ライフサイエンスコーパス: brain metastasis

1 pe in the brain, the astrocyte, in promoting brain metastasis.

2 ese drugs could be used to treat established brain metastasis.

3 RCC with vascular invasion, liver, lung and brain metastasis.

4 therapy can inhibit growth of breast cancer brain metastasis.

5 anged non-small-cell lung cancer (NSCLC) and brain metastasis.

6 n and recruitment of myeloid cell to promote brain metastasis.

7 to the neurological sequelae associated with brain metastasis.

8 tic target or serve as a prognostic tool for brain metastasis.

9 eural effusion and pericardial effusion; and brain metastasis.

10 enges in the development of therapeutics for brain metastasis.

11 d MET attenuation decreased the incidence of brain metastasis.

12 rvention of MMP-2-dependent diseases such as brain metastasis.

13 t patients with breast cancer suffering from brain metastasis.

14 presents a potential target for treatment of brain metastasis.

15 R2 signaling for HER2-positive breast cancer brain metastasis.

16 hanistic and therapeutic studies of melanoma brain metastasis.

17 Additional imaging showed no brain metastasis.

18 ted vessels in two separate murine models of brain metastasis.

19 GALNAC5, GJA1, and EGFR, all associated with brain metastasis.

20 nase in vitro cell invasion and experimental brain metastasis.

21 knowledge of the initial events that lead to brain metastasis.

22 with breast cancer, 362 developed subsequent brain metastasis.

23 and independently associated with subsequent brain metastasis.

24 cyte reactivity on neurovascular function in brain metastasis.

25 m could prove valuable for the inhibition of brain metastasis.

26 s, which served as a proxy for an orthotopic brain metastasis.

27 n contrast, ST6GALNAC5 specifically mediates brain metastasis.

28 is of melanoma cells, consequently promoting brain metastasis.

29 cases, 5/5 meningioma cases and 3/3 cases of brain metastasis.

30 s and treatment response in CNS lymphoma and brain metastasis.

31 be uniquely suited to the local treatment of brain metastasis.

32 are currently available for the treatment of brain metastasis.

33 active exudation, radiation maculopathy, and brain metastasis.

34 ival for patients with a single unresectable brain metastasis.

35 ages in 23 patients disclosed no evidence of brain metastasis.

36 nt immune response can eliminate established brain metastasis.

37 tial for study of the biology and therapy of brain metastasis.

38 r mechanisms of angiogenesis in experimental brain metastasis.

39 ich significantly decreased the incidence of brain metastasis.

40 y correlated with angiogenesis and growth of brain metastasis.

41 or patients following the first diagnosis of brain metastasis.

42 BB2+) metastatic breast cancer (MBC) develop brain metastasis.

43 barrier is a crucial, rate-limiting step of brain metastasis.

44 ties, and less than optimal efficacy against brain metastasis.

45 eatments inefficient for HER2+ breast cancer brain metastasis.

46 rred for patients who underwent resection of brain metastasis.

47 ial as a prognostic biomarker for predicting brain metastasis.

48 acological inhibition of BACE1 blocked NSCLC brain metastasis.

49 tion and chromatin accessibility that drives brain metastasis.

50 istinct transcriptional programs enriched in brain metastasis.

51 -acetyltransferase 10 (NAT10) as a driver of brain metastasis.

52 30-day readmission following craniotomy for brain metastasis.

53 significant risk factors for development of brain metastasis.

54 ive function (NCF) toxicity in patients with brain metastasis.

55 iated astrocyte reactivity, specifically, in brain metastasis.

56 matergic neurons, presenting a rationale for brain metastasis.

57 13 overexpression increased the incidence of brain metastasis.

58 tion and sialylated glycans in breast cancer brain metastasis.

59 ate the possible mechanisms of breast cancer brain metastasis.

60 result in an increase of sialylation during brain metastasis.

