoptosis and death of human neuroblastoma cell lines SH-SY5Y (SH-SY5Y) cells followi

94 In most neuroblastoma cell lines tested in vitro, apoptosis was

95 genetic manipulation of YAP in human-derived neuroblastoma cell lines to investigate YAP function in

96 In the present study, two p53-mutant neuroblastoma cell lines were used as in vitro models.

97 highly cytotoxic in vitro across a panel of neuroblastoma cell lines, directly causing double strand

98 highly cytotoxic in vitro across a panel of neuroblastoma cell lines, directly causing double-strand

99 ytotoxicity of (125)I-KX1 was assessed in 19 neuroblastoma cell lines, followed by in-depth pharmacol

100 transcript isoforms expressed in the brain, neuroblastoma cell lines, primary astrocytes and embryon

101 growth suppression, which we demonstrated in neuroblastoma cell lines, primary human cells, and xenog

102 ted RNA levels in a consistent manner in two neuroblastoma cell lines, SH-SY5Y and SK-N-BE(2).

103 tified that ITCH was expressed on p53-mutant neuroblastoma cell lines.

104 modulates GD2 expression in human and mouse neuroblastoma cell lines.

105 used complex bis(maltolato)oxovanadium(V) in neuroblastoma cell lines.

106 xpressing, non-ALT patient-derived high-risk neuroblastoma cell lines.

107 ate and was highly synergistic in decreasing neuroblastoma cell viability.

108 vity in a ligand-independent manner in mouse neuroblastoma cells (Neuro-2A).

109 ied, compared with MYCN-non-amplified, human neuroblastoma cells and also the most over-expressed in

110 not epilepsy-reduced Na+ current density in neuroblastoma cells and expectedly decreased neuronal fi

111 argeted Auger therapy is lethal to high-risk neuroblastoma cells and has the potential to be used in

112 ls as important metabolic master switches in neuroblastoma cells and identified critical nodes that r

113 NF-Y in two types of neuronal cells, neuro2a neuroblastoma cells and mouse brain striatal cells, and

114 motility, and invasiveness of MYCN-amplified neuroblastoma cells and patient-derived xenograft tumors

115 sfected wild-type or mutant channels in both neuroblastoma cells and primary cultured neurons reveale

116 uding vorinostat, enhanced GD2 expression in neuroblastoma cells beyond their individual effects.

117 nfection on protein degradation rates in N2a neuroblastoma cells by dynamic stable isotopic labeling

118 s the toxicity of the resulting oligomers to neuroblastoma cells by inhibiting their binding to the c

119 en Myc(oncogene)-On and Myc-Off Tet21N human neuroblastoma cells cultured with U-(13)C(6)-glucose med

120 AChE and microRNA-15b in protecting SH-SY5Y neuroblastoma cells from amyloid-beta (Abeta)-induced cy

121 ChIP-seq analysis of the human CLB-GA neuroblastoma cells harboring TERT rearrangement uncover

122 Neuroblastoma cells highly express the disialogangliosid

123 In contrast, knockdown of RUNX1 in neuroblastoma cells induced viral gene expression and in

124 te that resistant MYCN-amplified ALK-mutated neuroblastoma cells overexpress BORIS, resulting in wide

125 h of nonmalignant cells or MYCN-nonamplified neuroblastoma cells remained unaffected by reduced ABCE1

126 Forced expression of SHANK2 in neuroblastoma cells resulted in significant growth inhib

127 caused profound mitochondrial damage in MNA neuroblastoma cells through downregulation of the mitoch

128 w that LIN28B binds active gene promoters in neuroblastoma cells through protein-protein interaction

129 YAP1 depletion sensitized neuroblastoma cells to trametinib, while overexpression

130 protein, which mediated the apoptosis of the neuroblastoma cells upon irradiation treatment.

