ライフサイエンスコーパス: CNS tumor

1 agnosed between 1970 and 1986 with a primary CNS tumor.

2 CNS tumor or the cause of death listed as a CNS tumor.

3 9 years), 725 children were diagnosed with a CNS tumor.

4 2014, were followed up for a diagnosis of a CNS tumor.

5 tive and psychological function in AYAs with CNS tumor.

6 to ameliorate NI in pediatric patients with CNS tumor.

7 reatment with BBBD therapy for any malignant CNS tumor.

8 h recipients of organs from donors without a CNS tumor.

9 nts of organs from 177 donors with a primary CNS tumor.

10 pediatric patients treated for leukemia or a CNS tumor.

11 ontemporary long-term survivors of pediatric CNS tumor.

12 of neural origin, has been detected in human CNS tumors.

13 tumor donors when compared to donors with no CNS tumors.

14 re different from those elicited against non-CNS tumors.

15 radiation therapy are at risk for subsequent CNS tumors.

16 transcriptional regulation of these genes in CNS tumors.

17 ncidence of both spontaneous and ENU-induced CNS tumors.

18 s grade I or II by the WHO classification of CNS tumors.

19 t of an ongoing prospective investigation of CNS tumors.

20 treatment of pediatric patients with primary CNS tumors.

21 etastases in pediatric patients with primary CNS tumors.

22 vaccines for the treatment of patients with CNS tumors.

23 rveillance for early detection of subsequent CNS tumors.

24 apies, but also to other immunotherapies for CNS tumors.

25 rofiles of single cells of various pediatric CNS tumors.

26 creased risk of childhood cancer, especially CNS tumors.

27 P-value = 0.013) showed an increased risk of CNS tumors.

28 the paradoxical role of immune responses in CNS tumors.

29 of supervised learning models in classifying CNS tumors.

30 r patients affected by poorly differentiated CNS tumors.

31 an cancers and are associated primarily with CNS tumors.

32 World Health Organization classification of CNS tumors.

33 , and 51 (23%) had other histologic types of CNS tumors.

34 ite NRAS rarely being reported as mutated in CNS tumors.

35 tral nervous system (CNS) tumors and 494 non-CNS tumors.

36 med partial responses, both in patients with CNS tumors.

37 ed in children with recurrent or progressive CNS tumors.

38 ble findings in neuropathologies and primary CNS tumors.

39 h multifunctional effects in human embryonal CNS tumors.

40 history of or active central nervous system (CNS) tumor.

41 kemia, lymphoma, and central nervous system (CNS) tumors.

42 O) classification of central nervous system (CNS) tumors.

43 application against central nervous system (CNS) tumors.

44 luated for pediatric central nervous system (CNS) tumors.

45 2.91) for childhood central nervous system (CNS) tumors.

46 are the survivors of central nervous system (CNS) tumors.

47 malignancies 1.8 and at the manifestation of CNS tumors 2.7 years, respectively.

48 patients overall, including 10 patients with CNS tumors (38.5%).

49 1316 participants), central nervous system (CNS) tumors (488 participants), and Hodgkin lymphoma (HL

50 sarcomas on strength testing (score +/- SD: CNS tumors, 76.5 +/- 4.7; sarcoma 67.1 +/- 7.2 v sibling

51 childhood cancer with and without subsequent CNS tumors (82 participants and 228 matched controls).

52 Survivors of CNS tumors (9.5%; 95% CI, 5.2% to 13.8%) and bone tumors

53 ficantly increase prediction accuracy for 82 CNS tumors and 9 normal controls.

54 est scores were prevalent among survivors of CNS tumors and bone and soft tissue sarcomas on strength

55 ough good activity was also observed against CNS tumors and carcinomas of the breast and prostate.

56 rain metastases are more common than primary CNS tumors and confer grave prognosis on patients, as ex

57 s) for children with recurrent or refractory CNS tumors and DIPG.

