ライフサイエンスコーパス: brain cancer

1 Glioblastoma is a devastating form of brain cancer.

2 an aggressive and difficult to treat form of brain cancer.

3 are an efficacious therapeutic strategy for brain cancer.

4 s to treat patients with aggressive forms of brain cancer.

5 therapeutic strategies for the treatment of brain cancer.

6 on mechanisms of epigenetic deregulation in brain cancer.

7 es that are of interest for the treatment of brain cancer.

8 Glioblastoma remains an incurable brain cancer.

9 for glioma, which is a rare and highly fatal brain cancer.

10 urvival in an orthotopic model of aggressive brain cancer.

11 glioblastoma, a malignant and lethal form of brain cancer.

12 the most aggressive and common form of adult brain cancer.

13 ival from cancer with one glaring exception: brain cancer.

14 stoma (GBM), the most deadly form of primary brain cancer.

15 most common and devastating type of primary brain cancer.

16 pportunities for therapeutic intervention of brain cancer.

17 he diagnosis and prognosis of cancer such as brain cancer.

18 the most common type of aggressive malignant brain cancer.

19 ses of about 60 mGy might triple the risk of brain cancer.

20 ant therapeutic targets for the treatment of brain cancer.

21 d function and is commonly hyperactivated in brain cancer.

22 most common and the most aggressive type of brain cancer.

23 s in a hospital-based, case-control study of brain cancer.

24 glioblastoma multiforme (GBM), a devastating brain cancer.

25 (GBM) is the most common and lethal type of brain cancer.

26 Malignant glioma is a consistently fatal brain cancer.

27 Recent studies have identified stem cells in brain cancer.

28 a group of patients with different types of brain cancer.

29 s the most common and lethal form of primary brain cancer.

30 extended to solid tumors, such as breast and brain cancer.

31 distress symptoms for survivors of childhood brain cancer.

32 important role in the etiology of childhood brain cancer.

33 highly aggressive and heterogeneous form of brain cancer.

34 rly twice as likely as non-whites to develop brain cancer.

35 n 13 PRCA families with at least one case of brain cancer.

36 shown to be involved in breast, prostate and brain cancer.

37 the clinical symptoms seen in patients with brain cancer.

38 ons, such as epilepsy, and glioma, a form of brain cancer.

39 M) is the most aggressive and common type of brain cancer.

40 maging, and significant tumour inhibition of brain cancer.

41 blastoma (GBM) is a heterogeneous and lethal brain cancer.

42 ose derived from patients without history of brain cancer.

43 jor goal of advanced therapeutic systems for brain cancer.

44 flavine, and demonstrate its potency against brain cancer.

45 thout any obvious structural layers, such as brain cancer.

46 with neurological disorders, CNS injury, and brain cancer.

47 peutic strategies for these presently lethal brain cancers.

48 ure studies examining the role of lncRNAs in brain cancers.

49 contributes to altered GZ exit in pediatric brain cancers.

50 evelopment of novel therapies for metastatic brain cancers.

51 ovel targeted therapeutics for GBM and other brain cancers.

52 d G34, which have been reported in pediatric brain cancers.

53 in a high proportion of malignant pediatric brain cancers.

54 tly predicted poor survival in patients with brain cancers.

55 ent in epithelial tumors but not in blood or brain cancers.

56 and digestive system, prostate, kidney, and brain cancers.

57 riguing clues about targeting PTEN-deficient brain cancers.

58 n feature of a major subset of primary human brain cancers.

59 extended to solid tumors such as breast and brain cancers.

60 pancreatic, breast, lung, colon, bladder and brain cancers.

61 nd provide a therapeutic model for malignant brain cancers.

62 those induced by SV40 in animals, including brain cancers.

63 FF1 may behave as a tumor suppressor gene in brain cancers.

64 oration of cell cycle-targeting therapies in brain cancers.

65 cells that are potential cells of origin for brain cancers.

66 eterminant in the pathogenesis of paediatric brain cancers.

67 f genomic rearrangements identified in human brain cancers.

68 of origin, affects the outcome of malignant brain cancers.

