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 MPNSTs are highly aggressive, therapeutically resistant,

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

7 MPNSTs with PRC2 loss showed complete loss of trimethyla

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

9 (ARF)-specific exon 1beta were studied in 11 MPNST samples from 8 patients and 7 neurofibromas.

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

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

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

13 r overexpression was found in 10 of 35 (29%) MPNSTs, and it was lacking in NFs (P = 0.02).

14 Ki-67 expression was found in 20 of 34 (59%) MPNSTs but was absent in NFs (P < 0.001).

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

24 tifying novel genes driving neurofibroma and MPNST pathogenesis.

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

26 stained in mouse and human neurofibromas and MPNST.

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

28 tant therapeutic target in neurofibromas and MPNSTs.

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

30 e CDKN2A/p16 gene and p16 protein in NFs and MPNSTs from patients with NF1.

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

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

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

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

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

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

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

38 t reflect the genetics of patient-associated MPNST.

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

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

41 hyperactivation, as in human NF1-associated MPNSTs.

42 ssociated and 90% of radiotherapy-associated MPNSTs.

43 xpression of pRB, cyclin D1, and p21 between MPNSTs and NFs.

44 and E, in a cohort of 35 well-characterized MPNSTs and 16 NFs.

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

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

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

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

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

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

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

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

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

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

55 159-gene molecular signature distinguishing MPNST cell lines from normal Schwann cells, which was va

56 In contrast, all eight MPNSTs harbored NF1 deletions, regardless of S-100 prote

57 cal PNs, one cellular/atypical PN, and eight MPNSTs derived from 13 patients, seven of which had neur

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

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

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

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

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

63 r genetics to develop targeted therapies for MPNST in people with NF1.

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

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

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

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

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

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

70 ry information in the distinction of NF from MPNST.

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

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

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

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

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

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

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

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

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

80 ed from Nf1:p53 double mutant mice and human MPNST.

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

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

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

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

85 MAF was also downregulated in human MPNST.

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

87 tion and soft agar colony formation of human MPNST derived S100 positive cells and fibroblastoid cell

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

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

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

91 nant transformation in both murine and human MPNSTs.

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

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

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

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

96 these activated molecular pathways in human MPNSTs.

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

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

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

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

101 a unique approach for the treatment of human MPNSTs.

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

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

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

105 were found to induce productive autophagy in MPNST cells.

106 s implicate additional signaling cascades in MPNST pathogenesis.

107 PNs and that S-100 protein-negative cells in MPNST represent dedifferentiated Schwann cells, which ha

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

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

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

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

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

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

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

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

116 and scientists with specialist knowledge in MPNST and NF1 reviewed the current published and unpubli

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

118 -haploinsufficient tumor microenvironment in MPNST.

119 erative and causal role for p53 mutations in MPNST development.

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

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

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

123 ritical and potentially cooperative roles in MPNST pathogenesis.

124 that INK4A deletions are frequent events in MPNSTs and may participate in tumor progression.

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

126 to be the main target for hypomethylation in MPNSTs.

127 ng both p16 and p19(ARF), were identified in MPNSTs from 4 of 8 patients.

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

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

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

131 lysis and mutation analysis of CDKN2A/p16 in MPNSTs did not reveal any abnormalities.

132 r cyclin E expression was more pronounced in MPNSTs than in NFs.

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

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

135 if these enzymes might regulate signaling in MPNSTs.

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

137 be a prognostic factor for poor survival in MPNSTs (P = 0.03, relative risk = 2.4).

138 often in several tumor types, is uncommon in MPNSTs.

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

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

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

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

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

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

145 whereas others are underrepresented in many MPNSTs.

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

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

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

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

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

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

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

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

154 Nascent MPNSTs were identified within neurofibromas, suggesting

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

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

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

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

159 s did 7 of 7 other primary MPNSTs, a non-NF1 MPNST cell line, and the S100(+) cells from each of 9 be

160 nsistent with this hypothesis, growth of NF1 MPNST lines and the transformed NF1(-/-) mouse embryo Sc

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

162 provide new insights into the complexity of MPNST pathogenesis.