58 recipients of organs taken from donors with CNS tumors and found no evidence of a difference in over

59 (GBM) accounts for nearly half of malignant CNS tumors and has a dismal 5-year survival rate of 5.5%

60 l number of long-term survivors of pediatric CNS tumors and is most influenced by the initial tumor h

61 sly published studies in adult-onset primary CNS tumors and replicated these in survivors of childhoo

62 -seq data from 84,700 nuclei of 35 pediatric CNS tumors and three non-tumoral pediatric brain tissues

63 survivors at high or low risk for subsequent CNS tumors and validated these models in an independent

64 ted IDH2 gene in 445 central nervous system (CNS) tumors and 494 non-CNS tumors.

65 proach for targeting central nervous system (CNS) tumors and the constituency of the Tumor Immune Mic

66 rier, stimulates immune-cell infiltration of CNS tumors, and induces clinical responses in patients w

67 Internal malignancies, such as lung cancer, CNS tumors, and leukemia and/or lymphoma, occur at a you

68 eosarcomas, adrenocortical carcinomas (ACC), CNS tumors, and soft tissue sarcomas (STS) observed in 3

69 thy controls, 380 systemic cancers, 31 other CNS-tumors, and 120 IDH-mutant cartilaginous tumors, we

70 The survival of children with CNS tumors approaches 70%, yet health-related quality of

71 Survivors of pediatric CNS tumors are at risk of severe neurocognitive impairme

72 lmost all data on the treatment of embryonal CNS tumors are derived from the pediatric population, si

73 Central nervous system (CNS) tumors are exceptionally difficult to treat, and ox

74 Central nervous system (CNS) tumors are the leading cause of pediatric cancer de

75 Central nervous system (CNS) tumors are the most common solid tumors in children

76 of this review is to discuss the spectrum of CNS tumors arising in individuals with NF type 1 (NF1) a

77 ly useful for the treatment of MTX-sensitive CNS tumors, as it does not affect CSF MTX levels.

78 Lenalidomide was tolerable in children with CNS tumors at doses of 116 mg/m(2)/d during the initial

79 d augment antitumor immune responsiveness in CNS tumor-bearing mice treated with human gp100 + tyrosi

80 Continuous imiquimod administration in CNS tumor-bearing mice, however, was associated with the

81 between survivors diagnosed with leukemia or CNS tumor before 11 years old versus during later adoles

82 ics in children with central nervous system (CNS) tumors before intraventricular therapy has not been

83 essitated by rapidly increasing knowledge of CNS tumor biology and therapies, much of which is based

84 e nucleus of the nude rat resulted in lethal CNS tumor burden manifested by the onset of focal neurol

85 Organs from donors with CNS tumors can be used with a low risk of donor tumor tr

86 Information on pediatric CNS tumor cases for the period 1995-2011 was obtained fr

87 present study, we show that human embryonal CNS tumor cell lines and surgical tumor specimens expres

88 In parallel, we noted in CNS tumor cells that knockdown of BCL-xL (B-cell lymphom

89 our analyses to the central nervous system (CNS) tumor cells and to further define mechanisms of dru

90 To broaden the utility of methylation-based CNS tumor classification, we developed MNP-Flex, a platf

91 trated beneficial to central nervous system (CNS) tumor classification.

92 thers were less likely to have children with CNS tumors compared to non-Hispanic white mothers (OR 0.

93 ceps or vacuum delivery had a higher risk of CNS tumors compared to those born by spontaneous vaginal

94 In adults with advanced embryonal CNS tumors, conventional-dose intravenous cisplatin-base

95 In young children with CNS tumors, CSI and hemispheric location are associated

96 Despite 13,000 central nervous system (CNS) tumor deaths per year in the United States, CNS tum

97 ariants to pediatric central nervous system (CNS) tumor development remains understudied.

98 (HR) and incidence rate difference (IRD) of CNS tumors diagnosed at younger than 20 years.

