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

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

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

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

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

11 11.15 mmol/kg in individual patients with a PNET.

12 systemic therapy for patients with advanced PNETs.

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

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

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

16 tterns differed between medulloblastomas and PNETs.

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

18 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 ndication was found of an increased risk for PNET.

47 tic strategy and treatment armamentarium for PNETs.

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

49 d fifty-one patients underwent resection for PNETs.

50 (3 from VHL-related tumors including 1 from PNET), whereas only one control patient died due to unre

51 e poorer survival than those with functional PNETs.

52 +/- 3.5) with untreated brain tumors; 13 had PNETs, and 16 had other tumors.

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

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

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

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

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

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

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

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

61 omarker and target for anticancer therapy in PNET patients.

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

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

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

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

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

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

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

69 combination therapy against these targets in PNETs.

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

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

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

73 nd should be incorporated prospectively into PNET clinical trials.

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

75 inkage to the development of highly invasive PNETs.

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

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

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

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

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

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

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

83 19% at 3 years for patients with metastatic PNET/Ewing's sarcoma in first remission is encouraging.

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

85 n expanding treatment options for metastatic PNETs.

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

87 transgenic mice bearing advanced multifocal PNET.

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

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

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

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

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

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

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

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

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

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

98 nd treatment of resectable and nonresectable PNETs.

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

100 Multivariate analysis of PNET immunohistochemistry and clinical variables indicat

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

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

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

104 kinases, using a preclinical mouse model of PNET.

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

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

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

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

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

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

111 these abnormalities have in the formation of PNETs.

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

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

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

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

116 atients who are undergoing therapy for ES or PNET.

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

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

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

120 nose LMD in patients with medulloblastoma or PNET.

121 % to 18% of patients with medulloblastoma or PNET.

122 iagnosis in patients with medulloblastoma or PNET.

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

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

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

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

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

128 dulloblastomas are the most common pediatric PNETs.

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

130 targeted agents in patients with progressive PNETs.

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

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

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

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

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

136 3-kb IRBP promoter exhibit bilateral retinal PNET and PNET originating from the subependymal layer of

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

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

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

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

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

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

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

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

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

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

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

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

149 as expressed in three of five supratentorial PNETs.

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

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

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

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

154 4/5 were detected in 22, 9, and 19% of these PNET biopsies, respectively.

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

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

157 , 19 pediatric brain tumors other than these PNETs also were studied here, and they expressed these n

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

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

160 have potential clinical benefit in treating PNET.

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

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

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

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

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

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

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

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

169 ratentorial primitive neuroectodermal tumor (PNET).

170 blastoma or primitive neuroectodermal tumor (PNET).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 cerebellar primitive neuroectodermal tumors (PNETs).

186 stoma, and primitive neuroectodermal tumors (PNETs).

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

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

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

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

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

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

193 gulated in pancreatic neuroendocrine tumors (PNETs).

194 rapies for pancreatic neuroendocrine tumors (PNETs).

195 s in human pancreatic neuroendocrine tumors (PNETs).

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

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

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

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

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

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

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

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

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

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

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

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