61 ung cancer, and spontaneous melanoma-derived brain metastasis.

62 gy in mitigating lung cancer development and brain metastasis.

63 eking cell line 231BR, likely play a role in brain metastasis.

64 l movement were highlighted in breast cancer brain metastasis.

65 exhibited a significantly high incidence of brain metastasis.

66 for a better understanding of breast cancer brain metastasis.

67 e avenue for the prevention and treatment of brain metastasis.

68 intracranial control following resection of brain metastasis.

69 able therapeutic platform to target melanoma brain metastasis.

70 compared with WBRT in patients with resected brain metastasis.

71 al cues at the BBB affects the mechanisms of brain metastasis.

72 t during metastatic evolution is crucial for brain metastasis.

73 an experimental mouse model of breast cancer brain metastasis.

74 mutation carriers had a higher proportion of brain metastasis (27.1%) compared with nonmutation carri

75 of age with stage IV NSCLC with at least one brain metastasis 5-20 mm in size, not previously treated

76 In a syngeneic model of melanoma brain metastasis, a combination of MSC-oHSV and PD-L1 bl

77 Brain metastasis, a serious complication of cancer, hing

78 olid Tumors (RECIST) version 1.1, absence of brain metastasis, adequate organ function, and pre-treat

79 is a novel prognostic marker for lung and/or brain metastasis and a predictive marker for the respons

80 ions in the USA and Canada with one resected brain metastasis and a resection cavity less than 5.0 cm

81 cer: peripheral blood, the primary tumour, a brain metastasis and a xenograft derived from the primar

82 terface in 26 patients during resection of a brain metastasis and assessed mean diffusivity and fract

83 Rat models of brain metastasis and ciliary neurotrophic factor were us

84 ment for patients with a single unresectable brain metastasis and considered for patients with two or

85 we developed a model to study human melanoma brain metastasis and found that Stat3 activity was incre

86 ted an in vivo screen for vulnerabilities of brain metastasis and identified N-acetyltransferase 10 (

87 hting its role as a double agent in limiting brain metastasis and its local consequences.

88 mour tissues and exosomes from patients with brain metastasis and predicted brain metastasis progress

89 ical metabolic condition required to sustain brain metastasis and suggest that targeting gluconeogene

90 Brain metastasis and systemic responses were concordant,

91 ary but not sufficient for the production of brain metastasis and that the inhibition of VEGF represe

92 These patients were free of brain metastasis and underwent standard treatment and su

93 re also associated with development of NSCLC brain metastasis and were selectively enriched in brain

94 asis (BCBM) may allow for early diagnosis of brain metastasis and/or help for treatment choice and it

95 mately 50% of patients with melanoma develop brain metastasis, and currently there are no beneficial

96 ts with brain malignancies including glioma, brain metastasis, and primary and secondary CNS lymphoma

97 metabolism is a key element in breast cancer brain metastasis, and raise the possibility of targeting

98 Up to 40% of lung cancer patients develop brain metastasis, and the median survival of these patie

99 Coupling whole tissue imaging of brain metastasis animal models with SMART 3D, we demonst

100 iologic and therapeutic advances in melanoma brain metastasis are hampered by the paucity of reproduc

101 The current animal models for brain metastasis are highly variable, leading to a need

102 T-cell entry and response to these drugs in brain metastasis are poorly understood.

103 his increased Stat3 activation and effect on brain metastasis are unknown.

104 45 prostate cells, originally derived from a brain metastasis, are not responsive to PDGF.

105 ain metastases and data from an experimental brain metastasis assay, both indicative of a functional

106 Breast-to-brain metastasis (B2BM) is a common and disruptive form

107 blished a human breast cancer cell model for brain metastasis based on circulating tumor cells from a

108 gonucleotides led to decreased breast cancer brain metastasis (BCBM) in vivo.

