ライフサイエンスコーパス: brain tumour

1 cers, P=0.006 for breast cancers, P=0.05 for brain tumours).

2 ) is a highly aggressive, difficult to treat brain tumour.

3 comprise the most common malignant childhood brain tumour.

4 oblastoma is the most frequent and malignant brain tumour.

5 ears) had a confirmed diagnosis of cancer or brain tumour.

6 astoma, the most common paediatric malignant brain tumour.

7 toma is the most aggressive and lethal adult brain tumour.

8 is the most aggressive type of primary adult brain tumour.

9 glioblastoma (GB), the most aggressive adult brain tumour.

10 ther it is a developmental malformation or a brain tumour.

11 be useful in treating this uniformly lethal brain tumour.

12 (GBM) is the most common and most aggressive brain tumour.

13 Glioblastoma (GBM) is a lethal brain tumour.

14 rative scans of children with a history of a brain tumour.

15 ercome if we are to cure all patients with a brain tumour.

16 ayed by TAMs in glioblastoma, another common brain tumour.

17 transport of paclitaxel and methotrexate in brain tumour.

18 the most common and most aggressive primary brain tumour.

19 ant gliomas, the most common form of primary brain tumour.

20 mprove the design of trials in patients with brain tumours.

21 e design of clinical trials in patients with brain tumours.

22 ings improve classification and diagnosis of brain tumours.

23 stroke and, less frequently, head injury and brain tumours.

24 135 of 176,587 patients were diagnosed with brain tumours.

25 ng new and old cerebrovascular accidents and brain tumours.

26 tations in the pathogenesis and phenotype of brain tumours.

27 or the treatment of patients with high-grade brain tumours.

28 re absent in more than half of children with brain tumours.

29 are the main cause of death in children with brain tumours.

30 th an increased risk of radiation-associated brain tumours.

31 CT scans of abdominal organs and MR scans of brain tumours.

32 e structured MRI reporting of post-treatment brain tumours.

33 development of new, effective therapies for brain tumours.

34 ted to mount better immune responses against brain tumours.

35 ing cortical malformations and developmental brain tumours.

36 ty, intracranial bleeds, CNS infections, and brain tumours.

37 g epigenetic effects, such as in the case of brain tumours.

38 nd genomic landscape of childhood high-grade brain tumours.

39 used to distinguish low-grade and high-grade brain tumours.

40 rs to differentiate low-grade and high-grade brain tumours.

41 is an emerging therapeutic approach against brain tumours.

42 rogression in clinical studies of paediatric brain tumours.

43 y in distinguishing low-grade and high-grade brain tumours.

44 al immune response during oZIKV infection of brain tumours.

45 ve programs, which are also expressed by non-brain tumours.

46 s, had an 11-fold greater risk of developing brain tumours.

47 ccurate diagnosis and effective treatment of brain tumours.

48 suggest a new therapeutic approach to treat brain tumours.

49 of life in long-term survivors of paediatric brain tumours.

50 as potential future medicines for malignant brain tumours.

51 nificant neuroinflammation in TSC-associated brain tumours.

52 st mutated tumour suppressors, especially in brain tumours.

53 HFPL2 (function unknown) is overexpressed in brain tumours.

54 rse neurocognitive outcomes in patients with brain tumours.

55 on neurocognitive outcomes in patients with brain tumours.

56 mGy 0.036, 95% CI 0.005-0.120; p=0.0097) and brain tumours (0.023, 0.010-0.049; p<0.0001).

57 (MB) is the most common malignant childhood brain tumour(1,2), yet the origin of the most aggressive

58 s an aggressive and highly therapy-resistant brain tumour(1,2).

59 ents previously operated on for an embryonal brain tumour (13 patients prospectively diagnosed with p

60 mia began 2 years after the first CT and for brain tumours 5 years after the first CT.

