ライフサイエンスコーパス: neuroblastoma

1 gene member, MMP20, and 11q-deletion subtype neuroblastoma.

2 patients with NETs, especially children with neuroblastoma.

3 GF) as a potent prodifferentiating factor in neuroblastoma.

4 letion are associated with poor prognosis in neuroblastoma.

5 offer therapeutic perspectives for high-risk neuroblastoma.

6 vel anticancer agents against MYCN-amplified neuroblastoma.

7 elated prognostic factors of poor outcome in neuroblastoma.

8 t al. report GPC2 as a therapeutic target in neuroblastoma.

9 e to aim to optimise treatment for high-risk neuroblastoma.

10 o assess treatment response in children with neuroblastoma.

11 e an alternative strategy to treat high-risk neuroblastoma.

12 mide in patients with relapsed or refractory neuroblastoma.

13 2 inhibitors in patients with MYCN-amplified neuroblastoma.

14 tinct types of lymphoma, lung carcinoma, and neuroblastoma.

15 c strategy to induce cell differentiation in neuroblastoma.

16 resection of the primary tumor in high-risk neuroblastoma.

17 d refine response criteria for patients with neuroblastoma.

18 a rationale for chromosomal loss patterns in neuroblastoma.

19 ch are associated with poor outcome in human neuroblastoma.

20 inase inhibitor with preclinical activity in neuroblastoma.

21 contributes to high-risk and poor-prognosis neuroblastoma.

22 mide have activity in patients with advanced neuroblastoma.

23 s HAUSP) as a regulator of N-Myc function in neuroblastoma.

24 s highly expressed in many cancers including neuroblastoma.

25 apeutic activities in models of lymphoma and neuroblastoma.

26 has been shown to be a therapeutic target in neuroblastoma.

27 at could improve the treatment of metastatic neuroblastoma.

28 on of many neuroendocrine tumors, especially neuroblastoma.

29 es such as colon cancer, prostate cancer and neuroblastoma.

30 ational Neuroblastoma Staging System stage 4 neuroblastoma.

31 ated tumor-suppressive role for HIF2alpha in neuroblastoma.

32 ng of the mechanisms of perifosine action in neuroblastoma.

33 rgets in epithelial ovarian cancer (EOC) and neuroblastoma.

34 as a therapeutic target for the treatment of neuroblastoma.

35 e that functions as an oncogene in high-risk neuroblastoma.

36 vity in patients with relapsed or refractory neuroblastoma.

37 is a pathogenic effect of KIF1Bbeta loss in neuroblastomas.

38 (isotretinoin) in primary nf1a-/- zebrafish neuroblastomas.

39 ic Oncology European Neuroblastoma/High-Risk Neuroblastoma 1 (SIOPEN/HR-NBL1), is now reported.

40 selective HDAC8 inhibitors that showed anti-neuroblastoma activity in cellular testing.

41 For the childhood cancer neuroblastoma, amplification of the oncogene MYCN is ass

42 Neuroblastoma, an embryonal cancer of neural crest origi

43 Twenty-one patients were treated: 19 with neuroblastoma and 2 with MP.

44 Ten patients (5 with neuroblastoma and 5 with paraganglioma/pheochromocytoma)

45 2271338, reduced enhancer activity by 40% in neuroblastoma and astrocytoma cells (pBonferroni < .0001

46 r, ovarian, bladder, gastric, brain cancers, neuroblastoma and chronic lymphocytic leukemia.

47 which LMO1 and MYCN synergistically initiate neuroblastoma and contribute to metastatic disease progr

48 cale CRISPR-Cas9 screening of MYCN-amplified neuroblastoma and found a preferential dependency on gen

49 selectively expressed on the cell surface of neuroblastoma and is a dependency in this disease.

50 e (BSO) as effective agents in children with neuroblastoma and medulloblastoma.

