ライフサイエンスコーパス: MPNST

1 MPNST >or=10 cm at diagnosis, partial resection, and met

2 MPNST cells expressing shEYA4 either failed to form tumo

3 MPNST cells of both genotypes require laminin binding to

4 MPNST patients treated from 1986 to 2006 (n = 140) were

5 MPNST(LOSS) were also highly sensitive to DNA methyltran

6 MPNSTs are highly aggressive, therapeutically resistant,

7 MPNSTs are multidrug resistant, and thus long-term patie

8 MPNSTs occurred most often in the extremities (p = 0.006

9 MPNSTs with PRC2 loss showed complete loss of trimethyla

10 (CIS) analysis of 269 neurofibromas and 106 MPNSTs identified 695 and 87 sites with a statistically

11 analyzed whole exome sequencing data from 12 MPNST and SNP arrays for a subset of these.

12 Five of the 12 MPNST in our cohort (42%) contained such a mutation.

13 re retrospectively analyzed, representing 24 MPNSTs (all histologically confirmed) and 69 BNFs (26 hi

14 HG-MLPS: n = 65 [22.6%]; SS: n = 70 [24.4%]; MPNST: n = 27 [9.4%]; and LMS: n = 28 [9.8%]) were rando

15 block MEK activity and simultaneously ablate MPNSTs.

16 In the absence of retinoic acid, MPNST cells depleted of CRABP2 had reduced viability and

17 se neurofibroma transformation to aggressive MPNST (GEM-PNST).

18 All MPNST cell lines express the epidermal growth factor rec

19 RalA, however, was overactivated in all MPNST cells and tumor samples compared to nontransformed

20 nt somatic alterations of CDKN2A (81% of all MPNSTs) and NF1 (72% of non-NF1-associated MPNSTs), both

21 Tumor-forming potential is common among MPNST cells, but the assay conditions required to detect

22 hibitor FLLL32 delayed MPNST formation in an MPNST xenograft nude mouse model.

23 o study the clonal development of ANNUBP and MPNST and to identify new therapies to treat existing tu

24 vitro (immortalized human Schwann cells) and MPNST formation in vivo (transgenic mice).

25 AZ was predominately detected in AS, MLS and MPNST.

26 tifying novel genes driving neurofibroma and MPNST pathogenesis.

27 ntly proliferating cells in neurofibroma and MPNST, prolonged survival of mice implanted with human M

28 stained in mouse and human neurofibromas and MPNST.

29 nalyses of mouse and human neurofibromas and MPNSTs and identified global negative feedback of genes

30 tant therapeutic target in neurofibromas and MPNSTs.

31 or Schwann cells of skin, neurofibromas, and MPNSTs.

32 t neurofibromatosis type 1 (NF-1) associated MPNST.

33 Patients with NF1-associated MPNST appear to have worse outcomes than patients with s

34 ABP2 was established in human NF1-associated MPNST cell lines (S462, T265, NSF1), and functional effe

35 indicate a role for CXCR4 in NF1-associated MPNST development and identify a therapeutic target.

36 PNSTs and a majority of human NF1-associated MPNST lesions, suggesting that PTEN dosage and its contr

37 PNST that recapitulates human NF1-associated MPNST to identify a novel small chemical compound that i

38 s were also enriched in human NF1-associated MPNST.

39 t reflect the genetics of patient-associated MPNST.

40 l MPNSTs) and NF1 (72% of non-NF1-associated MPNSTs), both of which significantly co-occur with PRC2

41 e constitutively activated in NF1-associated MPNSTs, while PTT serves as a minimally invasive method

42 hyperactivation, as in human NF1-associated MPNSTs.

43 ssociated and 90% of radiotherapy-associated MPNSTs.

44 s malignant peripheral nerve sheath tumor (C-MPNST) and spindle cell melanoma (SCM) have not been wel

45 ndings support that the TME composition of C-MPNSTs and SCMs is at least partially independent on pro

46 and their effect on the TME composition of C-MPNSTs and SCMs.

47 8(+) T cells and macrophages in the TME of C-MPNSTs.

48 hRNA or pharmacological inhibition decreases MPNST cell growth in culture and inhibits tumorigenesis

49 acin-I inhibited the growth of NF1-deficient MPNST cells in vivo.

50 the lost PRC2 component in a PRC2-deficient MPNST cell line restored H3K27me3 levels and decreased c

51 y expressed in mouse models of NF1-deficient MPNSTs, but not in nontransformed precursor cells.