61 ath-promoting gene bax in a transgenic mouse brain tumour, a model in which p53-mediated apoptosis at

62 ), and nausea and vomiting (19%) for central brain tumours; abnormal gait and coordination (78%), cra

63 rcinoma, soft tissue sarcomas, osteosarcoma, brain tumours, adrenocortical carcinoma, Wilms' tumour a

64 d to assess the excess risk of leukaemia and brain tumours after CT scans in a cohort of children and

65 Rhabdoid brain tumours, also called atypical teratoid rhabdoid tu

66 The 8-year cumulative incidence of brain tumour among children with defective versus wild-t

67 The incidence of brain tumours among irradiated children (six of 52, 12.8

68 In children, stroke is as common as brain tumour and causes substantial mortality and long-t

69 s the most common and uncompromising primary brain tumour and is characterized by a dismal prognosis

70 flow (CBF) in areas of maximum perfusion in brain tumour and normal grey matter.

71 MB) is the most common aggressive paediatric brain tumour and, despite the recent progress in the tre

72 liomas are the most common primary malignant brain tumours and are classified into four clinical grad

73 nervous system (CNS) pathologies, including brain tumours and brain vascular malformations.

74 ours provides excellent anatomical detail of brain tumours and can also reveal the biology, cellular

75 for both systemic and localised delivery to brain tumours and discuss how recent engineering advance

76 nvolving patients with primary and secondary brain tumours and discuss their clinical implications.

77 rotron-generated X-rays for the treatment of brain tumours and drug-resistant epilepsies.

78 amyotrophic lateral sclerosis (ALS), stroke, brain tumours and epilepsy.

79 er cancers, paediatric sarcomas, leukaemias, brain tumours and other cancer types.

80 ent of disease progression in low back pain, brain tumours and primary epilepsy; (2) enhancing clinic

81 een features across the genetic landscape of brain tumours and show that generative network models re

82 erinatal conditions, traumatic brain injury, brain tumours and stroke were prominent underlying cause

83 plinary structures of care for patients with brain tumours and structured processes of diagnostic and

84 eas tissues and interfaces between xenograft brain tumours and the surrounding healthy brain matter.

85 ad no previous diagnosis of cancer or benign brain tumour, and were alive and cancer-free at least 5

86 of neurocognitive sequelae in children with brain tumours, and discuss various strategies to integra

87 g and genetic associations for patients with brain tumours, and emphasise the need for future researc

88 routine in-situ clinical assessment of human brain tumours, and its use was later extended for examin

89 increased risk for meningioma and childhood brain tumours, and possibly bladder cancer, melanoma, an

90 e programs, which are both unique to primary brain tumours, and systemic inflammatory and complement

91 ar factor NF-kappaB, and that ING4 regulates brain tumour angiogenesis through transcriptional repres

92 Primary and secondary brain tumours are associated with high mortality and mor

93 Malignant brain tumours are complex ecosystems containing neoplast

94 In this review the latest advances in MRI of brain tumours are discussed and their clinical applicati

95 Patients with brain tumours are motivated to participate in clinical t

96 Malignant brain tumours are the cause of a disproportionate level

97 Brain tumours are the commonest solid neoplasms in child

98 Brain tumours are the most common cause of cancer death

99 t the effectiveness of drugs against primary brain tumours as well as brain metastases.

100 Pathogenesis of malignant brain tumours as well as its mode of transformation to a

101 The incidence of secondary malignant brain tumour at 7 years was 2.3% (0-5.6) and brainstem n

102 treated for cancer (including leukaemia and brain tumours) at the Edinburgh Children's Cancer Centre

103 We compared the cumulative incidence of brain tumours between subgroups, and with that of 421 ch

104 stoblast (CB) and this fate is stabilised by Brain tumour (Brat) and Pumilio (Pum)-mediated post-tran

105 fluctuate in time and follow the changes in brain tumour burden providing biomarkers to monitor brai

106 ommonly occurring posterior fossa paediatric brain tumours can be classified using Apparent Diffusion

107 Pharmacotherapy of brain tumours can be limited by restricted drug delivery

108 d assessed excess incidence of leukaemia and brain tumours cancer with Poisson relative risk models.

109 ability to successfully treat patients with brain tumours, Cancer Research UK convened an internatio

110 ically relevant and diverse pro-inflammatory brain tumour cell secretome, including TNF-alpha.