69 ), with the highest risk among patients with brain cancer (200 per 1,000 person-years; 95% CI, 162 to

70 ase (7.6-fold), multiple myeloma (4.5-fold), brain cancer (3.5-fold), and seminoma (2.9-fold) were ra

71 ethod to 4 large-scale examples, combining 7 brain cancer, 9 prostate cancer, 8 idiopathic pulmonary

72 (EGFR) signaling pathway and angiogenesis in brain cancer act as an engine for tumor initiation, expa

73 Brain cancers activate core stem cell regulatory pathway

74 red (FTIR) spectroscopy for the detection of brain cancer, alongside machine learning technology, is

75 for the treatment of brain diseases such as brain cancer, Alzheimer's and Parkinson's diseases, is c

76 Increased risks were also found for brain cancer among men (O/E =1.91) and for cancers of th

77 one hundred one adult survivors of childhood brain cancer and 2,817 siblings completed a long-term fo

78 ed the expression of all lncRNAs in over 650 brain cancer and 70 normal brain tissue RNA sequencing d

79 tic potential in terms of early detection of brain cancer and better delimitation of the tumor bounda

80 Our model may impact mechanistic studies of brain cancer and better treatment outcomes through preci

81 athologic role of ACKR3 in breast, lung, and brain cancer and discuss its possible relevance as a pro

82 he treatment of breast, liver, prostate, and brain cancer and for the palliation of pain in bone meta

83 ontaining images from freshly resected human brain cancer and from a silica phantom acquired by a 131

84 5% confidence interval: 3.00, 18.37; and for brain cancer and homozygotes for haplotype CGGCT, hazard

85 ic analyses in the characterization of human brain cancer and identify a potentially useful genetic a

86 sion is associated with VTE in patients with brain cancer and may activate platelets.

87 GBs) are the most aggressive form of primary brain cancer and virtually incurable.

88 l antimitotic therapeutics, specifically for brain cancers and cancers that are resistant to standard

89 H3K27M, is associated with certain pediatric brain cancers and is linked to a global decrease of H3K2

90 impactful biomarkers in adult and pediatric brain cancers and it provides a perspective on the direc

91 tumor virus that is known to induce primary brain cancers and lymphomas in laboratory animals.

92 tients with neurological diseases, including brain cancers and neurodegenerative disorders.

93 ng SV40 in the pathogenesis of primary human brain cancers and NHL and discusses future research dire

94 to a human gene that had been identified in brain cancers and termed RTVP-1 or GLIPR.

95 HIP1 is overexpressed with high frequency in brain cancers and that this overexpression correlates wi

96 brain tissue but is upregulated in advanced brain cancers and, in particular, in GB tumors exhibitin

97 te cancer), PA-1 (ovarian cancer), and U118 (brain cancer); and human primary cells including lung fi

98 Glioblastoma (GBM) is the deadliest adult brain cancer, and all patients ultimately succumb to the

99 ve focused on Alzheimer's disease, pediatric brain cancer, and fetal alcohol syndrome, in addition to

100 edulloblastomas, a malignant neuroectodermal brain cancer, and other cancers.

101 e is the most common highly aggressive human brain cancer, and receptor tyrosine kinases have been im

102 risk of Hodgkin's disease, multiple myeloma, brain cancer, and seminoma.

103 -ag, or other viral markers in primary human brain cancers, and a systematic assessment of the data i

104 but also found in tissue from lung cancers, brain cancers, and bone marrow.

105 ous laboratories has revealed that malignant brain cancers are complex ecological systems composed of

106 t epigenomes define many childhood and adult brain cancers, as demonstrated by widespread changes to

107 The heterogeneity of brain cancers, as most solid tumors, complicates diagnos

108 lastoma, the most common malignant pediatric brain cancer; ASC is also expressed in human medulloblas

109 Using mosaic mouse models of the malignant brain cancer, astrocytoma, we report that tumor cells in

110 Because an excess of cases of primary brain cancer (BC) have been observed in some studies of

111 Further investigation of HIP1 function in brain cancer biology and validation of its use as a prog

112 Glioblastoma is the most malignant brain cancer but the early stages of disease progression

113 ar telephones is not associated with risk of brain cancer, but further studies are needed to account