109 Breast cancer brain metastasis (BCBM) is a devastating disease.

110 Breast cancer brain metastasis (BCBM) is a lethal disease with no effe

111 Breast cancer brain metastasis (BCBM) is an area of unmet clinical nee

112 anding of CTCs associated with breast cancer brain metastasis (BCBM) is necessary for early identific

113 TCs derived from breast cancer patients with brain metastasis (BCBM) may allow for early diagnosis of

114 Breast cancer brain metastasis (BCBM) remains a major clinical problem

115 medical need for Breast Cancer patients with brain metastasis (BCBM).

116 ts had at least one untreated or progressive brain metastasis between 5 and 20 mm in diameter without

117 their opinions on these important aspects of brain metastasis biology and management.

118 onse Assessment in Neuro-Oncology (RANO) for brain metastasis (BM) 1.0 criteria for metabolic respons

119 Brain metastasis (BM) carries a poor prognosis, yet the

120 Brain metastasis (BM) is a leading cause of death from n

121 Brain metastasis (BM) is a major cause of suffering and

122 t to identify candidate biomarkers for early brain metastasis (BM) recurrence in patients who underwe

123 mbination with radiotherapy in patients with brain metastasis (BM) since contrast-enhanced MRI often

124 The incidence of brain metastasis (BM) was evaluated with the logistic re

125 Plus, brain metastasis (BMs) is a major mortality cause for NS

126 Brain metastasis (br-met) develops in an immunologically

127 anslated into excellent efficacy in multiple brain metastasis breast cancer mouse models.

128 Brain metastasis (BrM) in gastroesophageal adenocarcinom

129 Brain metastasis (BrM) is a major problem associated wit

130 Brain metastasis (BrM) is the most common form of brain

131 Brain metastasis (BrM) represents the most common intrac

132 cally in the intracardially induced model of brain metastasis but with lower sensitivity because of s

133 ed a compound, parthenolide, that suppressed brain metastasis by blocking M2 polarization.

134 als cellular events during the initiation of brain metastasis by breast cancer cells and documents th

135 analyses, we discovered candidate drivers of brain metastasis by identifying genes with more frequent

136 Mito-LND blocks lung tumor development and brain metastasis by inhibiting mitochondrial bioenergeti

137 onal in LUAD and show that astrocytes oppose brain metastasis by mediating the downregulation of TRPA

138 Our results indicate that nicotine promotes brain metastasis by skewing the polarity of M2 microglia

139 ates the blood-brain barrier, could suppress brain metastasis by targeting c-Met signaling.

140 rostate cancer cell line, originating from a brain metastasis, carries a truncating mutation of EPHB2

141 gnitive symptoms; however, understanding how brain metastasis co-opts the function of neuronal circui

142 dtype) with no subtype enrichment within the brain metastasis cohort.

143 Accordingly, the study of brain metastasis could uncover new therapeutic targets a

144 on of lipid metabolism in these cells curbed brain metastasis development, suggesting a therapeutic s

145 s-induced HDAC8 activity as driving melanoma brain metastasis development.

146 CEMIP depletion in tumour cells impaired brain metastasis, disrupting invasion and tumour cell as

147 of brain metastasis (P = 0.02) and a shorter brain metastasis-free survival in lymph node-negative pa

148 uced MMP9 were significantly correlated with brain metastasis-free survival of breast cancer patients

149 nd Kaplan-Meier survival method (p = 0.0029, brain metastasis-free survival; p = 0.0007, overall surv

150 tion screen to identify molecular drivers of brain metastasis from an orthotopic xenograft model deri

151 FET) PET for differentiating local recurrent brain metastasis from radiation necrosis after radiation

152 By testing different preclinical models of brain metastasis from various primary sources and oncoge

153 One patient with occult brain metastasis had grade 4 intracranial hemorrhage.

154 Breast cancer brain metastasis has been recognized as one of the centr

155 the paucity of robust preclinical models of brain metastasis has severely limited such investigation

156 etween the primary lung tumor and respective brain metastasis; however, the identity of the genes cap

157 Primary brain tumor or brain metastasis (HR 2.5; P = .002), number of falls in

158 Studying spontaneous melanoma brain metastasis in a clinically relevant setting is the

159 as associated with metastatic progression to brain metastasis in a mouse xenograft model.