52 specific JAK2/STAT3 inhibitor FLLL32 delayed MPNST formation in an MPNST xenograft nude mouse model.

53 FLLL32 pharmacological inhibitor in delaying MPNST growth suggests that combination therapies targeti

54 n Schwann cells (P(0)-GGFbeta3 mice) develop MPNSTs.

55 (18)F-FDG PET/CT imaging in differentiating MPNSTs from BNFs in patients with NF1, with and without

56 hat reducing Group I Pak activity diminished MPNST cell proliferation and motility, and that these ef

57 rpretation of (18)F-FDG PET/CT discriminates MPNSTs from BNFs in NF1 patients with similar accuracy o

58 159-gene molecular signature distinguishing MPNST cell lines from normal Schwann cells, which was va

59 most effective single agents in eliminating MPNST cells without prohibitive toxicity.

60 xically, chronic MAF overexpression enhanced MPNST cell tumor growth in vivo, correlating with elevat

61 ts identified new and known driver genes for MPNST formation at these sites.

62 i resistance, with clinical implications for MPNST patients harboring NF1 alterations.

63 dies confirm the utility of mouse models for MPNST driver gene discovery and provide new insights int

64 Thus, an EGFR-STAT3 pathway is necessary for MPNST transformation and establishment of MPNST xenograf

65 found to be independent prognosticators for MPNST DSS in a multivariable analysis.

66 epresents a promising therapeutic target for MPNST treatment.

67 rgery is the primary course of treatment for MPNST, but with the limitation that these tumors are hig

68 To better understand the genetic basis for MPNSTs, we performed genome-wide or targeted sequencing

69 rgical resection is the standard of care for MPNSTs, but is often incomplete and can generate loss of

70 The mean SULmax was significantly higher for MPNSTs than BNFs on both early scans (6.5 vs. 2.0, P < 0

71 article-based photothermal therapy (PTT) for MPNSTs.

72 ing these seemingly disparate techniques for MPNSTs is based on several reports demonstrating the eff

73 e, we compared eight cell lines derived from MPNSTs and seven normal human Schwann cell samples.

74 e used adenovirus-Cre injections to generate MPNST in Nf1(Flox/Flox); Ink4a/Arf(Flox/Flox) and Nf1(Fl

75 ble chromosomal alterations in P(0)-GGFbeta3 MPNST cells (including universal chromosome 11 gains) an

76 P(0)-GGFbeta3 MPNSTs also exhibited abnormalities in the p16(INK4A)-cy

77 min expression was maintained, P(0)-GGFbeta3 MPNSTs exhibited Ras hyperactivation, as in human NF1-as

78 Human MPNST cell lines (Mash-1, YST-1, NMS-2 and NMS-2PC cells

79 we report the modulation of murine and human MPNST cell growth by the fatty acids docosahexaenoic aci

80 available in vitro models of MPNST and human MPNST cell lines, while remaining nontoxic to normally d

81 al stem cells, mouse glioma cells, and human MPNST cells through Ser(727) phosphorylation, leading to

82 TMs and protein expression in archival human MPNST illustrates how PRC2 loss promotes oncogenesis but

83 phosphorylated STAT3 (Tyr705) in both human MPNST and mouse GEM-PNST.

84 rmalin-fixed, paraffin-embedded (FFPE) human MPNST with and without PRC2 loss (MPNST(LOSS) vs. MPNST(

85 hila, were found to be dysregulated in human MPNST cell lines and solid tumors.

86 we report that restoration of KANK1 in human MPNST cells inhibits cell growth both in human cell cult

87 increased EGFR expression co-occur in human MPNST samples.

88 de of cancer-associated transcripts in human MPNST samples.

89 MAF was also downregulated in human MPNST.

90 ein (ABCB1), in the plasma membrane of human MPNST cells.

91 lative to rQLuc, rQT3-infected primary human MPNST and neuroblastoma cells exhibited equivalent virus

92 Using the human MPNST Schwann cell line ST88-14, we demonstrate that, in

93 engineered mice (GEM)-PNST similar to human MPNST, and tumors showed reduced p16INK4a protein and re

94 longed survival of mice implanted with human MPNST cells, and shrank neurofibromas in more than 80% o

95 nant transformation in both murine and human MPNSTs.

96 didate tumor suppressor gene (TSG) for human MPNSTs.

97 three Schwann cell lines derived from human MPNSTs possessed active p53.

98 the expression and action of NRG-1 in human MPNSTs and neurofibromas, the benign precursor lesions f

99 may function as a tumor suppressor in human MPNSTs, and thus it may be useful for targeted therapy.

