ライフサイエンスコーパス: metastasis

1 ironment that exert potent effects on cancer metastasis.

2 es, is essential for platelet-mediated tumor metastasis.

3 ay in tumor promotion and suppression and in metastasis.

4 beta signaling to promote tumor invasion and metastasis.

5 o ubiquitinate HIF-1alpha and inhibit cancer metastasis.

6 hat these two genes are suppressors of tumor metastasis.

7 on and independently predicts progression to metastasis.

8 asation, lung colonization, and postsurgical metastasis.

9 hat functions to regulate genes that promote metastasis.

10 it has been linked to increased invasion and metastasis.

11 00 nM) as modulators for cancer invasion and metastasis.

12 ractions and a p-EMT program associated with metastasis.

13 T6A efficiently suppresses TGF-beta-mediated metastasis.

14 ressed ROS production and the ability of HCC metastasis.

15 alone for patients with breast cancer liver metastasis.

16 and new function for LOXL2 in breast cancer metastasis.

17 une function or cell adhesion and tumor cell metastasis.

18 mutant p53 GOF in promoting tumor growth and metastasis.

19 and are hypothesized to be the initiators of metastasis.

20 enic fitness during the evolution of distant metastasis.

21 oted lung pre-metastatic niche formation and metastasis.

22 ing TNFalpha-activated MSCs to promote tumor metastasis.

23 atural killer (NK) cells, which help control metastasis.

24 l process that has been implicated in cancer metastasis.

25 eceptors, thereby promoting tumor growth and metastasis.

26 hibited migration, invasion, and spontaneous metastasis.

27 and biological properties and their role in metastasis.

28 ns such as neural circuit formation and cell metastasis.

29 tes Pin1, but also inhibits cells growth and metastasis.

30 and markedly inhibits cancer cell growth and metastasis.

31 arkers associated with HCC tumorigenesis and metastasis.

32 omoting cancer cell invasion, migration, and metastasis.

33 an be potentially targeted to control cancer metastasis.

34 ances transcriptional activity, facilitating metastasis.

35 tasis in an experimental mouse model of lung metastasis.

36 bone stromal activity in the absence of bone metastasis.

37 ms, embryogenesis, wound healing, and cancer metastasis.

38 plicated in tumor progression, invasion, and metastasis.

39 monstrated to play a role in host control of metastasis.

40 O-GlcNAcylation inhibits cancer invasion and metastasis.

41 ymal transition (EMT), which correlates with metastasis.

42 targeting Ncad in preclinical models of EOC metastasis.

43 rams currently proposed to be key drivers of metastasis.

44 and the cumulative rate of nonsentinel-node metastasis.

45 ped recurrence of retinoblastoma or systemic metastasis.

46 ated with histological grades and lymph node metastasis.

47 niches in remote microenvironments to favor metastasis.

48 ancer is characterized by early and frequent metastasis.

49 cranial control following resection of brain metastasis.

50 understood role during tumor progression and metastasis.

51 the solid tumor is a critical determinant of metastasis.

52 herapeutic platform to target melanoma brain metastasis.

53 as critical modifiers of tumorigenicity and metastasis.

54 ,, changes in tRNA amounts facilitate cancer metastasis.

55 in motility, a feature reminiscent of cancer metastasis.

56 BL oncogenic drivers and to characterize NBL metastasis.

57 ed in enhanced survival and markedly reduced metastasis.

58 , and migration and in vivo tumor growth and metastasis.

59 ilities to control unchecked cell growth and metastasis.

60 ions during the natural evolution of distant metastasis.

61 ifferent aspects of cancer cell survival and metastasis.

62 for tumor growth, survival, and cancer cell metastasis.

63 (MMPs) are central to cancer development and metastasis.

64 t an epigenetic process might operate during metastasis.

65 e, tumor microenvironment reprogramming, and metastasis.

66 s against thrombocytosis-induced increase in metastasis.

67 s a strong predictor of eventual relapse and metastasis.

68 lecules, AKT, RICTOR, and Rac1, to drive PCa metastasis.