111 y in immunocompromised mice, label-retaining brain tumour cells display elevated tumour-initiation pr

112 gether, these findings confirm dye-retaining brain tumour cells exhibit tumour-initiation ability and

113 lar interactions between microglia and AKT1+ brain tumour cells in zebrafish (Chia et al., 2018).

114 Before colonising the brain, tumour cells acquire specialised proficiencies th

115 Glioblastoma is the most aggressive adult brain tumour, characterised by resistance to therapy and

116 is a deadly and therapy resistant malignant brain tumour, characterized by an aggressive and diffuse

117 Canadian Institutes of Health Research, Brain Tumour Charity UK, University Health Network Found

118 Children with Cancer UK, The Brain Tumour Charity, and Academy of Medical Sciences.

119 The Brain Tumour Charity, Children with Cancer UK, Great Orm

120 In children treated for brain tumours, chronic neurocognitive effects are especi

121 ow that a subgroup of primary and metastatic brain tumours, classified as nodular on the basis of the

122 t diagnosis, especially of breast cancer and brain tumours, compared with families carrying protein t

123 Medulloblastoma is a malignant childhood brain tumour comprising four discrete subgroups.

124 lloblastoma is a highly malignant paediatric brain tumour currently treated with a combination of sur

125 peaks, from a widely tested SV 1H-MRS human brain tumour database.

126 diffuse glioma (HGG) is the leading cause of brain tumour death.

127 ical pathologies including ischaemic stroke, brain tumours, dementia and epilepsy.

128 The WHO classification of brain tumours describes 15 subtypes of meningioma.

129 lyses were performed using a dataset of 2314 brain tumour detection images.

130 in suppressing tumour cell proliferation and brain tumour development depends on TRIM33-promoted beta

131 role in cytokinesis, cell proliferation and brain tumour development.

132 epth view of the molecular routes leading to brain tumour development.

133 EGFR-promoted tumour cell proliferation and brain tumour development.

134 generalization to other adult and paediatric brain tumour diagnoses, demonstrating the potential for

135 geriatric dog groups were both enriched for brain tumour diagnoses, despite a lack of geriatric Boxe

136 Brain tumours disproportionately affect children and are

137 However, patients with brain tumours do not present with or present with low am

138 ion, in view of the low incidence of primary brain tumours--draws attention to the need to improve th

139 scular disease, other acquired brain injury, brain tumour, drug or alcohol misuse, or dementia were n

140 activity in the development of some types of brain tumours, elucidate a therapeutic strategy to reduc

141 These findings illuminate how aggressive brain tumours exploit glucose to suppress normal physiol

142 duced NEX/NeuroD6-Cre is sufficient to drive brain tumour formation in mice.

143 Our findings indicate that brain-tumour-generated solid stress impairs neurological

144 Here, we review recent advances in brain tumour genomics and highlight how these findings i

145 the European Society for Paediatric Oncology Brain Tumour Group and North American Children's Oncolog

146 ular mechanisms underlying the regulation of brain tumour growth and angiogenesis remain unresolved.

147 ressor gene, ING4, is involved in regulating brain tumour growth and angiogenesis.

148 blastoma, the most prevalent malignant adult brain tumour, harbouring a bias towards hypomethylation

149 Brain metastases are the most common type of brain tumours, harbouring an immune microenvironment tha

150 An association with brain tumours has also been demonstrated.

151 hich is the most common malignant paediatric brain tumour, has a 70% survival rate, but standard trea

152 Most children who have survived brain tumours have required surgical resection and focal

153 Gliomas, the most common and diverse brain tumours, have in parallel undergone changes in cla

154 f cancer (with pancreas, stomach and primary brain tumours having the highest risk) as well as on ind

155 59 glioblastoma patients from the Multimodal Brain Tumour Image Segmentation Benchmark (BraTS) 2019 C

156 a rapidly expanding sphere of investigation, brain-tumour imaging is producing great excitement.

157 edulloblastoma, a highly malignant childhood brain tumour, impose debilitating effects on the develop

158 multiforme (GBM), the most common malignant brain tumour in adulthood.