163 g understanding of the genomic complexity of MPNST.

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

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

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

167 n of hyaluronan oligomers inhibits growth of MPNST xenografts.

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

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

170 s and in spontaneous genetic mouse models of MPNST.

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

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

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

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

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

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

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

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

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

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

181 Treatment of MPNST cells with the hyaluronan oligomers causes disasse

182 urgical management, and medical treatment of MPNST in individuals with NF1.A multidisciplinary team a

183 ribute to the survival and tumorigenicity of MPNST cells.

184 invasiveness, and in vivo tumorigenicity of MPNST cells.

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

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

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

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

189 st NFs, but it was absent in the majority of MPNSTs, which displayed cytoplasmic staining (P < 0.001)

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

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

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

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

194 al, pathological, and genetic information on MPNST in NF1was collated, and a database was established

195 experience to produce a consensus summary on MPNST in NF1.

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

197 nes not previously linked to neurofibroma or MPNST pathogenesis.

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

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

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

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

202 STAT3 knockdown by shRNA prevented MPNST formation in vivo.

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

204 ix microarray data generated from 45 primary MPNSTs.

205 essed the EGF-R, as did 7 of 7 other primary MPNSTs, a non-NF1 MPNST cell line, and the S100(+) cells

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

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

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

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

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

211 53-mutant malignant peripheral nerve sheath (MPNST) and p53-null HCT116 cells with cisplatin (Cis) an

212 d CDKN2A/p16 deletions, whereas three of six MPNSTs appeared to have homozygous CDKN2A/p16 deletions.

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

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

215 ens in particular for patients with sporadic MPNST.

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

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

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

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

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

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

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

223 The MPNSTs, however, were essentially immunonegative for p16

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

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

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

227 ys are critical for transformation of NFs to MPNST.

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

229 of NF lesions and subsequent progression to MPNST.

230 to the conversion of benign neurofibromas to MPNSTs.

231 fibroma tumorigenesis and the progression to MPNSTs.

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

233 f 3 malignant peripheral nerve sheath tumor (MPNST) cell lines from NF1 patients expressed the EGF-R,

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

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

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

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

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

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

240 and malignant peripheral nerve sheath tumor (MPNST).

241 on (malignant peripheral nerve sheath tumor; MPNST), its neoplastic nature has been difficult to prov

242 ng malignant peripheral nerve sheath tumors (MPNST) and benign neurofibromas.

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

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

245 nd malignant peripheral nerve sheath tumors (MPNST) from neurofibromatosis type 1 (NF1) patients.

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

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

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

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

250 nd malignant peripheral nerve sheath tumors (MPNST).

251 nd malignant peripheral nerve sheath tumors (MPNST).

252 of malignant peripheral nerve sheath tumors (MPNST).

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

254 in malignant peripheral nerve sheath tumors (MPNSTs) and neurofibromas (NFs).

255 of malignant peripheral nerve sheath tumors (MPNSTs) and neurofibromas (NFs).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

275 op malignant peripheral nerve sheath tumors (MPNSTs), which supports a cooperative and causal role fo

276 me malignant peripheral nerve sheath tumors (MPNSTs).

277 as malignant peripheral nerve sheath tumors (MPNSTs).

278 to malignant peripheral nerve sheath tumors (MPNSTs).

279 to malignant peripheral nerve sheath tumors (MPNSTs).

280 to malignant peripheral nerve sheath tumors (MPNSTs).

281 ng malignant peripheral nerve sheath tumors (MPNSTs).These cancers are difficult to detect and have a

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

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

284 pathways may be beneficial for patients with MPNST.

285 effective in the treatment of patients with MPNSTs.

286 nanochemotherapy" for treating patients with MPNSTs.