51 e responsible for the majority of hereditary neuroblastoma and somatic ALK activating mutations are a

52 ortant mechanism for mHtt secretion in mouse neuroblastoma and striatal cell lines, as well as in pri

53 ntified significant loss of RD3 in high-risk neuroblastoma and the influential role of RD3 in tumor p

54 rigenic CAF in the tumor microenvironment of neuroblastoma and to STAT3 and ERK1/2 as mediators of th

55 o transport, providing a direct link between neuroblastomas and neurodegeneration.

56 KIF1Bbeta mutations previously identified in neuroblastomas and pheochromocytomas all fail to activat

57 G imaging is a mainstay in the evaluation of neuroblastoma, and (131)I-MIBG has been used for the tre

58 e findings, DEF is highly expressed in human neuroblastoma, and its depletion in human neuroblastoma

59 nactivation of a tumor suppressor program in neuroblastoma, and support testing EZH2 inhibitors in pa

60 es for children with relapsed and refractory neuroblastoma are dismal.

61 up clinical trial of patients with high-risk neuroblastoma at 128 institutions in 18 countries that i

62 or 28 days) were evaluated in chemoresistant neuroblastoma-bearing mice and compared with the standar

63 We identified novel ALK fusions in a neuroblastoma (BEND5-ALK) and an astrocytoma (PPP1CB-ALK

64 dently of well-defined prognostic factors in neuroblastoma, breast cancer, DLBCL, and medulloblastoma

65 confirm GPC2 to be highly expressed on most neuroblastomas, but not detectable at appreciable levels

66 oduct of the MYCN oncogene) is stabilized in neuroblastoma by the protein kinase Aurora-A in a manner

67 at 11q22.2 within MMP20 that associate with neuroblastoma cases harboring 11q deletion (rs10895322),

68 key molecules in Rho signaling, resulted in neuroblastoma cell differentiation and inhibition of neu

69 s agent, Roniciclib (BAY 1000394), inhibited neuroblastoma cell growth and induced apoptosis in vitro

70 stoma cell differentiation and inhibition of neuroblastoma cell growth, migration, and invasion.

71 and distant metastasis, which was linked to neuroblastoma cell invasion and migration, and elevated

72 Stathmin suppression significantly reduced neuroblastoma cell invasion of 3D tumor spheroids into a

73 Using a mouse neuroblastoma cell line (N2A), we also found that NLRX1

74 a p62-knock-down (p62 KD) human dopaminergic neuroblastoma cell line (SH-SY5Y).

75 resent evidence that loss of CSA or CSB in a neuroblastoma cell line converges on mitochondrial dysfu

76 y inhibit manganese toxicity not only in the neuroblastoma cell line SH-SY5Y in vitro but also in a m

77 phagy machinery homeostasis in human SH-SY5Y neuroblastoma cell line.

78 In 3 human neuroblastoma cell lines (SK-N-AS, SK-N-BE2, and SH-SY5Y

79 ye-Bourgeois and colleagues demonstrate that neuroblastoma cell lines and patient-derived xenografts

80 tivity of ALK inhibitor monotherapy in human neuroblastoma cell lines and xenograft models expressing

81 transendothelial migration in two different neuroblastoma cell lines in vitro.

82 suppress the growth of MYCN-amplified human neuroblastoma cell lines in xenograft mouse models.

83 an neuroblastoma, and its depletion in human neuroblastoma cell lines induces apoptosis.

84 We report in human brain and human SH-SY5Y neuroblastoma cell lines that DJ-1 predominantly forms h

85 that LIN28B is dispensable in MYCN-amplified neuroblastoma cell lines, despite de-repression of let-7

86 mitochondrial uncoupling using VCP knockdown neuroblastoma cell lines, induced pluripotent stem cells

87 elative to normal cells across a panel of 15 neuroblastoma cell lines, where both N-Myc and c-Myc dir

88 ells (designated CAF-MSCs) enhanced in vitro neuroblastoma cell proliferation, survival, and resistan

89 the ODC1 and E2F2 gene promoters and reduced neuroblastoma cell proliferation.

90 phosphorylation, resulting in suppression of neuroblastoma cell viability and inhibition of tumor gro

91 productive infection and IEtu1 GREs in mouse neuroblastoma cells (Neuro-2A).