159 he most common and most aggressive intrinsic brain tumour in adults.

160 gliomas are the commonest malignant primary brain tumour in adults.

161 s the most common and most malignant primary brain tumour in adults.

162 a (GBM) is the most common and fatal primary brain tumour in adults.

163 However, in many other types of brain tumour in both adults and children, the effect of

164 Pathway Glioma (OPG) is a relatively common brain tumour in childhood; however, there is scarce unde

165 edulloblastoma(3), the most common embryonal brain tumour in children(4).

166 loblastoma (MB) is the most common malignant brain tumour in children.

167 liomas are the most common malignant primary brain tumours in adults and cannot usually be cured with

168 iffuse gliomas are the most common malignant brain tumours in adults and include glioblastomas and Wo

169 mours, whereas mature astrocytes do not form brain tumours in adults.

170 tases are the most common cause of malignant brain tumours in adults.

171 dulloblastomas are the most common malignant brain tumours in children.

172 or about 30% of all newly diagnosed cases of brain tumours in children.

173 ostars enabled the precise treatment of deep brain tumours in freely behaving mice.

174 en deficiency-a risk factor for dementia and brain tumours in humans.

175 ake of PEGylated-CH1055 dye were observed in brain tumours in mice, suggesting that the dye was detec

176 o sensitively detect very small intracranial brain tumours in patient-derived xenograft models.

177 own to lead to an elevated risk of malignant brain tumours in patients with inborn errors of 2HG meta

178 rategy improves the sensitivity when imaging brain tumours in whole mice.

179 ARM was not associated with brain tumour incidence (HR = 0.998, 95% CI 0.988, 1.009)

180 ions in airborne magnetite nanoparticles and brain tumour incidence, further research is needed to ev

181 lastomas are molecularly distinct from other brain tumours including primitive neuroectodermal tumour

182 s in the USA exist for patients with primary brain tumours, independent of potential confounders incl

183 stem cells, but not astrocytes, gave rise to brain tumours, independent of their location.

184 Similarly, in brain tumours inhibition of OxPhos slows proliferation a

185 Silencing or inhibition of NHE9 in brain tumour-initiating cells attenuates tumoursphere fo

186 c delivery of therapeutic drug levels to the brain tumour is limited by the blood-brain barrier.

187 gh understanding of the biology of malignant brain tumours is likely to provide the background for th

188 ion of mature astrocytes to the formation of brain tumours is still not understood.

189 clinically challenging, malignant childhood brain tumour, is no exception.

190 ng the blood-brain barrier, namely malignant brain tumours, ischaemic stroke and haemorrhagic traumat

191 cal diseases such as traumatic brain injury, brain tumours, ischaemic stroke, multiple sclerosis, and

192 d with severe neurological disorders such as brain tumours, it is important to understand how astrocy

193 o measure the concentrations of this drug in brain tumour lesions of lung cancer patients, as penetra

194 xteen patients (22-56 years, 7 females) with brain tumours located in or near speech-eloquent areas o

195 ntified in 5% of patients with the malignant brain tumour medulloblastoma(3).

196 The brain tumour microenvironment (TME) is highly immunosupp

197 Brain tumour microstructure is potentially predictive of

198 th Darcy's law is applied to a 3-D realistic brain tumour model that is extracted from magnetic reson

199 r application in invasive, orthotopic rodent brain tumour models.

200 tance and inhibited GBM growth in orthotopic brain tumour models.

201 application of CE-CT for in-depth orthotopic brain tumour monitoring.

202 h and have already yielded new insights into brain tumours, multiple sclerosis, acute neurological in

203 b group were unknown (n=2), a second primary brain tumour (n=1), and acute myeloid leukaemia (n=1), a

204 tworks in control subjects and patients with brain tumours (n = 22).

205 ingioma (n=7; 12.0 [4.8-24.8]) and childhood brain tumours (n=3; 10.3 [2.1-30.1]), and for cancers of

206 iving grade-specific spatial distribution of brain tumour occurrence requires rich datasets from both

207 a (MB), the most common malignant paediatric brain tumour occurs in the cerebellum.

