ライフサイエンスコーパス: brain cancer

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

2 the most common type of aggressive malignant brain cancer.

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

4 ant therapeutic targets for the treatment of brain cancer.

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

6 d function and is commonly hyperactivated in brain cancer.

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

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

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

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

11 Malignant glioma is a consistently fatal brain cancer.

12 Recent studies have identified stem cells in brain cancer.

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

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

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

16 distress symptoms for survivors of childhood brain cancer.

17 important role in the etiology of childhood brain cancer.

18 jor goal of advanced therapeutic systems for brain cancer.

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

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

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

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

23 are an efficacious therapeutic strategy for brain cancer.

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

25 therapeutic strategies for the treatment of brain cancer.

26 on mechanisms of epigenetic deregulation in brain cancer.

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

28 Glioblastoma remains an incurable brain cancer.

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

30 urvival in an orthotopic model of aggressive brain cancer.

31 flavine, and demonstrate its potency against brain cancer.

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

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

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

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

36 pportunities for therapeutic intervention of brain cancer.

37 f genomic rearrangements identified in human brain cancers.

38 in a high proportion of malignant pediatric brain cancers.

39 tly predicted poor survival in patients with brain cancers.

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

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

42 riguing clues about targeting PTEN-deficient brain cancers.

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

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

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

46 nd provide a therapeutic model for malignant brain cancers.

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

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

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

50 id the exposed have an increased risk of all brain cancers.

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

52 contributes to altered GZ exit in pediatric brain cancers.

53 evelopment of novel therapies for metastatic brain cancers.

54 ovel targeted therapeutics for GBM and other brain cancers.

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

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

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

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

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

60 Brain cancers activate core stem cell regulatory pathway

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

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

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

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

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

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

67 5% confidence interval: 3.00, 18.37; and for brain cancer and homozygotes for haplotype CGGCT, hazard

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

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

70 ent personal histories of cancers other than brain cancer and most nervous system conditions, but the

71 to the child, in that no association between brain cancer and use of electric blankets (OR = 1.0, 95%

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 Brain cancer cells are diverse in their genetic, metabol

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

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

104 Brain cancer cells invade early on surrounding parenchym

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 0, 4.25) and an almost 5-fold higher risk of brain cancer death compared with nurses in the US cohort

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

121 e OCT attenuation mapping for intraoperative brain cancer detection.

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

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

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

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

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

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

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

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

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

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

132 (95% CI 1.46-6.94) and the relative risk of brain cancer for patients who received a cumulative dose

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

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

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

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

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

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

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

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

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

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

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

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

145 The vast majority of brain cancers (gliomas) express a receptor (R) for inter

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

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

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

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

150 tiforme is the most common form of malignant brain cancer in adults and, unfortunately, is not amenab

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 of the treatment of many forms of childhood brain cancer, including medulloblastoma.

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

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

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

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

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

173 11 481 persons who were treated for primary brain cancer, leukemia, Hodgkin disease, non-Hodgkin lym

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

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

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

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

178 an association between residential radon and brain cancer mortality.

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

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

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

182 hypothesis that there is a relation between brain cancer occurrence in children and 50-/60-Hz magnet

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

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

185 tly increased rates of ependymomas and other brain cancers, osteosarcomas, or mesotheliomas in the Un

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

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

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

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

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

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

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

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

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

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

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

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

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

199 Brain cancer risk did not vary by use in any trimester o

200 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 2.7 years for controls; no association with brain cancer was observed according to duration of use (

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

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

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

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

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

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

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

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

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

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

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

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

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