160 pared to those with high-BMI or other cancer brain metastasis in a pan-analysis of 7628 patients.

161 ritical role for Src activation in promoting brain metastasis in a preclinical model of breast cancer

162 astatic A375Br cells significantly inhibited brain metastasis in animal models (P<0.001).

163 as been implicated as an important driver of brain metastasis in breast cancer, but the critical targ

164 Brain metastasis in gastric cancer (GC) patients is a ra

165 Brain metastasis in gastric cancer is associated with si

166 transplantable model of spontaneous melanoma brain metastasis in immunocompetent mice and developed m

167 we show a significantly higher incidence of brain metastasis in low-BMI lung cancer patients compare

168 e a unifying mechanism for the initiation of brain metastasis in lung and breast cancers.

169 bust tool that is able to predict subsequent brain metastasis in patients with breast cancer with non

170 educed cell viability in HER2+ breast cancer brain metastasis in the presence of NRG1.

171 genesis-related genes and is associated with brain metastasis in triple-negative breast cancer.

172 Plasmin suppresses brain metastasis in two ways: by converting membrane-bou

173 ived cells showed an increased potential for brain metastasis in vivo and exhibited a unique protein

174 metabolic pathway decreased the incidence of brain metastasis in vivo Taken together, our results sho

175 cretion rescues the PTEN loss and suppresses brain metastasis in vivo.

176 In an experimental mouse model of brain metastasis, inhibition of PAK1 significantly reduc

177 , we analyzed the transcriptional profile of brain metastasis initiating cells (BMICs) at two distinc

178 Brain metastasis is a common characteristic of late-stag

179 Brain metastasis is a frequent occurrence in patients wi

180 Brain metastasis is a major cause of cancer mortality, b

181 Brain metastasis is a major cause of morbidity and morta

182 Brain metastasis is an end stage in breast cancer progre

183 Brain metastasis is an important cause of mortality in b

184 Brain metastasis is an important cause of mortality in p

185 Brain metastasis is an ominous complication of cancer, y

186 e development of effective therapies against brain metastasis is currently hindered by limitations in

187 etal imaging may be indicated if an isolated brain metastasis is detected.

188 the identity of the genes capable of driving brain metastasis is incompletely understood.

189 bility to be more inclusive of patients with brain metastasis is justified in many cases and may spee

190 oma, but activity in patients with untreated brain metastasis is less established.

191 survival time of breast cancer patients with brain metastasis is less than 6 months, and even a small

192 Brain metastasis is one of the chief causes of mortality

193 nical importance, the molecular basis of the brain metastasis is poorly understood.

194 Breast cancer brain metastasis is resistant to therapy and a particula

195 The incidence of brain metastasis is rising and poses a severe clinical p

196 A key event during brain metastasis is the migration of cancer cells throug

197 Brain metastasis is the most commonly occurring intracra

198 PURPOSE Brain metastasis is usually a fatal event in patients wi

199 inflammatory response has been documented in brain metastasis, its contribution to cancer progression

200 d quantify volumetric and spatial aspects of brain metastasis landscapes, including diverse tumor mor

201 + MBC and CNS disease, including parenchymal brain metastasis, leptomeningeal disease (LMD), or dural

202 In vivo, in a model of brain metastasis, low or high Her-2-overexpressing 231-B

203 tic phenotype with the unusual occurrence of brain metastasis, making it an important target for diag

204 hese data suggest that the glial response to brain metastasis may provide a sensitive biomarker of tu

205 patients with metastatic melanoma, melanoma brain metastasis (MBM) continues to represent a signific

206 adiosurgery group for patients with a single brain metastasis (median survival time 6.5 vs 4.9 months

207 these results indicate a novel mechanism of brain metastasis mediated by EVs that triggers the destr

208 e allowed the development of an experimental brain metastasis model and a postsurgical resection spon

209 Herein, we describe an experimental brain metastasis model that uses ultrasonographic guidan

210 Using an experimental brain metastasis model, we characterized the brain metas

211 ecycling of GI-101A cells in an experimental brain metastasis model.