208 , for example, are the most common malignant brain tumour of childhood, but their pathogenesis is unk

209 rogenase wild-type glioblastoma, a malignant brain tumour of glial origin, confers a poor prognosis w

210 lloblastoma is a highly malignant paediatric brain tumour, often inflicting devastating consequences

211 DC) can discriminate between posterior fossa brain tumours on a multicentre basis.

212 distinguish between low-grade and high-grade brain tumours on the basis of dynamic susceptibility con

213 er any clear evidence of an association with brain tumours or other malignancies.

214 y from the usual treatment of either primary brain tumours or systemic non-Hodgkin lymphoma.

215 It has been suggested that intrinsic brain tumours originate from a neural stem/progenitor ce

216 tactic radiosurgery (SRS) for the control of brain-tumours outweighs the potential neurocognitive ris

217 y motor area (SMA) is frequently involved by brain tumours (particularly WHO grade II gliomas).

218 indicate that ING4 has an important role in brain tumour pathogenesis.

219 ggests an important role for this pathway in brain tumour pathogenesis.

220 cal tract involvement in childhood embryonal brain tumour patients who developed posterior fossa synd

221 From MRI of brain tumour patients, we first constructed a grade-rela

222 d DNA, interrogating 739 plasma samples from brain tumour patients, were used to train and validate m

223 ess case of leukaemia and one excess case of brain tumour per 10,000 head CT scans is estimated to oc

224 Here, we have identified a dye-retaining brain tumour population that displays all the hallmarks

225 Paediatric brain tumours present distinct histopathological, molecu

226 Glioblastoma (GBM) is a highly lethal brain tumour presenting as one of two subtypes with dist

227 Medulloblastoma, a malignant brain tumour primarily diagnosed during childhood, has r

228 Magnetic resonance imaging (MRI) of brain tumours provides excellent anatomical detail of br

229 d for segmentation of CTVs to facilitate the brain tumour radiotherapy workflow.

230 Brain tumours rarely occur in survivors of childhood acu

231 cancers, and represent the leading cause of brain tumour-related death in both children and adults.

232 gh-grade gliomas (HGGs) account for the most brain tumour-related deaths in children and have a media

233 Despite decades of research, brain tumours remain among the deadliest of all forms of

234 Gliomas, the most common malignant primary brain tumours, remain universally lethal.

235 ctDNA) in the blood of patients with primary brain tumours remains challenging(11,12), sequencing of

236 astoma, the most common malignant paediatric brain tumour, requires simple yet realistic in vitro mod

237 In comparison, developmental brain tumours result from somatic variants in genes rela

238 suggest that advanced brain ageing enhances brain tumour risk in dogs and may be influenced by oestr

239 An unusually high frequency of brain tumours seen among children enrolled in one of our

240 datasets, with mean DICE scores of: 0.832 on brain tumour segmentation, and 0.894/0.841/0.853/0.847/0

241 a, allowing the identification of actionable brain tumour somatic mutations.

242 e we review the biological machinery used by brain tumour stem cells to commandeer tissues in the int

243 s in survival in patients with some types of brain tumours such as medulloblastoma.

244 In primary brain tumours, such as glioblastomas, as well as in brai

245 els of JHDM1B expression found in aggressive brain tumours, suggest a role for JHDM1B in cancer devel

246 sed as a general-purpose adjunct for guiding brain tumour surgeries.

247 er patient are lost as the result of primary brain tumours than any other form of cancer.

248 ely characterizes the genomic alterations of brain tumours than plasma, allowing the identification o

249 oblastoma (MB) is the most common paediatric brain tumour that arises from cerebellar precursor cells

250 Glioblastoma (GBM) is a heterogenous primary brain tumour that is characterised with unfavourable pat

251 astoma multiforme (GBM) is a highly invasive brain tumour that is unvaryingly fatal in humans despite

252 Medulloblastoma is the most common malignant brain tumour that occurs during childhood.

253 Ependymoma (EPN) is a paediatric brain tumour that relies on epigenomic remodelling to en

254 Glioblastoma are highly aggressive brain tumours that are associated with an extremely poor

255 rs (IGCTs) are a group of rare heterogeneous brain tumours that are clinically and histologically sim