100 these activated molecular pathways in human MPNSTs.

101 RA, which is important because ~78% of human MPNSTs have expression of wild-type PDGFRA, whereas only

102 FRA, which is important because 78% of human MPNSTs have expression of wild-type PDGFRA, whereas only

103 In surgical resections of human MPNSTs, HSF1 was overexpressed, translocated to the nucl

104 activity of PAK1/2/3 and the stage of human MPNSTs.

105 a unique approach for the treatment of human MPNSTs.

106 series, should be considered for an improved MPNST staging system useful for prognostic assessment an

107 ion as a novel cell signaling abnormality in MPNST that leads to important biological outcomes with t

108 nts for their ability to induce apoptosis in MPNST cells arising in nf1/tp53-deficient zebrafish.

109 found to diminish KANK1-induced apoptosis in MPNST cells.

110 were found to induce productive autophagy in MPNST cells.

111 s implicate additional signaling cascades in MPNST pathogenesis.

112 unogenic, as an adjuvant for chemotherapy in MPNST patients.

113 In contrast, in MPNST and HCTp53-/- cells, Nutlin-3a inhibited the bindi

114 retinoic acid binding protein 2 (CRABP2) in MPNST in vitro.

115 Rather, OHT-induced death in MPNST cells was associated with autophagic induction and

116 factor, p53, and pMEK were over-expressed in MPNST compared with benign neurofibromas.

117 Reducing TWIST1 expression in MPNST cells using small interfering RNA did not affect a

118 osfamide in SS; etoposide plus ifosfamide in MPNST; and gemcitabine plus docetaxel in UPS.

119 (EGFR) overexpression has been implicated in MPNST formation, but its precise role and relevant signa

120 stead, DNA methylation globally increased in MPNST(LOSS).

121 ly validated as a proto-oncogene involved in MPNST maintenance.

122 pression of glial differentiation markers in MPNST cells in vitro, decreased self-renewal of embryoni

123 -haploinsufficient tumor microenvironment in MPNST.

124 ted whether the absence of EZH2 mutations in MPNST is due to a PRC2-independent (i.e., noncanonical)

125 growth factor receptor (EGFR) gene occur in MPNST formation.

126 ate multiple essential oncogenic pathways in MPNST cells, including the Wnt/beta-catenin, YAP/TAZ, RB

127 AP1 nuclear expression was most prevalent in MPNST, SySa and MLS, whereas nuclear TAZ was predominate

128 l reduced the synthesis of viral proteins in MPNST cells.

129 sor gene mutations play an important role in MPNST pathogenesis, it is likely that dysregulated signa

130 ritical and potentially cooperative roles in MPNST pathogenesis.

131 leton regulator, its tumorigenic function in MPNSTs remains largely unknown.

132 to be the main target for hypomethylation in MPNSTs.

133 NRG-1) growth factors promote mitogenesis in MPNSTs, we examined the expression and action of NRG-1 i

134 icant global hypomethylation was observed in MPNSTs using methylome analysis by MeDIP-seq.

135 kers, SOX9 and TWIST1, were overexpressed in MPNSTs.

136 ossibly interacting SIX and DACH proteins in MPNSTs and suggest the EYA4 pathway as a rational therap

137 CNP, PMP22, and NGFR) was down-regulated in MPNSTs whereas neural crest stem cell markers, SOX9 and

138 if these enzymes might regulate signaling in MPNSTs.

139 eral cancers, it has not yet been studied in MPNSTs.

140 tumor cell phenotypes in vitro by increasing MPNST cell death and reducing metabolic activity and anc

141 ave a pathogenic effect in NF1 and inhibited MPNST growth in vivo.

142 f these two agents synergistically inhibited MPNST cell growth in vitro and dramatically decreased lo

143 Thus, KANK1 inhibits MPNST cell growth though CXXC5 mediated apoptosis.

144 gether, these data provide new insights into MPNST signaling deregulation and suggest that co-targeti

145 oxic effects of OHT by studying how it kills MPNST cells.

146 FPE) human MPNST with and without PRC2 loss (MPNST(LOSS) vs. MPNST(RET)).

147 whereas others are underrepresented in many MPNSTs.

148 dramatically decreased local and metastatic MPNST growth in animal models.

149 Most MPNST cells from Nf1(+/-); Ink4a/Arf(-/-) mice expressed

150 imated by quantitative real-time PCR in most MPNST cell lines.

