ライフサイエンスコーパス: PNET

1 PNET less than 15 mm left in place did not progress.

2 PNETs (</= 38 cases) were positively associated with int

3 PNETs also exhibited a higher ratio of Tau relative to c

4 PNETs are a heterogeneous group with varying clinical pr

5 stable silencing of RABL6A in cultured BON-1 PNET cells revealed that it is essential for their proli

6 (pancreatic ductal adenocarcinoma, n = 137), PNET (pancreatic neuroendocrine tumour, n = 15), and SC

7 Among the 15 PNET/Ewing's sarcoma patients, seven are in continuous C

8 pecimens from twenty-five Grade 1 or Grade 2 PNET patients, along with matched adjacent benign contro

9 behavior of medulloblastomas, we studied 29 PNET biopsy samples (27 of which were posterior fossa me

10 o air toxics during pregnancy/infancy for 43 PNET, 34 medulloblastoma, and 106 astrocytoma cases and

11 Three of 8 PNET cell lines tested were susceptible to TRAIL-induced

12 ors of survival and were incorporated into a PNET postresection prognostic score.

13 11.15 mmol/kg in individual patients with a PNET.

14 systemic therapy for patients with advanced PNETs.

15 but with discordant benefit in the PDAC and PNET GEMMs illustrates the potential value of linked pre

16 PDAC and PNET lesions were evaluated in 3 subgroups according to

17 promoter exhibit bilateral retinal PNET and PNET originating from the subependymal layer of the thir

18 of factors regulating AKT/mTOR signaling and PNET pathogenesis is needed to improve current therapies

19 n promoter exhibit bilateral lens tumors and PNET of the midbrain.

20 tterns differed between medulloblastomas and PNETs.

21 , that were classified histopatologically as PNET, was confirmed in 4 children.

22 ian Ki-67 index was 7% (range, 1% to 19%) at PNET diagnosis and 17.5% (range, 2.0% to 70.0%) at MHS o

23 expression levels of PD-L1 and FOXP3 between PNET and adjacent benign controls.

24 Silencing RABL6A caused PNET cell-cycle arrest that coincided with selective los

25 T)/medulloblastoma, three patients; cerebral PNET, three patients; glioblastoma multiforme, two patie

26 tumors into distinct medulloblastoma and CNS-PNET subgroups, indicating they resemble human Sonic hed

27 erapeutic targets in medulloblastoma and CNS-PNET.

28 erapeutic targets in medulloblastoma and CNS-PNET.

29 l genetic drivers of medulloblastoma and CNS-PNET.

30 first genetically induced mouse model of CNS-PNET and a rare model of group 3 and 4 medulloblastoma.

31 system primitive neuroectodermal tumors (CNS-PNET) are aggressive, poorly differentiated brain tumors

32 proportion of institutionally diagnosed CNS-PNETs display molecular profiles indistinguishable from

33 From the remaining fraction of CNS-PNETs, we identify four new CNS tumor entities, each ass

34 al tumors of the central nervous system (CNS-PNETs) are highly aggressive, poorly differentiated embr

35 primitive neuro-ectodermal brain tumors (CNS-PNETs) are rare tumors with ill-defined biological featu

36 For the current PNET surveillance protocol, the cumulative effective rad

37 significant role in immune modulation during PNET progression, highlighting the potential of combinin

38 inical trials in a mouse model of endogenous PNET suggest that combined targeting of the mTOR and EGF

39 agents with established activity against ES/PNET is reaching its efficacy and toxicity limits.

40 y mechanism utilized in the establishment ES/PNET tumors.

41 me was seen with use of active agents for ES/PNET-cyclophosphamide, ifosfamide, doxorubicin, dactinom

42 Ews/Fli-1 contributes to the etiology of ES/PNET by subverting the differentiation program of its ne

43 pecific markers and de novo expression of ES/PNET markers.

44 ortalized 3T3 fibroblasts and that 30% of ES/PNET tumors contain a homozygous deletion of the p16 loc

45 ths after transplantation (no evidence of ES/PNET); and one remains in CR at more than 7 years.

46 B cells resembled that observed in pooled ES/PNET cell lines and differed significantly from the NB p

47 sarcoma/primitive neuroectodermal tumor (ES/PNET) metastatic to bone/bone marrow (BM) have focused o

48 oma and primitive neuroectodermal tumors (ES/PNET) are characterized by the fusion of the N-terminus

49 erapy and delayed resection of chest wall ES/PNET.