92 of p11, 5-HTR1b and 5-HTR4 in mice and human neuroblastoma cells (SH-sy5y).

93 gregated form, in restoring the viability of neuroblastoma cells against Abeta-induced toxicity.

94 observed with SMN depletion in human SH-SY5Y neuroblastoma cells and human induced pluripotent stem c

95 -derived oxidants can be quantified in human neuroblastoma cells and midbrain dopamine neurons derive

96 n potential firing patterns of SH-SY5Y human neuroblastoma cells and neonatal cardiomyocytes.

97 42) and tracked its internalization by human neuroblastoma cells and neurons.

98 clein oligomers suppressed their toxicity in neuroblastoma cells and primary cortical neurons.

99 xplaining the activity of these compounds in neuroblastoma cells and providing a rational basis for t

100 degradation promotes the differentiation of neuroblastoma cells and reduces the proportion of stem-l

101 e also down-regulated global 5-hmC levels in neuroblastoma cells and the expression levels of some hy

102 ces tumor cell death in multiple myeloma and neuroblastoma cells as well as other cancer types in the

103 creen we observed a highly potent synergy in neuroblastoma cells between the EGFR kinase inhibitor la

104 Differentiation of SH-SY5Y human neuroblastoma cells by all-trans retinoic acid, or oxida

105 xicity of alpha-synuclein oligomers in human neuroblastoma cells by inhibiting their interactions wit

106 ion of gamma-tubulin-2 in mature neurons and neuroblastoma cells during oxidative stress may denote a

107 is investigated and recovery of viability of neuroblastoma cells exposed to Abeta (1-42) is observed

108 ough the ch14.18 scFv-gD chimera Fc bound to neuroblastoma cells expressing GD2.

109 Neuroblastoma cells expressing ORF2, MAML1, and beta-cat

110 on, oxidation, and nitrosylation) in SH-SY5Y neuroblastoma cells expressing the beta-amyloid precurso

111 5 effectively rescues neuroblastoma cells from Abeta-mediated cytotoxicity and

112 Inhibiting AIF rescued neuroblastoma cells from Ad.5/3-CTV-induced cell death,

113 ly inhibited proliferation of TP53 wild-type neuroblastoma cells harboring ALK amplification or mutat

114 ROCK, a key regulator of cell migration, in neuroblastoma cells highlighted that stathmin regulates

115 fore highlights an important role for S-type neuroblastoma cells in the invasion process and reveals

116 as depleted, RABV grew more quickly in mouse neuroblastoma cells in vitro This effect was replicated

117 This paper shows that human neuroblastoma cells incorporated small amounts of uraniu

118 Ad.5/3-CTV infection of neuroblastoma cells increased ATM phosphorylation instig

119 Sustained O-GlcNAc elevation in SH-SY5Y neuroblastoma cells increased OGA expression and reduced

120 at stathmin may influence these processes in neuroblastoma cells independent of tubulin binding.

121 s of endogenous alpha-Syn from SH-SY5Y human neuroblastoma cells indicates a potential functional rel

122 zation of alpha-synuclein amyloid fibrils in neuroblastoma cells is dependent on heparan sulfate, whe

123 In neuroblastoma cells it was found that the aggregation pr

124 -24-induced caspase-independent apoptosis in neuroblastoma cells mediated through modulation of AIF,

125 bust approach to differentiate human SH-SY5Y neuroblastoma cells over 2.5 weeks, producing a uniform

126 Downregulation in neuroblastoma cells reduced cell proliferation and induc

127 Silencing of SOX5 in human SH-SY5Y neuroblastoma cells resulted in a significant repression

128 ifferentiation in vivo, knockdown of FIG4 in neuroblastoma cells resulted in vacuologenesis and cell

129 expression of MYCN in zebrafish and in human neuroblastoma cells results in the appearance of interme

130 Reduced stathmin expression in neuroblastoma cells significantly increased the activati

131 Finally, stathmin suppression in neuroblastoma cells significantly reduced whole body, lu

132 In mice xenografts of neuroblastoma cells stably expressing doxycycline-induci

133 out, a single kind of cellular assay system: neuroblastoma cells that are persistently infected with