151 rf(-/-) mice expressed laminin, whereas most MPNST cells from Nf1(+/-); p53(+/-) mice did not.

152 cell gene signature, and accordingly, mouse MPNST-like melanomas were also extensively infiltrated b

153 udy, we show that among five different mouse MPNST cell lines, only the ones with elevated levels of

154 A transplantable mouse MPNST-like melanoma cell line recapitulated mast cell re

155 e in PTEN expression was found in all murine MPNSTs and a majority of human NF1-associated MPNST lesi

156 Nascent MPNSTs were identified within neurofibromas, suggesting

157 ta3 mice accurately model human neurofibroma-MPNST progression, cohorts of these animals were monitor

158 ice represent a robust model of neurofibroma-MPNST progression useful for identifying novel genes dri

159 hat accurately models plexiform neurofibroma-MPNST progression in humans would facilitate identificat

160 enign neurofibromas; subsequent neurofibroma-MPNST progression is caused by aberrant growth factor si

161 f MEK and SHP2 is effective in models of NF1-MPNST, both those naive to and those resistant to MEKi,

162 was superior to MEKi alone in models of NF1-MPNST, including those with acquired resistance to MEKi.

163 ransplantation, whereas only 1.8% to 2.6% of MPNST cells from Nf1(+/-); p53(+/-) mice did.

164 provide new insights into the complexity of MPNST pathogenesis.

165 g understanding of the genomic complexity of MPNST.

166 Given the exceptional dependency of MPNST cells on HuR for survival, proliferation, and diss

167 To identify genetic drivers of MPNST development, we used the Sleeping Beauty (SB) tran

168 or MPNST transformation and establishment of MPNST xenografts growth but not for tumor maintenance.

169 eam effectors occurred in only a fraction of MPNST cell lines.

170 n of hyaluronan oligomers inhibits growth of MPNST xenografts.

171 robust genetically engineered mouse model of MPNST that recapitulates human NF1-associated MPNST to i

172 s growth of all available in vitro models of MPNST and human MPNST cell lines, while remaining nontox

173 nhibition demonstrated activity in models of MPNST and may therefore be effective in patients with MP

174 s and in spontaneous genetic mouse models of MPNST.

175 ccelerated onset and increased penetrance of MPNST formation in fish overexpressing both the wild-typ

176 xogenous laminin increased the percentage of MPNST cells from Nf1(+/-); p53(+/-) but not Nf1(+/-); In

177 oduce fatty acids as a possible regulator of MPNST development in NF1 patients.

178 divergent turning point for the response of MPNST cells to an assault by oncolytic herpes.

179 parison using a gene expression signature of MPNST-like mouse melanomas identified a subset of human

180 e, high-dose DHA reversed the stimulation of MPNST cell growth by a number of growth factors suggeste

181 uppressor role of CRABP2 for the survival of MPNST cells in vitro.

182 of K-Ras, which is critical for survival of MPNST cells.

183 ting tumor growth and increasing survival of MPNST-bearing animals.

184 and/or therapeutic targets for treatment of MPNST and support the use of the MPNST cell lines as a p

185 Treatment of MPNST cells with the hyaluronan oligomers causes disasse

186 ribute to the survival and tumorigenicity of MPNST cells.

187 invasiveness, and in vivo tumorigenicity of MPNST cells.

188 Genomic analyses of MPNSTs arising in neuregulin-1 and epidermal growth fact

189 tudy helps understand the complex biology of MPNSTs and may enable future therapeutic development.See

190 gesting that fgf6a itself may be a driver of MPNSTs.

191 ar pathways contributing to the formation of MPNSTs in NF1 patients, we used a zebrafish tumor model

192 Consistent with the observation that half of MPNSTs develop in neurofibromatosis type 1 (NF1) patient

193 bromas, with 70% carrying smaller numbers of MPNSTs.

194 overexpresses fgf8 accelerated the onset of MPNSTs in fish bearing a mutation in p53, suggesting tha

195 the p53 gene have been found in a subset of MPNSTs and mouse models support a role for p53 mutations

196 A subset of MPNSTs was found to be highly sensitive to HDACis, espec

197 Paraffin-embedded neurofibroma or MPNST blocks were assembled in a tissue microarray; mark

198 nes not previously linked to neurofibroma or MPNST pathogenesis.

199 ound that 18% of primary and 49% of passaged MPNST cells from Nf1(+/-); Ink4a/Arf(-/-) mice formed tu

200 model (Nf1(fl/fl);Dhh-Cre) or in NF1 patient MPNST cell xenografts.