212 Characterizing clinically relevant brain metastasis models and assessing the therapeutic ef

213 stemic delivery of OV, we developed melanoma brain metastasis models in immunocompromised and immunoc

214 In cell-based culture and brain metastasis models, we found that downregulation of

215 ave developed an in vivo imageable breast-to-brain metastasis mouse model.

216 Brain metastasis occurred as the sole site of first fail

217 Brain metastasis occurs in 20-40% of cancer patients.

218 Brain metastasis occurs in about 50% of all women with m

219 Brain metastasis occurs in up to 40% of patients with no

220 rats with HER2-positive cells derived from a brain metastasis of a breast cancer patient (MDA-MB-361)

221 Brain metastasis of advanced breast cancer often results

222 suggest that miR-509 has a critical role in brain metastasis of breast cancer by modulating the RhoC

223 metastatic cancer cell-derived EVs promoted brain metastasis of breast cancer cell lines and are pre

224 In contrast, the calculated pore size of a brain metastasis of breast cancer was approximately 10-f

225 rve as biomarkers or therapeutic targets for brain metastasis of breast cancer.

226 levels support the importance of DDR in the brain metastasis of CRC.

227 l possesses the unique capability to examine brain metastasis of human lung, breast and melanoma cell

228 on with a dominant-negative Stat3 suppressed brain metastasis of human melanoma cells in animal model

229 Brain metastasis of lung cancer causes high mortality, b

230 an brain metastatic cells and contributes to brain metastasis of melanoma.

231 nvasion of melanoma cells and contributes to brain metastasis of melanoma.

232 R2 signaling for HER2-positive breast cancer brain metastasis.Oncogene advance online publication, 24

233 Brain metastasis only group and multiple sites metastasi

234 and < .001, respectively), whereas a single brain metastasis or initial treatment with SRS versus WB

235 ode status, along with a higher incidence of brain metastasis (P = 0.02) and a shorter brain metastas

236 sis therapies, especially of consequence for brain metastasis patients.

237 In patients with brain metastasis, PET using labeled amino acids has gain

238 Brain metastasis poses formidable clinical challenges du

239 patients with brain metastasis and predicted brain metastasis progression and patient survival.

240 In 29% of patients, the cause of death was brain metastasis progression.

241 of the 2 patients, subsequent resection of a brain metastasis proved HER2-positive disease, confirmin

242 cerebrovascular dysfunction associated with brain metastasis, providing a potential therapeutic aven

243 time-activity curve can differentiate local brain metastasis recurrence from radionecrosis with high

244 The molecular changes that lead to brain metastasis remain poorly understood.

245 ever, how smoking impacts the development of brain metastasis remains elusive.

246 Brain metastasis represents a substantial source of morb

247 is review, we discuss the latest advances in brain metastasis research, with special emphasis on the

248 Thus, the use of SRS after brain metastasis resection could be an alternative to wh

249 ndividuals who had undergone craniotomy with brain metastasis resection from January 2010 to December

250 h ICIs, specifically following neurosurgical brain metastasis resection, are scarce.

251 After brain metastasis resection, whole brain radiotherapy dec

252 t was the proportion of patients achieving a brain metastasis response (partial response or complete

253 col evaluation scan and were unevaluable for brain metastasis response as a result of progression or

254 The primary endpoint was brain metastasis response assessed in all treated patien

255 A brain metastasis response was achieved in four (22%; 95%

256 Brain metastasis response, the primary end point, was as

257 15.9-47.0]) of 37 patients in cohort 1 had a brain metastasis response.