114 r stem-like cells (CSC) are thought to drive brain cancer, but their cellular and molecular origins r

115 tiforme (GBM), an aggressive form of primary brain cancer, by enhancing drug biodistribution to the t

116 These findings demonstrate that brain cancers cause multifaceted immunosuppression and p

117 expression of BCCIPalpha inhibits breast and brain cancer cell growth, but fails to inhibit HT1080 ce

118 s from five breast cancer cell lines and one brain cancer cell line to investigate the possible mecha

119 lastoma multiforme and neuroblastoma), human brain cancer cell lines (D54 and D54-EGFRvIII), and gene

120 Here, we cultured 3 primary human brain cancer cell lines under 3 different culture condit

121 ability and drug resistance of the following brain cancer cell lines: primary cancers (glioblastoma m

122 roteins in hundreds of isolated glioblastoma brain cancer cell pairs and to monitor their relative mo

123 Brain cancer cells are diverse in their genetic, metabol

124 o investigate the PI3K pathway activities of brain cancer cells expressing mutant epidermal growth fa

125 associated cytotoxicity in human breast and brain cancer cells in vitro.

126 Brain cancer cells invade early on surrounding parenchym

127 Experimental evidence indicates that human brain cancer cells proliferate or migrate, yet do not di

128 terestingly, ectopic expression of TMEFF1 in brain cancer cells resulted in their growth inhibition.

129 terrogate a dose-dependent response of model brain cancer cells to EGFR inhibition.

130 LT) of 505 V/cm and 1316 V/cm were found for brain cancer cells when 100 mus IRE and 2 mus symmetric

131 xploited therapeutically to selectively kill brain cancer cells while sparing the surrounding brain p

132 ne and glycine metabolism in the survival of brain cancer cells within the ischaemic zones of gliomas

133 liver, colorectal, lung, breast, kidney, and brain cancer cells, at clinically achievable doses, sora

134 Glioblastoma is an incurable brain cancer characterized by high genetic and pathologi

135 Glioblastoma is a highly aggressive form of brain cancer characterized by uncontrolled cell growth r

136 we developed a novel three-dimensional (3D) brain cancer chip composed of photo-polymerizable poly(e

137 is; esophageal, stomach, pancreas, lung, and brain cancer; cirrhosis; organ transplantation; and preg

138 orders like AD, PD, schizophrenia, epilepsy, brain cancer, CNS infection (viral and fungal), multiple

139 Risk of brain cancer compared by use of handheld cellular teleph

140 Glioblastoma the most aggressive form of brain cancer, comprises a complex mixture of tumor cells

141 ncogenic mutant form of EGFR linked to human brain cancers, confers transforming activity while it is

142 tiforme (GBM) is a lethal, therapy-resistant brain cancer consisting of numerous tumor cell subpopula

143 urthermore, serum samples from patients with brain cancer contained anti-HIP1 antibodies more frequen

144 0, 4.25) and an almost 5-fold higher risk of brain cancer death compared with nurses in the US cohort

145 In aggressive breast and brain cancers, defective laminin anchoring was often due

146 e OCT attenuation mapping for intraoperative brain cancer detection.

147 and multifunctional materials applicable to brain cancer diagnostics, imaging, and therapy, with an

148 potential to make an impact in the field of brain cancer diagnostics.

149 gh low-grade gliomas and glioblastomas, both brain cancers, driven by EGFR amplifications are highly

150 also displayed resistance to the widely used brain cancer drug temozolomide.

151 including human breast, ovary, prostate and brain cancer, due to amplification of the PAK1 gene in a

152 Cranial irradiation for the treatment of brain cancer elicits progressive and severe cognitive dy

153 Glioblastoma is the most common human brain cancer entity and is maintained by a glioblastoma

154 cted central nervous system (CNS) disorders (brain cancer, epilepsy, and anxiety) and using them as e

155 Brain cancer, especially the most common type of gliobla

156 e in the treatment of primary and metastatic brain cancers, especially in children.