201 t increase in neurofibroma and grade 3 PNST (MPNST) formation compared with single transgenic control

202 Genetic analysis of human malignant PNSTs (MPNST) also revealed downregulation of PTEN expression,

203 STAT3 knockdown by shRNA prevented MPNST formation in vivo.

204 c and microenvironmental features of primary MPNST-like melanomas.

205 Primary MPNSTs mostly occurred unifocally as multilobulated or o

206 ix microarray data generated from 45 primary MPNSTs.

207 NSTs were significantly smaller than primary MPNSTs (p = 0.003).

208 While primary MPNSTs mostly appear unifocally as multilobulated or ovo

209 onally redundant in the slowly proliferating MPNST precursors.

210 ceptor CXCR4 and its ligand, CXCL12, promote MPNST growth by stimulating cyclin D1 expression and cel

211 Twenty patients with histologically proven MPNST underwent post-treatment 1.5 T MRI.

212 Recurrent MPNSTs purely occurred multifocally as mostly nodular (p

213 Recurrent MPNSTs were significantly smaller than primary MPNSTs (p

214 Primary and recurrent MPNSTs were examined for configuration, contrast enhance

215 s multilobulated or ovoid lesions, recurrent MPNSTs purely occur multifocally as mostly nodular lesio

216 Moreover, Cpd21 can reduce MPNST burden in a mouse allograft model, underscoring th

217 bal loss of PRC2-mediated repression renders MPNST differentially dependent on DNA methylation to mai

218 with the MEK inhibitor trametinib to retard MPNST progression in transgenic fish overexpressing the

219 ting hyaluronan-CD44 interactions sensitizes MPNSTs to doxorubicin in vitro and in vivo.

220 and negative predictive value for separating MPNSTs from BNFs of 91%, 84%, 67%, and 96% versus 91%, 8

221 53-mutant malignant peripheral nerve sheath (MPNST) and p53-null HCT116 cells with cisplatin (Cis) an

222 Sixteen MPNSTs but none of the neurofibromas tested were found t

223 e worse outcomes than patients with sporadic MPNST, but the mechanism underlying this correlation is

224 ens in particular for patients with sporadic MPNST.

225 a panel of human NF1-associated and sporadic MPNSTs in vitro and in vivo.

226 rs (MPNSTs) compared with unmatched sporadic MPNSTs (P = .001).

227 In contrast, as a group the sporadic-MPNST cells were markedly resistant to HDACi treatment.

228 a reciprocal activity in vitro, stimulating MPNST cell growth at comparable concentrations and reduc

229 We found that MPNST lines are heterogeneous in their in vitro growth r

230 d those resistant to MEKi, as well as in the MPNST precursor lesion plexiform neurofibroma.

231 Comparative analysis of the MPNST and Schwann cell methylomes identified 101,466 can

232 reatment of MPNST and support the use of the MPNST cell lines as a primary analytic tool.

233 These MPNST lines are NRG-1 responsive and demonstrate constit

234 ignaling and thus contributes importantly to MPNST development-a prediction supported by the ability

235 h the molecular mechanisms underlying NF1 to MPNST malignant transformation remain unclear, alteratio

236 ys are critical for transformation of NFs to MPNST.

237 Although loss of the NF1 gene predisposes to MPNST induction, relatively long tumor latency in NF1 pa

238 ately phenocopy human ANNUBP and progress to MPNST with high penetrance.

239 of NF lesions and subsequent progression to MPNST.

240 d further changes underlie transformation to MPNST.

241 to the conversion of benign neurofibromas to MPNSTs.

242 fibroma tumorigenesis and the progression to MPNSTs.

243 important new therapeutic strategy to treat MPNST, including in combination with autophagy blocking

244 in malignant peripheral nerve sheath tumor (MPNST) cell lines.

245 ent malignant peripheral nerve sheath tumor (MPNST) cells.

246 Malignant peripheral nerve sheath tumor (MPNST) is an aggressive sarcoma with recurrent loss-of-f

247 Malignant peripheral nerve sheath tumor (MPNST) is an aggressive soft tissue sarcoma.

248 for malignant peripheral nerve sheath tumor (MPNST) prognostication and management are needed.

249 and malignant peripheral nerve sheath tumor (MPNST) xenografts.

250 S), malignant peripheral nerve sheath tumor (MPNST), and undifferentiated pleomorphic sarcoma (UPS).

251 g a malignant peripheral nerve sheath tumor (MPNST).