134 ome provide a novel site of vulnerability in neuroblastoma cells that could be exploited for targeted

135 n primary cortical neurons and human SH-SY5Y neuroblastoma cells to prevent mitochondrial respiratory

136 tinoblastoma cells and CD44-negative SK-N-DZ neuroblastoma cells transduced with adenoviral vectors i

137 Furthermore, human and mouse neuroblastoma cells treated with the amyloid-beta(1-42)

138 tylome after perifosine treatment in SK-N-AS neuroblastoma cells using SILAC labeling, affinity enric

139 between TDP-43 and RACK1 on polyribosomes of neuroblastoma cells with mis-localization of RACK1 on TD

140 rtic smooth muscle cells) and SH-SY5Y (human neuroblastoma cells).

141 transporter 2 (VMAT2) and alpha-synuclein in neuroblastoma cells, and endogenous THSer(P)-31 was dete

142 In a mouse model of orthotopically implanted neuroblastoma cells, inhibition of JAK2/STAT3 and MEK/ER

143 ) when transfected into scrapie-infected N2a neuroblastoma cells, likely due to segregation of transm

144 insight into the biology of ARC channels in neuroblastoma cells, these findings provide evidence for

145 Using Tet21N human neuroblastoma cells, we also found that Myc(oncogene)-in

146 Furthermore, using neuroblastoma cells, we demonstrated the neurotoxicity a

147 Using knockout mice and RNAi in human neuroblastoma cells, we showed that nELAVL intronic and

148 ules in neurites of differentiated N2a mouse neuroblastoma cells, where it shows partial colocalizati

149 nfluence the viability and poor prognosis of neuroblastoma cells, where MYC is often overexpressed.

150 , which is frequently expressed in resistant neuroblastoma cells, which allowed prolonged and elevate

151 ant, TH1-S31A, was restricted to the soma of neuroblastoma cells, with decreased association with the

152 these motifs and is essential for binding to neuroblastoma cells, with the E138K mutation abrogating

153 %) alter transcription factor-DNA binding in neuroblastoma cells.

154 coactivation of JAK2/STAT3 and MEK/ERK1/2 in neuroblastoma cells.

155 in primary neurons but also in SH-SY5Y human neuroblastoma cells.

156 ormation of TDP-43 cytoplasmic inclusions in neuroblastoma cells.

157 etastatic process via RhoA/ROCK signaling in neuroblastoma cells.

158 bolism and gene expression, in human SH-SY5Y neuroblastoma cells.

159 72 and RAB7L1 was confirmed in human SH-SY5Y neuroblastoma cells.

160 inhibited AIF changes in Ad.5/3-CTV-infected neuroblastoma cells.

161 hat is potently cytotoxic to GPC2-expressing neuroblastoma cells.

162 reduced tau mRNA and protein level in human neuroblastoma cells.

163 ion and proliferation of MYCN gene-amplified neuroblastoma cells.

164 synthesized and evaluated in SH-SY5Y (human neuroblastoma) cells for MGE.

165 igin of intra-tumor genetic heterogeneity in neuroblastoma.Chromosomal abnormalities such as 11q dele

166 , and copy number variations in 105 cases of neuroblastoma, complemented by primary tumor- and cell l

167 erential screening-selected gene aberrant in neuroblastoma (DAN), a bone morphogenetic protein (BMP)

168 l insights into the genetic underpinnings of neuroblastoma, demonstrating that the inherited common v

169 al growth factor-like growth factor promotes neuroblastoma differentiation.

170 We demonstrate high GPC2 expression in neuroblastoma due to MYCN transcriptional activation and

171 se de novo or as a result of maturation of a neuroblastoma either spontaneously or after chemotherapy

172 high-risk primary tumors from patients with neuroblastoma exhibited strong repression of EZH2-regula

173 s without MYCN amplification, MYCN-amplified neuroblastomas expressed higher levels of EZH2.