131 internalisation into differentiated SH-SY5Y neuroblastoma cells using fluorescence and electron micr

132 iferase reporter assays and its synthesis in neuroblastoma cells was increased under hypoxic conditio

133 Remarkably, cell-death in NB1 neuroblastoma cells was solely induced by ferroptosis, i

134 Neuroblastoma cells with c-MYC overexpression also requi

135 Co-treatment of neuroblastoma cells with inhibitors of MCT1 and LDHA, th

136 ven more effective in sensitizing aggressive neuroblastoma cells with p53 cytoplasmic accumulation.

137 Treatment of neuroblastoma cells with the MCT1 inhibitor SR13800 incr

138 Akt2, stimulated neurite formation in mouse neuroblastoma cells, a requirement for neurogenesis.

139 Here, we found that in human neuroblastoma cells, activation of ADAM10 with the musca

140 l encapsulation, bioavailability in cultured neuroblastoma cells, and effective cytotoxic or differen

141 n this study, INCENP was highly expressed by neuroblastoma cells, and its expression decreased follow

142 uroblastoma cells, nonspecifically active in neuroblastoma cells, and nonactive.

143 f regulatory elements specifically active in neuroblastoma cells, as compared with the others.

144 We analyzed GLS2 expression in HCC, GBM and neuroblastoma cells, as well as in monkey COS-7 cells.

145 n regulatory elements specifically active in neuroblastoma cells, nonspecifically active in neuroblas

146 an brains and spinal cords, as well as human neuroblastoma cells, suggesting evolutionary conservatio

147 ficantly enhanced neurite formation in mouse neuroblastoma cells, which correlates with repairing dam

148 overexpression on metabolic reprogramming in neuroblastoma cells.

149 nosis in a range of human cancers, including neuroblastoma, cervical, brain, breast, prostate, pancre

150 ma cells and also the most over-expressed in neuroblastoma compared with all other cancers.

151 taneous transgenic (TH-MYCN) murine model of neuroblastoma, comparing histological features and immun

152 nd ISL1-all members of the adrenergic (ADRN) neuroblastoma core regulatory circuitry (CRC).

153 member and LMO1 is a coregulator of the ADRN neuroblastoma CRC.

154 ve metastatic disease or refractory/relapsed neuroblastoma currently face a dismally low chance of su

155 g two real-world cancer datasets (i.e., SEQC neuroblastoma dataset and the NIH/NCI TCGA lung adenocar

156 gene expression may have relevant effects in neuroblastoma development.

157 atic mutations have relevant implications in neuroblastoma development.

158 on decreased following retinoic acid-induced neuroblastoma differentiation.

159 The majority of patients with neuroblastoma due to MYCN oncogene amplification and con

160 clude glial brain tumors, relapsed high-risk neuroblastoma, embryonal rhabdomyosarcoma, acute myeloid

161 em stages 1/2A/2B, from 3 cohorts: Localized Neuroblastoma European Study Group I/II and Children's O

162 ncluding rhabdomyosarcoma, synovial sarcoma, neuroblastoma, Ewing sarcoma, and osteosarcoma) identifi

163 mouse model of high-risk treatment-resistant neuroblastoma exhibits changes in the tumor microenviron

164 n = 7) breast cancer xenografts, and Th-MYCN neuroblastomas (G (d) = 3.5 +/- 0.2 kPa, G (l) = 2.3 +/-

165 ranial solid tumors of childhood and include neuroblastoma, ganglioneuroblastoma, and ganglioneuroma.

166 uroblastoma, caused long-term suppression of neuroblastoma growth in vivo, highlighting the clinical

167 s cohort, approximately 1 in 6 patients with neuroblastoma had ocular manifestations, but only 3% pre

168 Neuroblastoma has a low mutation rate for the p53 gene.

169 ired resistance to ALK inhibition therapy in neuroblastoma have not yet been elucidated.

170 ons of resectable non-MYCN-amplified stage 2 neuroblastomas have a distinct age-dependent prognostic

171 abdomyosarcoma, Ewing sarcoma, osteosarcoma, neuroblastoma, Hodgkin lymphoma, non-Hodgkin lymphoma, a

172 ibody (mAb) has proven efficacy in high-risk neuroblastoma (HR-NB).