252 and malignant peripheral nerve sheath tumor (MPNST).

253 Malignant peripheral nerve sheath tumors (MPNST) are highly invasive soft tissue sarcomas that ari

254 Malignant peripheral nerve sheath tumors (MPNST) develop in approximately 10% of neurofibromatosis

255 of malignant peripheral nerve sheath tumors (MPNST) harboring loss-of-function polycomb-repressive co

256 in malignant peripheral nerve sheath tumors (MPNST) where estrogen is not involved.

257 in malignant peripheral nerve sheath tumors (MPNST) where NF1 mutations also occur.

258 in malignant peripheral nerve sheath tumors (MPNST), a class of highly aggressive, therapeutically re

259 to malignant peripheral nerve sheath tumors (MPNST), a main cause of mortality.

260 s, malignant peripheral nerve sheath tumors (MPNST), solitary fibrous tumors, synovial sarcomas (SySa

261 of malignant peripheral nerve sheath tumors (MPNST).

262 of malignant peripheral nerve sheath tumors (MPNST).

263 nd malignant peripheral nerve sheath tumors (MPNST).

264 ve malignant peripheral nerve sheath tumors (MPNST).

265 nd malignant peripheral nerve sheath tumors (MPNST).

266 of malignant peripheral nerve sheath tumors (MPNST).

267 se malignant peripheral nerve sheath tumors (MPNSTs) and found that 18% of primary and 49% of passage

268 Malignant peripheral nerve sheath tumors (MPNSTs) are a type of rare sarcomas with a poor prognosi

269 Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive neoplasms that commonly occur in

270 Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive sarcomas without effective therap

271 Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive tumors with low survival rates an

272 Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive, frequently metastatic sarcomas t

273 Malignant peripheral nerve sheath tumors (MPNSTs) are devastating sarcomas for which no effective

274 Malignant peripheral nerve sheath tumors (MPNSTs) are genetically diverse, aggressive sarcomas tha

275 Malignant peripheral nerve sheath tumors (MPNSTs) are sarcomas of Schwann cell lineage origin that

276 Malignant peripheral nerve sheath tumors (MPNSTs) are soft tissue sarcomas that arise in connectiv

277 Malignant peripheral nerve sheath tumors (MPNSTs) are soft-tissue sarcomas that frequently arise i

278 AS malignant peripheral nerve sheath tumors (MPNSTs) compared with unmatched sporadic MPNSTs (P = .00

279 Malignant peripheral nerve sheath tumors (MPNSTs) develop sporadically or in the context of neurof

280 an malignant peripheral nerve sheath tumors (MPNSTs) driven by NF1 loss, HSF1 was overexpressed and a

281 ng malignant peripheral nerve sheath tumors (MPNSTs) from benign neurofibromas (BNFs) in patients wit

282 om malignant peripheral nerve sheath tumors (MPNSTs) overexpress PDGF receptor-beta and generate an a

283 Malignant peripheral nerve sheath tumors (MPNSTs) represent a group of highly aggressive soft-tiss

284 at malignant peripheral nerve sheath tumors (MPNSTs) that arise in zebrafish as a result of mutations

285 of malignant peripheral nerve sheath tumors (MPNSTs), benign neurofibromas, and normal Schwann cells.

286 e, malignant peripheral nerve sheath tumors (MPNSTs), is thought to result in the overactivation of t

287 In malignant peripheral nerve sheath tumors (MPNSTs), Polycomb repressive complex 2 (PRC2), which pla

288 to malignant peripheral nerve sheath tumors (MPNSTs), rare Schwann cell-derived malignancies that occ

289 or malignant peripheral nerve sheath tumors (MPNSTs), which are highly aggressive sarcomas that origi

290 to malignant peripheral nerve sheath tumors (MPNSTs).

291 me malignant peripheral nerve sheath tumors (MPNSTs).

292 as malignant peripheral nerve sheath tumors (MPNSTs).

293 to malignant peripheral nerve sheath tumors (MPNSTs).

294 with and without PRC2 loss (MPNST(LOSS) vs. MPNST(RET)).

295 mas, the benign precursor lesions from which MPNSTs arise.

296 orm future clinical trials for patients with MPNST harboring alterations in NF1.

297 may therefore be effective in patients with MPNST harboring genetic alterations in NF1.

298 Patients with MPNST may also receive doxorubicin as therapy, but this

299 pathways may be beneficial for patients with MPNST.

300 nanochemotherapy" for treating patients with MPNSTs.

301 effective in the treatment of patients with MPNSTs.