69 ing tumor cells (CTC) during prostate cancer metastasis.

70 senchymal transition (EMT), invasiveness and metastasis.

71 es anoikis to suppress PDAC tumor growth and metastasis.

72 ar disease (CVD), and cancer progression and metastasis.

73 ed liver endothelial cell adhesion and liver metastasis.

74 activation of STAT3 and inhibit the EMT and metastasis.

75 ded, and all patients were free from distant metastasis.

76 he pre-metastatic niche and other aspects of metastasis.

77 s SMAD2 function in NSCLC cells and promotes metastasis.

78 that miR-194 is a driver of prostate cancer metastasis.

79 o tissue regeneration and the suppression of metastasis.

80 gent for the prevention or treatment of bone metastasis.

81 stalk may be a therapeutic approach to block metastasis.

82 nancies, owing in part to its propensity for metastasis.

83 istant organs, thus fueling tumor growth and metastasis.

84 significant in colon cancer, as it regulates metastasis.

85 d increased neutrophil recruitment and tumor metastasis.

86 w) lymphangiogenesis contributes to visceral metastasis.

87 ortant in both normal development and cancer metastasis.

88 a retrograde developmental transition in PDA metastasis.

89 mportant influence on cancer progression and metastasis.

90 s to promote their growth, angiogenesis, and metastasis.

91 edict those CAF-specific lncRNAs involved in metastasis.

92 or the study of angiosarcoma development and metastasis.

93 regional recurrence and one (2%) had distant metastasis; 2-year progression-free survival was 92% (95

94 enase with fewer than three organ sites with metastasis (5 years, 51%).

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

96 the radial growth phase (WM35) and from lung metastasis (A375-P).

97 mplification and/or overexpression, frequent metastasis and a dismal prognosis.

98 w, we evaluate the importance of ERs in bone metastasis and discuss new avenues of investigation for

99 e of breast cancer cells are associated with metastasis and disease relapse.

100 s could be novel agents for the treatment of metastasis and for skeletal complications in prostate ca

101 elopment of advanced and relapsed peritoneal metastasis and its impact on patients' outcomes.

102 e the genes involved in both the stages- non metastasis and metastatsis and change in their expressio

103 extent by reflecting molecular features of a metastasis and might be a useful tool for future clinica

104 y correlated with invasion depth, lymph node metastasis and negatively correlated with the patients'

105 tion correlates with colorectal cancer (CRC) metastasis and prognosis.

106 However, the role of IL-35 in cancer metastasis and progression is not well understood.

107 omal compartment, is associated with reduced metastasis and prolonged survival in pancreatic ductal a

108 MAOA inhibitor treatment effectively reduces metastasis and prolongs mouse survival by disengaging th

109 that is lost during melanoma progression to metastasis and provides the ability to identify melanoma

110 dered as a well-established marker for tumor metastasis and recurrence.

111 initiate cancer formation and are linked to metastasis and resistance to therapies.

112 contrast, TIM-4(+) B cells decreased B16-F10 metastasis and s.c. tumor growth, and this was IFN-gamma

113 pression of prostate tumor growth and distal metastasis and substantially prolonged overall survival.

114 kinesin-1 motor functions and breast cancer metastasis and suggest PLD2 as a potential therapeutic t

115 -specific 6 (GAS6), are important drivers of metastasis and therapeutic resistance in human cancers.

116 he idea that cancer cell plasticity promotes metastasis and tumor recurrence, resulting in patient mo

117 BCBM) may allow for early diagnosis of brain metastasis and/or help for treatment choice and its effi

118 may help restore vessel structure, minimize metastasis, and aid in drug delivery.

119 naling-mediated breast cancer tumorigenesis, metastasis, and cancer stem cell (CSC) maintenance.