174 used for the treatment of relapsed high-risk neuroblastoma for several years, however, the outcome re

175 tumor groups were greater than that for the neuroblastoma group (P = .01).

176 le inhibition of ROCK suppressed MYCN-driven neuroblastoma growth in TH-MYCN homozygous transgenic mi

177 of IGFBP3, a direct EZH2 target, suppressed neuroblastoma growth in vitro and in vivo.

178 harmacological suppression of EZH2 inhibited neuroblastoma growth in vitro and in vivo.

179 Here we show that neuroblastoma harbors frequent mutations of genes contro

180 onal Society of Paediatric Oncology European Neuroblastoma/High-Risk Neuroblastoma 1 (SIOPEN/HR-NBL1)

181 ent-free survival in patients with high-risk neuroblastoma; however, which regimen has the greatest p

182 High-risk neuroblastoma (HR-NB) is the most frequent, aggressive,

183 primary cancers (glioblastoma multiforme and neuroblastoma), human brain cancer cell lines (D54 and D

184 pathogenic KIF1Bbeta mutations identified in neuroblastoma impair TRKA transport.

185 t EZH2 represses neuronal differentiation in neuroblastoma in a PRC2-dependent manner.

186 s sufficient to suppress the acceleration of neuroblastoma in nf1-deficient fish, but not the hypertr

187 prolonging survival of mice bearing GD2-high neuroblastomas in vivo.

188 ng qPCR analysis of an independent cohort of neuroblastomas, including a subset of tumors without MYC

189 DRP1 are silenced in 1p36 hemizygous-deleted neuroblastomas, indicating that deregulation of calcineu

190 LMO1 as an important oncogene that promotes neuroblastoma initiation, progression, and widespread me

191 ound that genetic loss of let-7 is common in neuroblastoma, inversely associated with MYCN amplificat

192 Thus, even though neuroblastoma is a classical "developmental tumor", NF1

193 Neuroblastoma is a pediatric cancer characterized by var

194 Neuroblastoma is a pediatric solid tumor with high expre

195 Neuroblastoma is a pediatric tumor characterized by hist

196 Neuroblastoma is a peripheral neural system tumor that o

197 Poor prognosis in neuroblastoma is associated with genetic amplification o

198 High-risk neuroblastoma is characterized by undifferentiated neuro

199 f ALK inhibitors in patients with ALK-mutant neuroblastoma is limited, highlighting the need to impro

200 While neuroblastoma is often RD3-positive, the adrenal medulla

201 One feature of high-risk neuroblastoma is the high level of DNA methylation of pu

202 Neuroblastoma is the most common cancer in infancy and e

203 Neuroblastoma is the most common childhood extracranial

204 lines, including glioblastoma, astrocytoma, neuroblastoma, lung adenocarcinoma, and breast cancer.

205 c ability of this signature was evaluated in neuroblastoma, medulloblastoma, diffuse large B-cell lym

206 stathmin, has recently been shown to mediate neuroblastoma metastasis although precise functions rema

207 f SPHK1 or YAP/TAZ was sufficient to inhibit neuroblastoma metastasis in vivo Overall, we identify ge

208 nderstand the molecular mechanisms mediating neuroblastoma metastasis, we developed a mouse model usi

209 h7 and C2C12 cells and abrogated it in mouse neuroblastoma N2A cells.

210 stant ALK(F1174L) mutation arises de novo in neuroblastoma (NB) and is acquired in ALK translocation-

211 ymphoma kinase (ALK) is sufficient to induce neuroblastoma (NB) in mouse sympathoadrenal cells.

212 Neuroblastoma (NB) is a childhood tumor that arises from

213 Neuroblastoma (NB) is a pediatric malignant neoplasm of

214 Neuroblastoma (NB) is the most common extracranial tumor

215 transcription factor CASZ1 to function as a neuroblastoma (NB) tumor suppressor.