256 stic oligodendroglioma (AO) are rare primary brain tumours that are generally incurable, with heterog

257 Gliomas are primary brain tumours that are thought to develop from neural st

258 Sonic Hedgehog (SHH) medulloblastomas are brain tumours that arise in the posterior fossa.

259 Gangliogliomas (GGs) are low-grade brain tumours that cause intractable focal epilepsy in c

260 Motor weakness in subjects with brain tumours that do not involve primary motor structur

261 Ependymomas are common childhood brain tumours that occur throughout the nervous system,

262 These are well differentiated primary brain tumours that typically develop in young adults.

263 Current clinical brain tumour therapy practices are based on tumour resec

264 resistance mechanisms and vulnerabilities in brain tumour therapy.

265 We also tested SDT against advanced-stage brain tumours to verify its efficacy further.

266 alise on scientific and clinical advances in brain tumour treatment in neuro-oncology to accelerate a

267 nd targeted therapy hold promise for primary brain tumour treatment, but require more specific and ef

268 sed in clinical studies of discrimination of brain tumour types and follow-up of patients bearing abn

269 supervised methods for the discrimination of brain tumour types, as it accounts for their increasingl

270 were quantified across a range of paediatric brain tumours using (1)H-High-Resolution Magic Angle Spi

271 lastoma (the most common malignant childhood brain tumour), using scant/low-quality samples remaining

272 patients and by using mouse models of human brain tumours, we show that a subgroup of primary and me

273 Forty-one patients with brain tumours were evaluated by 3-Tesla MRI.

274 severe weakness following surgery for their brain tumours were followed longitudinally, and the subj

275 asets from sixty-six patients with different brain tumours were retrospectively analysed and plasma g

276 This need is particularly acute in brain tumours where biopsy is a highly invasive procedur

277 ontine Gliomas (DIPGs) are deadly paediatric brain tumours where needle biopsies help guide diagnosis

278 ns for chemoresistant cancers, especially of brain tumours where the use of temozolomide is frequentl

279 echanism that enables stem cells to generate brain tumours, whereas mature astrocytes do not form bra

280 s (GBM) are aggressive and therapy-resistant brain tumours, which contain a subpopulation of tumour-p

281 Glioblastomas are highly aggressive primary brain tumours, which display heterogeneous characteristi

282 provide insight into the biology of primary brain tumours, which face similar challenges to brain me

283 lso occur in other diseases, like metastatic brain tumours, which we describe in this case report.

284 Ependymomas are chemotherapy-resistant brain tumours, which, despite genomic sequencing, lack e

285 Glioblastoma (GBM) is a malignant brain tumour with a dismal prognosis, despite best treat

286 Glioblastoma is a highly aggressive brain tumour with a high risk of recurrence after surger

287 astoma multiforme is an aggressive, invasive brain tumour with a poor survival rate.

288 Glioblastoma (GBM) is a brain tumour with high invasiveness and poor prognosis.

289 grade gliomas remain the most common primary brain tumour with limited treatments options and early r

290 ished that diffuse low-grade gliomas (DLGG), brain tumours with a slow-growth rate, induce a compensa

291 (ETMRs) are aggressive paediatric embryonal brain tumours with a universally poor prognosis(1).

292 Glioblastomas (GBMs) are highly lethal brain tumours with current therapies limited to palliati

293 DNA repair gene and p53 efficiently induces brain tumours with hallmark characteristics of human pro

294 Glioblastomas remain the deadliest brain tumour, with a dismal ~12-16-month survival from d

295 tiforme is the most common primary malignant brain tumour, with a median survival of about one year.

296 glioma is the most common and lethal primary brain tumour, with dismal survival rates and no effectiv

297 Meningiomas are mostly benign brain tumours, with a potential for becoming atypical or

298 low-grade glioma occurrence, placing primary brain tumours within a well established framework of neu

299 e diffusion MRI signal permits monitoring of brain tumours without invasive intervention.

300 nables continuous and on-demand treatment of brain tumours, without open-skull surgery and toxicologi