99 of these tools has the potential to advance CNS tumor diagnostics by providing broad access to rapid

100 ys a central role in central nervous system (CNS) tumor diagnostics but currently used assays pose li

101 ee distinct components: the first classifies CNS tumors directly from slide images ('direct model'),

102 tumor deaths per year in the United States, CNS tumor donors comprise only 1% of cadaveric donors re

103 e UK experience of transplanting organs from CNS tumor donors found no transmission in 448 recipients

104 There is a wide variation in the number of CNS tumor donors utilized by individual organ procuremen

105 CNS tumor donors were not used more often for either urg

106 ifference in patient survival of organs from CNS tumor donors when compared to donors with no CNS tum

107 focused on the treatment of the most common CNS tumors encountered in children and adults with NF1 a

108 fraction of CNS-PNETs, we identify four new CNS tumor entities, each associated with a recurrent gen

109 ble from those of various other well-defined CNS tumor entities, facilitating diagnosis and appropria

110 one of the transgenic mice formed detectable CNS tumors, even when aged.

111 The growing complexity of CNS tumor genetics has required reorganization of tumor

112 iquimod resulted in synergistic reduction in CNS tumor growth compared with melanoma-associated Ag-pu

113 gnancies; however, benefit for patients with CNS tumors has been limited.

114 s into the causes and potential treatment of CNS tumors have come from discovering connections with g

115 Mortality rates for AYAs with CNS tumors have increased by 0.6% per year for males and

116 Survivors of a CNS tumor, head and neck tumor, and leukemia are particu

117 By 60 years of age, 9%, 6%, and 5% of CNS tumor, head and neck tumor, and leukemia survivors,

118 tory and global collaborations, underscoring CNS tumor heterogeneity.

119 .8-39.6) and was particularly pronounced for CNS tumors (HR, 111.7; 95% CI, 96.8-128.8), except among

120 ha knockout (KO) mice and studied their anti-CNS tumor immune responses.

121 llular interactions involved in NK cell anti-CNS tumor immunity are even less well understood.

122 sponse to chemotherapy of advanced embryonal CNS tumors in adults.

123 econd leading cause of cancer-related death, CNS tumors in AYAs require improved clinical management.

124 Gliomas are the most common CNS tumors in children and adolescents, and they show an

125 s and also for modified incidence of primary CNS tumors in rats treated with a single dose of the neu

126 POLD1], and rs11615 [ ERCC1]) and subsequent CNS tumors in survivors of childhood cancer.

127 ent innate antitumor immune response against CNS tumors in the absence of toxicity.

128 count for approximately 80% of all malignant CNS tumors in the AYA age group, with the most common ty

129 The incidence of central nervous system (CNS) tumors in children appears to be increasing, yet fe

130 mmonly used to treat central nervous system (CNS) tumors in patients of all ages, young children trea

131 us tumorigenicity of central nervous system (CNS) tumors in the offspring of pregnant rats and also f

132 aited for a donor who did not have a primary CNS tumor, in addition to the life years gained by the t

133 Spontaneous CNS tumor incidence in control groups was 1.1-4.4% but s

134 The primary CNS tumors included medulloblastoma (n = 29), astrocytom

135 tended survival in both TNBC and BRCA-mutant CNS tumors, including complete regressions and prolonged

136 n and young adults with recurrent/refractory CNS tumors, including diffuse midline glioma.

137 recently been associated with several human CNS tumors, including medulloblastomas and a broad range

138 total tumor remission in mice bearing human CNS tumors, including metastatic tumor growth, after int

139 ancer effects against primary and metastatic CNS tumors, including sources of therapeutic NK cells, c

140 Because of the difficulty in treating CNS tumors, innovative treatments and alternative delive

141 0.95 ([95% CI, 0.74-1.23]; 84 children with CNS tumors; IRD, -0.3 [95% CI, -1.6 to 1.0]) for recent

142 0.86 ([95% CI, 0.72-1.02]; 421 children with CNS tumors; IRD, -0.8 [95% CI, -1.7 to 0.0]) for previou

143 than 3 years with newly diagnosed embryonal CNS tumors is 14 mg.

144 on the understanding of tumor biology of AYA CNS tumors is emphasized.

145 points in clinical trials for patients with CNS tumors is in its infancy, so that long-term outcomes

146 d points in clinical trials of patients with CNS tumors is increasing.