157 hese genes have established relevance to the brain cancers examined herein, with others having known

158 ss than 1.0 for all histologic categories of brain cancer except for uncommon neuroepitheliomatous ca

159 bserved familial caregivers of patients with brain cancer for a year after diagnosis and tracked chan

160 (95% CI 1.46-6.94) and the relative risk of brain cancer for patients who received a cumulative dose

161 express a module of suppressed microRNAs in brain cancer for therapeutic purposes.

162 We calculated the relative risk of dying of brain cancers for each municipality and correlated this

163 antibodies more frequently than age-matched brain cancer-free controls.

164 CMDS to two real datasets of lung cancer and brain cancer from Affymetrix and Illumina array platform

165 or the accuracy of identifying a particular brain cancer from the background of all phenotypes, was

166 vel connection between neurotransmitters and brain cancer, further highlighting the critical influenc

167 tation associated with an aggressive form of brain cancer generates an immunogenic T cell epitope res

168 Here we demonstrate that the highly lethal brain cancer glioblastoma (GBM) is remarkably dependent

169 y resistance, including in the highly lethal brain cancer glioblastoma (GBM).

170 The malignant brain cancer glioblastoma multiforme (GBM) displays inva

171 ene expression profiles of 202 tumors of the brain cancer glioblastoma multiforme (GBM) given at the

172 ls sustain propagation of the deadly primary brain cancer glioblastoma.

173 hesis, is overexpressed in the highly lethal brain cancer glioblastoma.

174 ium catalysts, with their specific uptake in brain cancer (glioblastoma) cells, while maintaining the

175 The most common and deadly form of primary brain cancer, glioblastoma (GBM), is characterized by si

176 We have previously shown that the aggressive brain cancer, glioblastoma (GBM), maintains stem-like fe

177 , computational method that models a type of brain cancer (glioma) only by using the topological prop

178 Among primary brain cancers, gliomas are the most deadly and most refr

179 Liver, bone, stomach, and brain cancer had greater-than-average reported:expected

180 oblastoma (GBM), the most aggressive form of brain cancer, has witnessed very little clinical progres

181 Some studies of brain cancer have found an excess risk for farmers.

182 ; P = 0.001), predicting higher contrast for brain cancer imaging.

183 iforme is the most common and lethal primary brain cancer in adults.

184 e (GBM) is the most common primary malignant brain cancer in adults.

185 ncluding the most common but least treatable brain cancer in children and adults: glioblastoma multif

186 s associated with municipal mortality due to brain cancer in Galicia, Spain.

187 astoma multiforme, the most common malignant brain cancer in humans, are aggressive growth and the ab

188 Astrocytomas are the leading cause of brain cancer in humans.

189 n normal brain but can effectively eliminate brain cancer in multiple preclinical tumor models in viv

190 The authors examined the risk of childhood brain cancer in relation to parental exposure to classes

191 There was no evidence of increased brain cancer in the entire cohort (standardized mortalit

192 ear, over 16,000 patients die from malignant brain cancer in the US.

193 astoma (GBM), are the most common and deadly brain cancers in adults.

194 dulloblastomas are the most common malignant brain cancers in children.

195 lastomas are among the most common malignant brain cancers in the pediatric population and consist of

196 lth-status variables, survivors of childhood brain cancer, in the aggregate, appear to report signifi

197 st common and malignant of all human primary brain cancers, in which drug treatment is still one of t

198 ponent for improving gene-based therapies of brain cancer includes tumor suppressor genes that exhibi

199 and destroyed two different types of deadly brain cancer, including glioblastoma and melanoma.

200 brain and targeted and completely destroyed brain cancer, including high-grade glioblastoma and mela

201 mmunosuppression in three distinct models of brain cancer, including mice harbouring GL261 glioma, B1

202 Reciprocally, brain cancers influence neuronal function, increasing ne

203 e significant in therapy to prevent or treat brain cancer invasion.

204 nism that mediates this neural regulation of brain cancer is activity-dependent cleavage and secretio

205 nologic factors might cause or prevent human brain cancer is of interest.

206 Glioblastoma (GBM), a uniformly lethal brain cancer, is characterized by diffuse invasion and a

207 in serum samples of children, suffering from brain cancer, is demonstrated.