173 reening of 23 drugs used in the treatment of neuroblastoma identified several drugs with the potentia

174 highlight the potential of targeting MCT1 in neuroblastoma in conjunction with strategies that involv

175 ctivity in patients with relapsed/refractory neuroblastoma in the randomized Children's Oncology Grou

176 There were 523 patients with neuroblastoma in the study cohort.

177 to the rich histopathologic heterogeneity of neuroblastoma in the Th-MYCN transgenic model.

178 ic ductal adenocarcinoma, ovarian cancer and neuroblastoma in vitro and in orthotopic and metastatic

179 st common cause of driver point mutations in neuroblastoma, including most ALK and Ras-activating var

180 the ALT DNA biomarker C-circles to stratify neuroblastoma into three groups, with distinct overall s

181 provides precise stratification of high-risk neuroblastoma into three subgroups with substantially di

182 Neuroblastoma is a cancer of the developing sympathetic

183 Neuroblastoma is a childhood cancer with heterogeneous c

184 Neuroblastoma is a common solid tumor of young children

185 Neuroblastoma is a deadly pediatric solid tumor with inf

186 Childhood neuroblastoma is a hypervascular tumor of neural origin,

187 Neuroblastoma is a malignancy of the developing sympathe

188 Neuroblastoma is a paediatric cancer with a poor prognos

189 Neuroblastoma is a pediatric malignancy with heterogeneo

190 The cell of origin of neuroblastoma is mysterious due to the complexity of neu

191 onal role in the aggressive pediatric cancer neuroblastoma is not well-characterized.

192 Neuroblastoma is the most common malignant disease of in

193 Neuroblastoma is the most commonly diagnosed extracrania

194 Neuroblastoma is the most commonly diagnosed extracrania

195 en injected intratumorally into mice bearing neuroblastoma lesions, significantly prolonged survival

196 sis revealed strong associations between the neuroblastoma lincRNAs MIAT and MEG3 and MYCN and PHOX2B

197 ndard 3D conditions for rodent cells support neuroblastoma lines used as human CNS models, but not hN

198 her than that of (124)I-MIBG in an MIBG-avid neuroblastoma model.

199 le biological representations including sex, neuroblastoma MYCN amplification, and cell types.

200 ted NK cells represses oncogenic proteins in neuroblastoma (MYCN and AURKA) and components of the TGF

201 In MYCN-amplified neuroblastoma, MYCN invaded active enhancers, driving a

202 nd human kidney cells HEK293), animal cells (neuroblastoma N115 and sheep red blood cells), cancer ce

203 utant PS1E280A and mutant PS1Delta9 in mouse neuroblastoma N2a cells.

204 , decreasing its intracellular levels in the neuroblastoma (N2a) cell line.

205 naptic and mitochondrial toxicities in mouse neuroblastoma (N2a) cells that express mutant APP.

206 Neuroblastoma (NB) is a malignant embryonal tumor of the

207 s promising responses in heavily pre-treated neuroblastoma (NB) patients.

208 ity treatments, prognosis for advanced stage neuroblastoma (NB) remains challenging with residual lon

209 Neuroblastoma (NB), derived from the neural crest (NC),

210 entify resistance mechanisms in ALK-positive neuroblastoma (NB), we herein employ genome-wide CRISPR

211 entiation and is activated by N-Myc in human neuroblastoma (NB).

212 ) to CPT-11 was compared in: (i) spontaneous neuroblastomas (NB) in transgenic TH-MYCN mice; (ii) ort

213 und that screening chemical libraries across neuroblastoma (NBL) tumor subtypes for selectively-letha

214 in-15 in children with relapsed or resistant neuroblastoma (NCT03294954).

215 G) stratifies the treatment of patients with neuroblastoma on the basis of a combination of biomarker

216 cells within many tumor cell lines including neuroblastoma or glioblastoma.