147 The management of CNS tumors is limited by the blood-brain barrier (BBB),

148 for the treatment of central nervous system (CNS) tumors is a major challenge to the development of s

149 Treatment of animals carrying orthotopic CNS tumor isolates with lapatinib- and obatoclax-prolong

150 Lapatinib and obatoclax killed multiple CNS tumor isolates.

151 fficking of tumor antigen-specific CTLs into CNS tumor lesions.

152 atric and adolescent central nervous system (CNS) tumor localized along the midline structures of the

153 Due to the low prevalence of pediatric CNS tumors, major advances in targeted therapies have be

154 ss, immunotherapeutic targeting of malignant CNS tumors may be enhanced by the administration of the

155 ncer Cell, Sill et al. expand the Heidelberg CNS Tumor Methylation Classifier from 91 to 184 subclass

156 We present the Heidelberg CNS Tumor Methylation Classifier version 12.8 (v12.8), t

157 We tested whether modulation of the CNS-tumor microenvironment by delivery of IFN-alpha-tran

158 donor with a primary central nervous system (CNS) tumor necessitates offsetting the risk of tumor tra

159 Health Organization's 5th Classification of CNS Tumors now designates DMG as, 'H3 K27-altered', sugg

160 care, and both pediatric-type and adult-type CNS tumors occur at that age.

161 emangioblastomas are central nervous system (CNS) tumors of unknown histogenesis, which can occur spo

162 Meningiomas are the most common primary CNS tumors, often managed conservatively due to their be

163 od cancer at high or low risk for subsequent CNS tumors on the basis of genetic and clinical informat

164 r donors of whom 397 had a past history of a CNS tumor or the cause of death listed as a CNS tumor.

165 histology and were higher for patients with CNS tumors or enrolled at Pediatric Early Phase Clinical

166 especially those with a history of leukemia, CNS tumors, or neuroblastoma, may be at increased risk f

167 one-tailed; P < 0.16 two-tailed; ENU-induced CNS tumors, P < 0.08 one-tailed, P < 0.16 two-tailed), t

168 cance in the experiment overall (spontaneous CNS tumors, P < 0.08 one-tailed; P < 0.16 two-tailed; EN

169 In glioblastoma and non-CNS tumor panels, 806 was reactive with a high proportio

170 rapy may represent an effective modality for CNS tumors, particularly when combined with strategies t

171 ts in cancer predisposition genes across 830 CNS tumor patients from the Pediatric Brain Tumor Atlas

172 of immuno-methylomic profiling in pediatric CNS tumor patients that may ultimately inform approach t

173 The adjusted incidence rate of CNS tumors per 100 000 person-years was 5.0 for children

174 e use of kidneys from a donor with a primary CNS tumor provides a further 8 years of life over someon

175 ndard for adjusting rates; underreporting of CNS tumor rates resulting from the exclusion of nonmalig

176 ) to induce glioma-specific type 1 CTLs with CNS tumor-relevant homing properties and the mechanism o

177 Development of novel therapies for CNS tumors requires reliable assessment of response and

178 eutic strategies for central nervous system (CNS) tumors requires a firm understanding of factors reg

179 development are illustrated by three common CNS tumors: retinoblastoma, glioblastoma, and medullobla

180 f cancer and leukemia but did not indicate a CNS tumor risk (incidence rate ratio = 1.03, 95% CI: 0.7

181 n most cancer registries; and information on CNS tumor risk factors, including concerns related to no

182 any maternal hormonal contraception use and CNS tumor risk.

183 Survivors of central nervous system (CNS) tumors (SHR=4.6, 95% confidence interval, 4.3-5.0),

184 nitial diagnosis of leukemia (SMR = 15.5) or CNS tumor (SMR = 15.7).

185 clinical outcomes observed in patients with CNS tumors, such as gliomas.

186 nd consistent with its established role as a CNS tumor suppressor, we find that SMARCB1 is essential

187 , racial and ethnic disparities in childhood CNS tumor survival appear to have their roots at least p

188 memory impairment was associated with CRT in CNS tumor survivors (RR, 1.97; 95% CI, 1.33-2.90) and al

189 The excess risk of cerebral infarction among CNS tumor survivors increases with attained age.

190 nd; P = .04 and .01, respectively) and among CNS tumor survivors on the TUG (score +/- SD: 5.1 +/- 0.