50 s were suppressed in the hybrids, whereas ES/PNET-specific markers were unaffected.

51 large series of unselected patients with ES/PNET metastatic to bone/BM showed similarly unsatisfacto

52 Patients < or =30 years of age with ES/PNET of the chest wall were entered in 2 consecutive pro

53 ifferentiation markers, we generated NB x ES/PNET somatic cell hybrids.

54 atures of the sympathetic nervous system, ES/PNETs express markers consistent with parasympathetic di

55 resulting from a translocation unique to ES/PNETs, might account for the loss of NB-specific markers

56 The patients with Ewing/PNET who had a CR have remained disease free on therapy

57 resents a promising therapeutic approach for PNET that deserves further investigation.

58 ative regulator of Rb1 that is essential for PNET proliferation and survival.

59 mor-associated macrophages are important for PNET development and progression.

60 therapeutic strategy to enhance outcomes for PNET patients.

61 ndication was found of an increased risk for PNET.

62 tic strategy and treatment armamentarium for PNETs.

63 predicting survival after pancreatectomy for PNETs and to establish a postresection prognostic score.

64 d fifty-one patients underwent resection for PNETs.

65 (3 from VHL-related tumors including 1 from PNET), whereas only one control patient died due to unre

66 ectively(5,6), and 84% of 142 non-functional PNETs expressed one or the other factor, occasionally bo

67 latory programs, we find that non-functional PNETs fall into two major subtypes, with epigenomes and

68 to cell lineage correlates of non-functional PNETs, accurately predicts disease course and can inform

69 e poorer survival than those with functional PNETs.

70 +/- 3.5) with untreated brain tumors; 13 had PNETs, and 16 had other tumors.

71 neuroectodermal brain tumor (PNET), 8 human PNET cell lines were tested for TRAIL-induced apoptosis.

72 ing and dysfunction of p53 are seen in human PNETs, we investigated what role these abnormalities hav

73 into the biology and classification of human PNETs and suggest that multiple tumor types or variants

74 pressor and an essential activator of AKT in PNET cells.

75 tinib reduced blood flow both in PDAC and in PNET, concomitant with a reduction in vessel density; ne

76 cently garnered FDA and European approval in PNET, whereas two antiangiogenic drugs failed to demonst

77 High TrkC mRNA expression in PNET is a powerful independent predictor of favorable cl

78 Thus, RABL6A promotes G1 progression in PNET cells by inactivating Rb1, an established suppresso

79 n important mechanism of TRAIL-resistance in PNET cells.

80 omarker and target for anticancer therapy in PNET patients.

81 e 1 (DNMT1) was significantly upregulated in PNET samples, positively correlated with higher tumor gr

82 concentration was significantly elevated in PNETs and was useful in the differentiation of PNETs fro

83 r cognate receptor proteins are expressed in PNETs as well as in other pediatric brain tumors may imp

84 findings indicate that expression of GFAP in PNETs has prognostic power comparable with the most sign

85 s expressed at significantly lower levels in PNETs from invasion-resistant C3H mice compared with inv

86 epigenetic regulators and immune markers in PNETs to evaluate the potential for a combination of epi

87 ve clinical relevance for targeting c-MET in PNETs.

88 tocyte growth factor (HGF) receptor c-MET in PNETs.

89 ogical factors of prognostic significance in PNETs, the expression of glial, neuronal, or photorecept

90 combination therapy against these targets in PNETs.

91 (den)/VP(den) and Tm(den)/PanP(den) indicate PNET.

92 These c-Myc+beta-catenin-induced PNETs are histologically similar to large cell/anaplasti

93 xpressed in medulloblastomas (infratentorial PNETs) but was expressed in three of five supratentorial

94 iological markers, and treatments at initial PNET diagnosis and MHS onset.

95 nd should be incorporated prospectively into PNET clinical trials.

96 g the appearance of recurrent intramedullary PNET affecting the cervical spinal cord.

97 inkage to the development of highly invasive PNETs.

98 Moreover, SMAP treatment effectively killed PNET cells in a RABL6A-dependent manner and suppressed P

99 of a comprehensive case-control study of MB/PNET, this study explored parental exposure to heat and

100 ion in future animal and human studies of MB/PNET.