216 In patients with neuroblastoma (NB), treatment with anti-GD2 monoclonal a

217 paucity of druggable mutations in high-risk neuroblastoma (NB), we undertook chromatin-focused small

218 Moreover, in solid tumors such as stage 4 neuroblastomas (NB), imatinib showed benefits that might

219 Neuroblastoma (NBL) is an embryonal cancer of the sympat

220 Furthermore, in neuroblastoma neuro-2A cells and primary superior cervic

221 ta-catenin and/or HMGA1 in transfected mouse neuroblastoma (Neuro-2A) cells.

222 anscriptional activation of target genes and neuroblastoma oncogenesis.

223 hese findings validate GPC2 as a non-mutated neuroblastoma oncoprotein and candidate immunotherapeuti

224 nts had to have histological verification of neuroblastoma or ganglioneuroblastoma at diagnosis or ha

225 atients with recurrent or refractory stage 4 neuroblastoma or metastatic paraganglioma/pheochromocyto

226 D3-positive, the adrenal medulla, where many neuroblastomas originate, is RD3-negative.

227 ment of neuroendocrine tumors, especially in neuroblastoma, paraganglioma, and pheochromocytoma.

228 role in some neuroendocrine tumors, such as neuroblastoma, paraganglioma/pheochromocytoma, and carci

229 e how epigenetic deregulation contributes to neuroblastoma pathogenesis, with novel implications for

230 the neuroblastoma tumor microenvironment in neuroblastoma pathogenesis.-Gaviglio, A.

231 In two independent neuroblastoma patient cohorts, high DKC1 expression corr

232 inhibited tumor growth is reflected in large neuroblastoma patient datasets.

233 Seventeen of 19 neuroblastoma patients continued on further chemotherapy

234 High-risk neuroblastoma patients receive myeloablative chemotherap

235 defined (MET-75) that predicted survival of neuroblastoma patients with metastatic disease.

236 RhoA is activated in tumors from neuroblastoma patients, and elevated expression of Rho-a

237 on, we demonstrate that GPC2 is required for neuroblastoma proliferation.

238 The broad clinical spectrum of neuroblastoma ranges from spontaneous regression to rapi

239 Activating mutations in neuroblastoma RAS viral oncogene homolog (NRAS) are freq

240 escence features prominently in PSC and that neuroblastoma RAS viral oncogene homolog (NRAS) is activ

241 Neuroblastoma RAS viral oncogene homolog was mutated in

242 lanoma, mutant and thereby constantly active neuroblastoma rat sarcoma (NRAS) affects 15-20% of tumor

243 o induction therapy, nearly 50% of high-risk neuroblastomas recur because of chemoresistance.

244 ranscriptomic analyses show that unfavorable neuroblastomas resemble mouse sympathetic neuroblasts la

245 The International Neuroblastoma Response Criteria (INRC) require serial me

246 working group established the International Neuroblastoma Response Criteria (INRC) to assess treatme

247 Response was assessed by International Neuroblastoma Response Criteria or (for MP) by changes i

248 5-Aza-deoxycytidine (AZA) restores high-risk neuroblastoma sensitivity to RA.

249 entiated neural progenitor cells (dNPCs) and neuroblastoma SH-SY5Y (dSY5Y) cells.

250 on of wild type and mutant 4R-Tau isoform in neuroblastoma SH-SY5Y cell lines is sufficient to induce

251 P(+)-induced neurotoxicity in cultured human neuroblastoma SH-SY5Y cells, a widely used in vitro Park

252 -methyl-4-phenylpyridinium (MPP(+)) in human neuroblastoma SH-SY5Y cells.

253 ry tumor response in children with high-risk neuroblastoma should therefore be evaluated in accordanc

254 , yielding an IC50 value of 356 +/- 21 nM in neuroblastoma SHSY5Y cells and proved even to efficientl

255 ressed only in stromal compartments of human neuroblastoma specimens, with tissue from high-stage dis

256 ts exhibited (123)I-MIBG-avid, International Neuroblastoma Staging System stage 4 neuroblastoma.