208 Glioblastoma, the most lethal primary brain cancer, is extremely proliferative and invasive.

209 Glioblastoma, the most malignant form of brain cancer, is responsible for 23% of primary brain tu

210 11 481 persons who were treated for primary brain cancer, leukemia, Hodgkin disease, non-Hodgkin lym

211 ors across 7 histological types of childhood brain cancer: low-grade glioma (n = 93), ependymoma (32)

212 sue images for the mathematical diagnosis of brain cancer (malignant glioma).

213 and Classifiers (ISSAC)--that resulted in a brain cancer marker panel of 44 unique genes.

214 EORTC) Quality of Life Questionnaire C30 and Brain Cancer Module.

215 t correlation between residential radon with brain cancer mortality for males and females and the int

216 an association between residential radon and brain cancer mortality.

217 herapy has been linked to the development of brain cancer (most commonly astrocytomas), and Tpmt stat

218 te, colon, liver, ovarian, bladder, gastric, brain cancers, neuroblastoma and chronic lymphocytic leu

219 Interventions for diseases like brain cancer, neurodegeneration, or age-associated infla

220 reast cancer and the U251 xenograft model of brain cancer, NSC48300 produced effective tumor growth i

221 trocytoma grade IV is a malignant and lethal brain cancer of unknown origin.

222 s a transcriptional repressor mutated in the brain cancer oligodendroglioma.

223 se of two samples of infiltrating astrocytic brain cancers (oligodendroglioma and high-grade astrocyt

224 , with implications for our understanding of brain cancer pathogenesis.

225 d cancer cells is a fundamental component of brain cancer pathophysiology, both for primary gliomas a

226 tion-based case-control study in Iowa of 375 brain cancer patients and 2,434 controls.

227 t of radiation and chemotherapy efficacy for brain cancer patients is traditionally accomplished by m

228 and medical advances, the prognosis for most brain cancer patients remains dismal and the median surv

229 In brain cancer patients, Kaplan-Meier analysis showed that

230 In a subset of brain cancer patients, parameters from blood samples and

231 or early prediction of treatment response in brain cancer patients.

232 els in the sera of ovarian, renal, lung, and brain cancer patients.

233 d time-to-diagnosis and a poor prognosis for brain cancer patients.

234 r receptors have failed to show efficacy for brain cancers, potentially due to their inability to ach

235 ults identify Norrin as a modulator of human brain cancer progression and reveal an unanticipated Not

236 To determine the biological role of Fn14 in brain cancer progression, we examined the activity of Fn

237 ies an unanticipated role of Norrin in human brain cancer progression.

238 ray datasets generated from three studies on brain cancer, prostate cancer, and lung disease, respect

239 e was no evidence for linkage to CAPB in the brain cancer-prostate cancer subset.

240 Brain cancers recently overtook leukemia as the number o

241 .g. we use neighborhood analysis to identify brain cancer related genes.

242 glioma is a highly malignant and metastatic brain cancer, resistant to many existing anticancer trea

243 s of leukemia (RR, 2.21; 95% CI, 2.02-2.42), brain cancer (RR, 1.93; 95% CI, 1.86-2.00), and Hodgkin

244 ted in the context of regenerative medicine, brain, cancer, skin, and immune diseases.

245 or tumor development and therapy resistance, brain cancer stem cells (BCSCs).

246 maintains normal neural stem cells, but also brain cancer stem cells, indicating an oncogenic role.

247 -1), a marker for both neural stem cells and brain cancer stem cells, is enriched after radiation in

248 Ms), which are the poorest prognosis primary brain cancers, strongly resemble developmental systems,

249 Studies in patients with pancreatic or brain cancer suggest that elevated levels of PAI-1 may c

250 e intrinsic pontine glioma (DIPG) is a fatal brain cancer that arises in the brainstem of children, w

251 Glioblastoma is an immunosuppressive, fatal brain cancer that contains glioblastoma stem-like cells

252 Glioblastoma (GBM) is a primary brain cancer that contains populations of stem-like canc

253 BM), or grade IV astrocytoma, is a malignant brain cancer that contains subpopulations of proliferati

254 Glioblastoma is a universally lethal form of brain cancer that exhibits an array of pathophysiologica

255 Glioblastoma is a highly lethal brain cancer that frequently recurs in proximity to the

256 toma multiforme (GBM) is a highly aggressive brain cancer that is characterized by the paradoxical fe