101 e to any heat source were associated with MB/PNET in a dose-response fashion (for high exposure: odds

102 ng up to 1% of all CpG islands in primary MB/PNETs and 6% in MB cell lines.

103 gest series of patients with average-risk MB/PNETs treated with a combination of reduced-dose RT and

104 nervous system, including medulloblastomas (PNET/MB), are the most common malignant brain tumor of c

105 ive neuroectodermal tumors/medulloblastomas (PNETs/medulloblastomas) are suspected to originate from

106 19% at 3 years for patients with metastatic PNET/Ewing's sarcoma in first remission is encouraging.

107 g Sema3A in cancer cells converts metastatic PNETs and cervical carcinomas into benign lesions.

108 n expanding treatment options for metastatic PNETs.

109 miR-431 may be targeted to manage metastatic PNETs.

110 The cell lines Daoy and MHH-PNET-5 in which the p16(INK4A) promoter was methylated d

111 ges of tumorigenesis in both human and mouse PNETs.

112 transgenic mice bearing advanced multifocal PNET.

113 Sixteen (70%) patients with VHL had multiple PNET; lesions less than 15 mm were left in place in 11 p

114 e, RABL6A, in primary human pancreatic NETs (PNET) that correlated with high-level RABL6A protein exp

115 ween a p53 null peripheral neuroepithelioma (PNET) cell line and a cervical carcinoma HeLa cell line

116 and a p53 null peripheral neuroepithelioma (PNET) cell line.

117 retrospective analysis was performed for NF-PNET patients who underwent resection at the University

118 Ninety-seven NF-PNET patients underwent surgical resection.

119 We recommend that NF-PNET patients at high risk of recurrence undergo initial

120 ctional pancreatic neuroendocrine tumors (NF-PNETs) have poorer survival than those with functional P

121 In patients with NF-PNETs, risk factors associated with recurrence were high

122 h VHL (n = 23) operated on for nonmetastatic PNET were reviewed.

123 nd treatment of resectable and nonresectable PNETs.

124 Although the p53 null PNET parent lacked detectable p21 protein, introduction

125 Multivariate analysis of PNET immunohistochemistry and clinical variables indicat

126 were identified more often in the context of PNET progression and increased Ki-67 indices.

127 nths (range, 7 to 219) and in the context of PNET progression, stability, and tumor response in 8, 6,

128 vered that RABL6A, a new oncogenic driver of PNET proliferation, is required for AKT activity.

129 A better understanding of the drivers of PNET tumorigenesis is urgently needed.

130 The common finding of PNET arising from the subependymal layer of the dienceph

131 kinases, using a preclinical mouse model of PNET.

132 th xenograft and spontaneous mouse models of PNET.

133 oad traffic sources may increase the risk of PNET and medulloblastoma, with limited support for incre

134 An increased risk of PNET was observed for only herbicides (OR = 1.5).

135 , the molecular basis of other subclasses of PNET remains unclear.

136 activating Rb1, an established suppressor of PNET proliferation and development.

137 Treatment of PNET cells with Erk inhibitor or locked nucleic acids se

138 ificant metabolite in the differentiation of PNETs from other tumors (6.09 mmol/kg +/- 2.24 vs 0.76 m

139 ETs and was useful in the differentiation of PNETs from other tumors.

140 these abnormalities have in the formation of PNETs.

141 to active Ras/Erk and promote metastasis of PNETs.

142 whether miR-431 contributes to metastasis of PNETs.

143 nt predictors of survival after resection of PNETs (P < 0.0001).

144 on, and epithelial-mesenchymal transition of PNETs.

145 rategy of PP2A reactivation for treatment of PNETs as well as other human cancers driven by RABL6A ov

146 Furthermore, we have obtained one PNET with marked epithelial differentiation having histo

147 es were obtained from 28 patients with ES or PNET at initial presentation or at relapse.

148 with both nonmetastatic and metastatic ES or PNET, which implies that occult tumor cells are present

149 atients who are undergoing therapy for ES or PNET.

150 Twelve medulloblastoma or PNET cell lines were screened for c-myc genomic amplific

151 WMLs in medulloblastoma or PNET patients treated with conformal radiotherapy and HD

152 ents newly diagnosed with medulloblastoma or PNET were evaluated with concurrent lumbar CSF cytology

153 nose LMD in patients with medulloblastoma or PNET.

154 % to 18% of patients with medulloblastoma or PNET.

155 iagnosis in patients with medulloblastoma or PNET.