191 Beyond 60 years of age, every year, 0.4% of CNS tumor survivors were hospitalized for a cerebral inf

192 adiation (CRT), 25.8% (95% CI, 22.6%-29.0%); CNS tumor survivors, 34.7% (95% CI, 30.0%-39.5%); and HL

193 atosis type 2 (NF2) is an autosomal-dominant CNS tumor syndrome that affects 1:25,000 children and yo

194 ma (DIPG) is a fatal central nervous system (CNS) tumor that confers a median survival of 11 months.

195 herapy for malignant central nervous system (CNS) tumors that has been linked to poorly understood pi

196 This is partly because, unlike some CNS tumors, the blood-brain barrier (BBB) of DMG tumor v

197 malignant peripheral nerve sheath tumors and CNS tumors, the cancers traditionally associated with NF

198 ize the criteria that are used for different CNS tumors, the Response Assessment in Neuro-Oncology (R

199 n of HuR in 35 freshly resected and cultured CNS tumors to determine whether there was any correlatio

200 ecurrent, refractory, or progressive primary CNS tumors to estimate the maximum-tolerated dose (MTD)

201 PLOY), a deep learning model that classifies CNS tumors to ten major categories from histopathology.

202 ,200 newly diagnosed pediatric patients with CNS tumors, to assess their utility in routine neuropath

203 omprised 643 pediatric patients with primary CNS tumor treated at St Jude Children's Research Hospita

204 eview of patients with primary or metastatic CNS tumors treated between 2003 and 2018 (15 y).

205 and cell type-specific targets for pediatric CNS tumor treatment.

206 This review will focus on new or revised CNS tumor types and subtypes, beyond infiltrating glioma

207 the CNS WHO classification, as well as other CNS tumor types common in the AYA population.

208 y transcriptomic alterations among pediatric CNS tumor types compared to non-tumor tissues, while acc

209 three broad immune clusters associated with CNS tumor types/subtypes.

210 e large diversity of central nervous system (CNS) tumor types in children and adolescents results in

211 diagnosis of diverse central nervous system (CNS) tumor types is crucial for optimal treatment.

212 scribe the TIME of >6000 primarily pediatric CNS tumors using a deconvolution approach (methylCIBERSO

213 s an appealing option to specifically target CNS tumors using the immune system.

214 ife factors, risk, and survival of pediatric CNS tumors, using data from one of the world's largest a

215 Larger CNS tumor volume at baseline allowed the identification

216 CNS tumor volume at baseline may allow to identify patie

217 Promising activity, particularly in CNS tumors, warrants phase II evaluation of this regimen

218 ncer at highest or lowest risk of subsequent CNS tumors was 87.5% and 83.5%, respectively.

219 B16/F10 murine melanoma (B16) as a model for CNS tumor, we show that vaccination with bone marrow-gen

220 As B7-H3 is expressed on pediatric CNS tumors, we conducted BrainChild-03, a single-center,

221 stration of cell therapies for patients with CNS tumors, we define TIAN, propose a toxicity grading s

222 which poses a unique challenge in AYAs with CNS tumors, we propose encouraging referrals to neuro-on

223 ive vaccines against central nervous system (CNS) tumors, we evaluated the ability of vaccines with s

224 d thirty-nine infants with a newly diagnosed CNS tumor were treated with chemotherapy, with or withou

225 Results for CNS tumors were less consistent, but the most comprehens

226 vated in adolescents treated for leukemia or CNS tumors when compared with siblings.

227 Embryonal central nervous system (CNS) tumors, which comprise medulloblastoma, are the mos

228 generate tumor-specific immune responses to CNS tumors while the immuno-modulatory properties are be

229 Participants included 224 survivors of CNS tumors who were treated at St Jude Children's Resear

230 ss HRQOL rapidly and easily in children with CNS tumors, who have significantly worse HRQOL than heal

231 study for the treatment of both CNS and non-CNS tumors with MTAP loss.

232 DEPLOY to assist pathologists in diagnosing CNS tumors within a clinically relevant short time frame