258 Six patients (26%) had a brain metastasis response.

259 interactions in both animal models and human brain metastasis samples.

260 gression, and death caused by progression of brain metastasis, seemed to be improved compared with hi

261 eviously, we reported a protein signature of brain metastasis showing increased ability of brain meta

262 e N-methyltransferase 2 (KMT2) and prevented brain metastasis similar to direct downregulation of Mmp

263 f activated Stat3 is also increased in human brain metastasis specimens when compared with that in th

264 After resection of a brain metastasis, SRS radiosurgery should be considered

265 Analysis of treatment by brain metastasis status demonstrated EGFR-TKI plus bevac

266 Here, we report that breast cancer brain metastasis stromal cell interactions in 3D cocultu

267 ts with cutaneous melanoma only), 71% in the brain metastasis subgroup, 36% in the ocular/uveal melan

268 d in brain metastases, led to a reduction in brain metastasis, suggesting that some niche-specific EC

269 the outstanding antitumor activity of C1a in brain metastasis, support clinical investigation of this

270 ancer (NSCLC) to try to improve incidence of brain metastasis, survival, and eventually quality of li

271 s undergo morphologic changes in response to brain metastasis, switching to a reactive phenotype, whi

272 e using a PC model (DU145/RasB1) of bone and brain metastasis that EGR1 expression regulates angiogen

273 In this work, we developed a robust model of brain metastasis that empowers quantitative tracking of

274 Glial cells are masterminds of brain metastasis that orchestrate tumor-supportive signa

275 However, in patients with brain metastasis, the blood-brain barrier limits its use

276 w discusses recent advances in breast cancer brain metastasis therapy and potential approaches for su

277 pG-C treatment as a new intervention against brain metastasis, through an essential activation of mic

278 A sequencing was performed on eight resected brain metastasis tissue samples and revealed B-cell rela

279 d validated in a cohort of 128 patients with brain metastasis treated at the Cross Cancer Institute (

280 ear survival was similar to patients without brain metastasis treated with anti-programmed cell death

281 mouse model of HER2-amplified breast cancer brain metastasis using an orthotopic xenograft of BT474

282 d EGFR-TKI plus bevacizumab in patients with brain metastasis was associated with significant OS bene

283 A nomogram to predict brain metastasis was constructed and validated in a coho

284 Brain metastasis was reported in 368 (0.62%) patients.

285 Brain metastasis was the most common site of failure.

286 s of protein concentration in a rat model of brain metastasis, we determined that the proportion of A

287 metastases but limited to those with 1 to 4 brain metastasis were eligible.

288 for the correct identification of recurrent brain metastasis were evaluated by receiver-operating-ch

289 disorders or psychosis, substance abuse, or brain metastasis were excluded.

290 th a constitutively activated Stat3 enhanced brain metastasis, whereas blockade of Stat3 activation b

291 ting to genomic instability in breast cancer brain metastasis which is of potential translational sig

292 Brain metastasis, which commonly arises in patients with

293 -713 in the intracerebrally induced model of brain metastasis, which was significantly greater than t

294 We found that nicotine enhanced brain metastasis, while a depletion of microglia suppres

295 thologically confirmed diagnosis of melanoma brain metastasis who underwent surgical resection at a s

296 enriched patient population at high risk for brain metastasis will facilitate the design of trials ai

297 ate deep learning (DL) methods for detecting brain metastasis with MRI to aid in treatment planning f

298 eir kind that provide insight into targeting brain metastasis with stem-cell mediated delivery of pro

299 ent (observation group, 46 patients) for the brain metastasis, with median follow-up of 48 weeks and

300 rvival in two murine models of breast cancer brain metastasis, without any apparent local or systemic