156 outcomes of patients with Ewing's sarcoma or PNET of bone with metastases at diagnosis.

157 tic and therapeutic targets in MBs and other PNETs of the CNS.

158 oplastic cells in medulloblastomas and other PNETs resemble progenitor cells of the developing centra

159 reatment of human brain tumors, particularly PNET/MB.

160 trospectively found in 8 of 14 of pathologic PNET specimens obtained before MHS diagnosis.

161 dulloblastomas are the most common pediatric PNETs.

162 anaplastic astrocytoma, one patient; pineal PNET, one patient) are alive and disease free at a media

163 targeted agents in patients with progressive PNETs.

164 l mechanisms whereby macrophages can promote PNET progression, we crossed the RIP1-Tag2 (RT2) mouse m

165 that macrophages are important for promoting PNET development and suggest that additional factors con

166 We report a case of primary renal PNET/EES of the kidney in an adult patient and describe

167 tein, while none of the five TRAIL-resistant PNET cell lines expressed caspase-8 protein.

168 RAIL-sensitivity in formerly TRAIL-resistant PNET cells, suggesting that gene methylation inhibits ca

169 3-kb IRBP promoter exhibit bilateral retinal PNET and PNET originating from the subependymal layer of

170 odermal tumor/extraskeletal Ewing's sarcoma (PNET/EES) is a very rare renal tumor.

171 Adult patients with Ewing's sarcoma/PNET at highest risk for death are those who are older t

172 Ewing's sarcoma/PNET is a disease of childhood rarely seen in adults.

173 atients with newly diagnosed Ewing's sarcoma/PNET were evaluated and treated at the Adult Sarcoma Pro

174 overexpression in a mouse insulin-secreting PNET cell line, MIN6, downregulates c-Met expression.

175 In the rapamycin-sensitive PNET/MB cell line DAOY, rapamycin exhibited additive cyt

176 However, all TRAIL-sensitive PNET cell lines expressed caspase-8 mRNA and protein, wh

177 rm outcome of resected VHL-PNET and sporadic PNET.

178 h those in patients operated on for sporadic PNET, matched for tumor size, stage, and Ki-67 index.

179 ted VHL-PNET is better than that of sporadic PNET.

180 in a RABL6A-dependent manner and suppressed PNET growth in vivo.

181 e abnormalities, we generated supratentorial PNET (sPNET) in mice using somatic cell gene transfer.

182 patients with medulloblastoma/supratentorial PNET with aggressive supportive care.

183 as expressed in three of five supratentorial PNETs.

184 ve radiation doses were compared between the PNET surveillance algorithms by analyses of variance, an

185 nt role of an initial Rb loss in driving the PNET phenotype.

186 n epigenetics and immune infiltration in the PNET tumor microenvironment remains poorly understood.

187 study, we introduced wild-type p53 into the PNET parent to investigate whether p53 retained wild-typ

188 cording to one or other treatment arm of the PNET 3 controlled trial.

189 TRAIL-sensitivity of the PNET cell lines was correlated with mRNA expression leve

190 4/5 were detected in 22, 9, and 19% of these PNET biopsies, respectively.

191 nohistochemical studies of a subset of these PNETs using antibodies to neurotrophins that primarily a

192 in 8 (27%), 18 (62%), and 14 (48%) of these PNETs, respectively.

193 , 19 pediatric brain tumors other than these PNETs also were studied here, and they expressed these n

194 with MHSs died during follow-up, all due to PNETs, including 4 patients with insulin-related MHSs.

195 anding of hereditary syndromes in regards to PNETs, as well as in the diagnosis and treatment of rese

196 have potential clinical benefit in treating PNET.

197 dhood primitive neuroectodermal brain tumor (PNET), 8 human PNET cell lines were tested for TRAIL-ind

198 blastoma or primitive neuroectodermal tumor (PNET) and document the associated clinical, radiologic,

199 peripheral Primitive Neuroectodermal Tumor (PNET) are associated with aberrant transcription factors

200 ma (MB) and primitive neuroectodermal tumor (PNET) are histologically similar brain tumors that occur

201 vement with primitive neuroectodermal tumor (PNET) demonstrated mild hypometabolism relative to corti

202 /peripheral primitive neuroectodermal tumor (PNET) family are pediatric cancers derived from neural c

203 sarcoma or primitive neuroectodermal tumor (PNET) of bone were entered onto a randomized trial evalu

204 vous system primitive neuroectodermal tumor (PNET), and astrocytoma before 6 years of age diagnosed i

205 ratentorial primitive neuroectodermal tumor (PNET).