217 rgeted delivery of miR-186 to MYCN-amplified neuroblastoma or NK cells resulted in inhibition of neur

218 To better understand neuroblastoma pathogenesis, here we analyze whole-genome

219 LIN28B in transcriptional regulation during neuroblastoma pathogenesis.

220 ology classified by age-linked International Neuroblastoma Pathology Classification (INPC) criteria.

221 e sequencing, and clinical covariates in 134 neuroblastoma patient samples at diagnosis.

222 re sensitive than (123)I-MIBG WBS in staging neuroblastoma patients and evaluating disease persistenc

223 GFbeta1-dependent immune escape in high-risk neuroblastoma patients as well as the inclusion of ex vi

224 ted with poor prognosis in primary tumors of neuroblastoma patients with high-risk disease.

225 nrolled 16 high-risk and 2 intermediate-risk neuroblastoma patients.

226 ing increases the penetrance of MYCN-induced neuroblastoma, potentiates the invasion and migration of

227 of chromosomal passenger complex and inhibit neuroblastoma progression.

228 ional control network, that is essential for neuroblastoma proliferation.

229 fts treated in vivo, which may contribute to neuroblastoma recurrence.

230 We investigated whether cases of bilateral neuroblastoma represented independent tumors in two chil

231 intent-to-treat basis per the International Neuroblastoma Response Criteria.

232 lid Tumours version 1.1 or the International Neuroblastoma Response Criteria.

233 s of gene expression data from patients with neuroblastoma revealed that MYCN was associated with inc

234 tion between these parameters, the principal neuroblastoma risk factors, and outcome.

235 th and are incorporated in the International Neuroblastoma Risk Group classification schema.

236 Here, we analyzed data in the International Neuroblastoma Risk Group Data Commons to validate the pr

237 The CNV had a substantial impact on neuroblastoma risk, with an odds ratio of 13.9 (95% conf

238 Here we show that the neuroblastoma risk-associated locus 6p22.3-derived tumor

239 t to 46 adult glioblastoma and 146 pediatric neuroblastoma samples sequenced by Illumina and Complete

240 y was active in human ganglioneuroma but not neuroblastoma samples.

241 ole-exome and/or transcriptome data from 702 neuroblastoma samples.

242 tic potential of tumor-suppressive miRNAs in neuroblastoma.See related article by Neviani and colleag

243 In the whole genome neuroblastoma set, VCF2CNA identified MYCN high-level am

244 vestigated the effects of repotrectinib in a neuroblastoma setting in vitro and in vivo.

245 The human neuroblastoma SH-SY5Y cell line expresses only kindlin-2

246 -pathway aggregation and toxicity in a human neuroblastoma SH-SY5Y cell line.

247 operties, showing target engagement in human neuroblastoma SH-SY5Y cells and a desirable pharmacokine

248 haracterised in human rhabdomyosarcoma (RD), neuroblastoma (SH-SY5Y) and peripheral blood mononuclear

249 Like many childhood cancers, neuroblastoma shows a relative paucity of somatic single

250 ional Society of Pediatric Oncology European Neuroblastoma (SIOPEN) Biology Group.

251 G-P-TAT was synthesized and evaluated in the neuroblastoma SK-N-FI cell line for improved targeting a

252 anges characteristic of human MYCN-amplified neuroblastoma, specifically copy number gains at mouse c

253 lus other COG-risk biomarkers (International Neuroblastoma Staging System [INSS] stage, MYCN status,

254 were obtained from 317 tumors, International Neuroblastoma Staging System stages 1/2A/2B, from 3 coho

255 t protocols of the SIOP Europe International Neuroblastoma Study Group, Children's Oncology Group, an

256 ical Committees of SIOP Europe International Neuroblastoma Study Group, Children's Oncology Group, an

257 ys of p53 inactivation have been proposed in neuroblastoma, such as abnormal cytoplasmic accumulation

258 egulation of genes associated with high-risk neuroblastoma, such as the cell-cycle regulator cyclin B

259 The International Neuroblastoma Surgical Report Form is the first universa

260 The "International Neuroblastoma Surgical Report Form" provides a structure

261 ess toxic, more tumor-specific treatment for neuroblastoma than conventional cytotoxic therapies.