257 These findings in cardiac ischaemia and in neuroblastoma suggest that TRPM2 has a basic role in sus

258 M-domain-only transcriptional cofactor, as a neuroblastoma susceptibility gene that functions as an o

259 LMO1 is a high-risk neuroblastoma susceptibility gene, but how LMO1 cooperat

260 a MYCN-driven transgenic zebrafish model of neuroblastoma that arises in the PSNS.

261 entially expressed cell-surface molecules in neuroblastoma that meet criteria for optimal immunothera

262 activation of RAS signaling in MYCN-induced neuroblastomas that arise in these precursors, and that

263 1Bbeta-deficient mouse neuroblasts and human neuroblastomas that lack KIF1Bbeta.

264 Advanced stages of neuroblastoma, the most common extracranial malignant so

265 Neuroblastoma, the most common solid tumor of young chil

266 igh levels of DOT1L gene expression in human neuroblastoma tissues correlated with high levels of MYC

267 therapeutic potential of CXCR4 inhibition in neuroblastoma treatment and provide a rationale to test

268 he Children's Oncology Group (COG) high-risk neuroblastoma trial, COG A3973, with a postinduction CS

269 nd resistance to chemotherapy and stimulated neuroblastoma tumor engraftment and growth in immunodefi

270 mechanisms by which CXCR4 signaling controls neuroblastoma tumor growth and response to therapy.

271 as been shown to be effective in controlling neuroblastoma tumor growth.

272 data support a role for loss of HBEGF in the neuroblastoma tumor microenvironment in neuroblastoma pa

273 nation (i.e. lapatinib plus YM155) decreased neuroblastoma tumor size in an in vivo model.

274 y gene, but how LMO1 cooperates with MYCN in neuroblastoma tumorigenesis is unclear.

275 have demonstrated that N-Myc is a driver of neuroblastoma tumorigenesis, therapies that directly sup

276 of CXCR4 or stimulation with CXCL12 supports neuroblastoma tumorigenesis.

277 esent in three independent high-risk stage 4 neuroblastoma tumors (COA/UAB-3, COA/UAB -6 and COA/UAB

278 Here, we have isolated from primary human neuroblastoma tumors a population of alphaFAP- and FSP-1

279 Analysis of human neuroblastoma tumors also confirmed the presence of alph

280 Neuroblastoma tumors arise in children and are character

281 HBEGF mRNA expression is decreased in human neuroblastoma tumors compared with benign tumors, with l

282 CXCR4 expression in neuroblastoma tumors correlates with disease severity.

283 mutations not reported previously in primary neuroblastoma tumors.

284 yses and was further validated in 42 primary neuroblastomas using qPCR.

285 pound YM155 that is preserved across several neuroblastoma variants.

286 Mean 5-year overall survival (+/-SD) for neuroblastoma was 37% +/- 11%.

287 sight into perifosine anti-tumor activity in neuroblastoma we have studied changes in the proteome an

288 he development and pathogenesis of high-risk neuroblastoma, we generated a MYCN-driven genetically en

289 ers of ABT-199 sensitivity in MYCN-amplified neuroblastomas, we demonstrate that the Aurora Kinase A

290 Patients (age 1-20 years) with neuroblastoma were eligible to be randomly assigned if t

291 pse is the major cause of death in pediatric neuroblastoma, where there remains a lack of therapies t

292 de an effective treatment for TP53 wild-type neuroblastoma with ALK aberrations.

293 ent-free survival in children with high-risk neuroblastoma with an adequate response to induction tre

294 hese new molecular entities, designated "CNS neuroblastoma with FOXR2 activation (CNS NB-FOXR2)," "CN

295 s to improve the treatment of very high-risk neuroblastomas with aberrant RAS-MAPK activation.

296 in tumors without any treatment, and 18 with neuroblastoma without brain metastatic disease).

297 Moreover, compared with neuroblastomas without MYCN amplification, MYCN-amplifie

298 gous transgenic mice and MYCN gene-amplified neuroblastoma xenograft growth in nude mice.

299 esulted in complete and durable responses in neuroblastoma xenografts derived from these cells.

300 rodialysis in patient-derived GD2-expressing neuroblastoma xenografts.