206 blastoma or primitive neuroectodermal tumor (PNET).

207 ) patients (primitive neuroectodermal tumor (PNET)/medulloblastoma, three patients; cerebral PNET, th

208 (ES) and/or primitive neuroectodermal tumor (PNET)] sarcoma, treated with chemotherapy and surgery or

209 ncidence of pancreatic neuroendocrine tumor (PNET) is increasing, and it presents with various clinic

210 uced in the pancreatic neuroendocrine tumor (PNET) model, the latter results confirming and extending

211 DAC) and in pancreatic neuroendocrine tumor (PNET), respectively.

212 lloblastoma/primitive neuroectodermal tumor (PNETs) in location, histologic appearance, and expressio

213 nosed with primitive neuroectodermal tumors (PNET) in the United States and Canada between 1986 and 1

214 astoma and primitive neuroectodermal tumors (PNET) of the midbrain.

215 (EWS) and primitive neuroectodermal tumors (PNET), are highly aggressive malignancies predominantly

216 oninvasive pancreatic neuroendocrine tumors (PNET) and invasive carcinomas with varying degrees of ag

217 Pancreatic neuroendocrine tumors (PNET) have a poorly defined natural history, and a stagi

218 Primitive neuroectodermal tumors (PNETs) are a family of primary malignant brain tumors th

219 Primitive neuroectodermal tumors (PNETs) of the central nervous system (CNS) are poorly un

220 Primitive neuroectodermal tumors (PNETs) of the central nervous system, including medullob

221 and other primitive neuroectodermal tumors (PNETs) of the childhood CNS we performed a systematic an

222 d cerebral primitive neuroectodermal tumors (PNETs), gliomas, and cell lines derived from a variety o

223 cerebellar primitive neuroectodermal tumors (PNETs).

224 stoma, and primitive neuroectodermal tumors (PNETs).

225 f six with primitive neuroectodermal tumors (PNETs)/ medulloblastoma.

226 Pancreatic neuroendocrine tumors (PNETs) are rare tumors, with an incidence of one per 100

227 agement of pancreatic neuroendocrine tumors (PNETs) associated with von Hippel-Lindau disease (VHL) i

228 Most pancreatic neuroendocrine tumors (PNETs) do not produce excess hormones and are therefore

229 ib in both pancreatic neuroendocrine tumors (PNETs) in RIP-Tag2 mice and cervical carcinomas in HPV16

230 Pancreatic neuroendocrine tumors (PNETs) may evolve and cause hormonal hypersecretion-rela

231 Pancreatic neuroendocrine tumors (PNETs), although rare, often metastasize, such that surg

232 driver of pancreatic neuroendocrine tumors (PNETs), yet the interplay between epigenetics and immune

233 allmark of pancreatic neuroendocrine tumors (PNETs).

234 gulated in pancreatic neuroendocrine tumors (PNETs).

235 rapies for pancreatic neuroendocrine tumors (PNETs).

236 s in human pancreatic neuroendocrine tumors (PNETs).

237 ients with pancreatic neuroendocrine tumors (PNETs; 124 patients and 381 scans) were compared between

238 generated primitive neuroectodermal tumours (PNET), indicating an important role of an initial Rb los

239 (BCCs) and primitive neurectodermal tumours (PNETs).

240 including primitive neuroectodermal tumours (PNETs), atypical teratoid/rhabdoid tumours (AT/RTs) and

241 004), patients were identified who underwent PNET resection.

242 ompare the long-term outcome of resected VHL-PNET and sporadic PNET.

243 The long-term outcome of resected VHL-PNET is better than that of sporadic PNET.

244 ategy seems appropriate in patients with VHL-PNET, who may develop more life-threatening tumors of ot

245 less, PDAC tumors continued to grow, whereas PNET were growth impaired.

246 rlier reports on the association of JCV with PNETs in humans and the involvement of the Wnt signaling

247 aid in treatment planning for patients with PNETs and should be incorporated prospectively into PNET

248 d in the tumor specimens of 86 patients with PNETs by immunohistochemistry after microwave antigen en

249 Of 435 patients with PNETs, 15 (3.4%) were identified as having MHSs involvin