262 dy the involvement of regulatory variants in neuroblastoma that could be extended to other cancers an

263 romoted a mesenchymal phenotype in high-risk neuroblastoma that modulated tumor growth and therapy re

264 In neuroblastoma, the interplay between immune cells of the

265 e cancer progression is well demonstrated in neuroblastoma, the most common extracranial pediatric so

266 Restoration of miR-186 levels in neuroblastoma through NK cell-derived exosomes or by nan

267 an epigenetically regulated component of the neuroblastoma transcriptional control network, that is e

268 erexpression of AHR significantly suppressed neuroblastoma tumor growth.

269 -TAT demonstrated significant suppression of neuroblastoma tumor progression, growth, and viability i

270 ion, induces apoptosis in vitro and leads to neuroblastoma tumor regression in mice, which are signif

271 Dysregulation of INCENP contributes to neuroblastoma tumorigenesis and targeting INCENP present

272 astoma or NK cells resulted in inhibition of neuroblastoma tumorigenic potential and prevented the TG

273 ALT was identified in 23.4% of high-risk neuroblastoma tumors and genomic alterations in ATRX wer

274 ollowing chemotherapy and relapse, high-risk neuroblastoma tumors harbor more genomic alterations tha

275 tance to MCT1 inhibitor treatment in hypoxic neuroblastoma tumors.

276 rived neuroblastoma cell lines and high-risk neuroblastoma tumors.

277 tion of somatic structural variation (SV) in neuroblastoma using a combination of whole-genome sequen

278 Infants with stage 4S neuroblastoma usually have favorable outcomes with obser

279 prove chemotherapy response in patients with neuroblastoma via its regulation of HRK, thus providing

280 nd CDK2, selectively targeted MYCN-amplified neuroblastoma via multiple mechanisms.

281 MYCN overexpression in mesenchymal neuroblastoma was sufficient to induce adrenergic identi

282 nism (TMM) on clinical outcomes in high-risk neuroblastoma, we integrated the C-circle assay [a marke

283 Patients with high-risk neuroblastoma were classified into three subgroups (TERT

284 Newly diagnosed patients with high-risk neuroblastoma were randomly assigned or assigned to rece

285 Noncoding somatic mutations of 151 neuroblastomas were integrated with ENCODE data to locat

286 ys confirmed the hypomethylation of GATA3 in neuroblastoma, which correlated with high expression at

287 In patients with stage 4 high-risk neuroblastoma who have responded to induction therapy, C

288 including leukaemia, lymphoma, CNS tumours, neuroblastoma, Wilms tumour, soft-tissue sarcomas, and b

289 leukaemia, lymphoma, malignant CNS tumours, neuroblastoma, Wilms' tumours, and bone and soft tissue

290 th symptomatic and/or unfavorable biology 4S neuroblastoma with a uniform treatment approach using a

291 n summary, we describe a unique mechanism in neuroblastoma with TERT overexpression and an epigenetic

292 y cotargeting Brd4 and Cdks suppresses human neuroblastoma with TERT overexpression by inhibiting the

293 f TERT and multiple TERT-associated genes in neuroblastoma with TERT overexpression or MYCN amplifica

294 Signature 18 is enriched in neuroblastomas with MYCN amplification, 17q gain, and in

295 xpressed gene signature in MYCN nonamplified neuroblastomas with telomerase reverse transcriptase (TE

296 hese molecules have in vivo activity towards neuroblastoma, with essentially no toxicity.

297 For localized, resectable neuroblastoma without MYCN amplification, surgery only i

298 le derivative that induced growth delay in a neuroblastoma xenograft model with minimal toxicity.

299 of the ITCH siRNA using nanoparticles to the neuroblastoma xenograft mouse model showed around 15-20%

300 but this combination was ineffective against neuroblastoma xenografts.