257 (GBM) is the most common and lethal primary brain cancer that is driven by aberrant signaling of gro

258 oid tumors (ATRTs) are challenging pediatric brain cancers that are predominantly associated with ina

259 Glioblastomas (GBMs) are lethal brain cancers that are resistant to current therapies.

260 Gliomas are primary brain cancers that spread exclusively within the brain,

261 ress were to find large relative effects for brain cancer, the absolute increase in risk would probab

262 -crossing nanoplatforms for highly efficient brain cancer theranostics.

263 n-1 pathways may be a promising strategy for brain cancer therapy.

264 ch as PDZ1i hold promise to advance targeted brain cancer therapy.

265 a precluding the genomic characterization of brain cancer through plasma ctDNA.

266 This study implicates ion channels in brain cancer, thus expanding on knowledge of their roles

267 ed glioblastoma cells (U87), which formed 3D brain cancer tissues on the chip, and used the GBM chip

268 oproteinase, is also abnormally expressed in brain cancer tissues.

269 Glioblastoma (GB) is one of the deadliest brain cancers to afflict humans, and it has a very poor

270 anscriptomic data for the primary classes of brain cancers to study the feasibility of separating all

271 roperties favor further development of 1 for brain cancer treatment by intratumoral injections.

272 er-associated PTEN defects and may lead to a brain cancer treatment that targets PTEN mono-ubiquitina

273 Radiotherapy is a mainstay of brain cancer treatment, but it causes significant compli

274 High-grade glioma is the most common primary brain cancer type and is characterized by invasive and f

275 is and EGFR modules to study the response of brain cancer under tyrosine kinase inhibitors (TKIs) tre

276 investigate the properties of populations of brain cancer undergoing electrotaxis, a phenomenon where

277 f E2F1 in the development and maintenance of brain cancer using a transgenic mouse model engineered t

278 2.7 years for controls; no association with brain cancer was observed according to duration of use (

279 Interrogating the genomes of over 4000 brain cancers we identified ZEB1 deletion in 15% (grade

280 To better understand the role of lncRNAs in brain cancer, we performed a global analysis to identify

281 ter multivariate adjustment, odds ratios for brain cancer were 1.0, 1.1, 1.6, and 1.3 for exposure to

282 Survivors of brain cancer were also most likely to report restricted

283 ndings from 60 patients with head, neck, and brain cancer were used to train and validate A-CycleGAN,

284 When molecular signatures of brain cancers were constructed from all currently availa

285 stoma (GBM) is the most lethal type of human brain cancer, where deletions and mutations in the tumou

286 nase isoform 2 (JNK2) is reported in primary brain cancers, where it associates with the histologic g

287 ularly in hard-to-treat cancer types such as brain cancer which suffer from a lack of clinical sample

288 pontine glioma (DIPG) is a lethal pediatric brain cancer whose median survival time is under one yea

289 High-grade gliomas are lethal brain cancers whose progression is robustly regulated by

290 ltiforme (GBM) is a highly malignant primary brain cancer with a dreadful overall survival and for wh

291 GBM) - the most common and malignant type of brain cancer with no effective cure.

292 (GBM) is the most common aggressive form of brain cancer with overall dismal prognosis (10-12 months

293 common and aggressive histologic subtype of brain cancer with poor outcomes and limited treatment op

294 Glioblastoma (GBM) is an aggressive type of brain cancer with remarkable cell migration and adaptati

295 ed rosettes (ETMRs) are highly lethal infant brain cancers with characteristic amplification of Chr19

296 Glioblastoma (GBM) is the deadliest form of brain cancer, with a median survival of less than 2 year

297 unraveled the unique genetic makeup of this brain cancer, with nearly 80% found to harbor a p.Lys27M

298 w that HRGP expression is increased in human brain cancers, with the protein heavily localized to the

299 Glioblastomas (GBM) are the most aggressive brain cancers without effective therapeutics.

300 orphan RTK ROS is a frequent event in human brain cancers, yet the pathologic significance of this e