120 elay tumor onset and to impair tumor growth, metastasis, and cancer stem-like cell formation in this

121 primary tumor, the sole treatment-resistant metastasis, and germline tissue to explore mechanisms of

122 n (nal-IRI) prevented tumor relapse, reduced metastasis, and increased both progression-free survival

123 t MCPIP1 regulated ccRCC cell motility, lung metastasis, and mesenchymal phenotype by regulating key

124 hts into how macrophages enhance cancer cell metastasis, and they identify TNFalpha and TGFbeta1 dual

125 poor survival as patients with more distant metastasis, and thus may not benefit from surgery.

126 n = 5/group), the latter through a syngeneic metastasis approach.

127 , intrahepatic lymph invasion and lymph node metastasis are poor prognostic factors.

128 Cancer chemoresistance and metastasis are tightly associated features.

129 l; n = 2,042), or who developed locoregional metastasis as a first recurrence some time after primary

130 ue Thr(567) phosphorylation in regulation of metastasis-associated behaviors, ovarian cancer cells th

131 s a prominent downstream signaling target of metastasis-associated in colon cancer 1 (MACC1) in color

132 Metastasis-associated lung adenocarcinoma transcript 1 (

133 ine the role of long noncoding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (

134 ich AR can either increase or decrease ccRCC metastasis at different sites and may help us to develop

135 atients and provide an unprecedented view of metastasis at single-cell genomic resolution.

136 rived from breast cancer patients with brain metastasis (BCBM) may allow for early diagnosis of brain

137 Metastasis, biochemical recurrence, overall survival, pr

138 ls are highly efficient at preventing cancer metastasis but are infrequently found in the core of pri

139 n associated with increased tumor growth and metastasis but the mechanistic details of this interacti

140 e for Twist1-induced migration, invasion and metastasis, but less responsible for Twist1-induced mese

141 prognostic and therapeutic implications for metastasis by cancers that preferentially exploit nerve

142 to infection and promoting tumor growth and metastasis by converting resting B and T cells into IL-1

143 ritical roles in PDAC cell extravasation and metastasis by facilitating the adhesion to endothelial c

144 iency induced aggressive tumor formation and metastasis by promoting the disruption of adherens junct

145 , which may account for tumor recurrence and metastasis by regenerating new tumors.

146 Early detection of metastasis can be aided by circulating tumor cells (CTC)

147 e necessity for radiation or surgery to bone metastasis cause considerable morbidity, decrements in q

148 mplanted with 5 x 10(6) rat colorectal liver metastasis cell line cells.

149 pha-activated MSCs strikingly enhanced tumor metastasis compared with normal MSCs.

150 Metastasis-competent circulating tumour cells (CTCs) exp

151 As the body of research concerning metastasis continues to grow at a rapid rate, the biolog

152 For colorectal liver metastasis (CRLM), intrahepatic lymph invasion and lymph

153 l for the formation and maintenance of liver metastasis derived from colorectal cancers.

154 Metastasis detection by routine metabolic imaging with [

155 d either as a screening tool for brain micro-metastasis detection or for making rational treatment de

156 They thus hold promise for metastasis diagnosis, image-guided surgery, and theranos

157 Purpose Retrospective studies suggest that metastasis-directed therapy (MDT) for oligorecurrent pro

158 ase-related outcome (local recurrence, nodal metastasis, distant metastasis, or disease-specific deat

159 he bone marrow microenvironment mediate bone metastasis during prostate cancer progression, with pote

160 The antitumor and anti-metastasis efficacy of CREKA-loaded liposome was more ob

161 We showed that synchronous metastasis entropy was correlated across 5 Spatial Scale

162 ith bone metastasis versus soft-tissue or no metastasis for both (18)F-FDG (P = 0.037) and (68)Ga-DOT

163 gs versus negative scan findings for osseous metastasis for IS and FOM; more extensive disease versus

164 matory tumor microenvironment contributes to metastasis, for instance, by recruiting blood and lymph

165 unosuppressive microenvironment conducive to metastasis formation.

166 offer a new possibility for diminishing bone metastasis formation.Significance: These findings establ

167 r predicting worse overall survival (OS) and metastasis-free survival (MFS).

168 ecurrence-free survival [bRFS], 29%; distant metastasis-free survival [DMFS], 53%; prostate cancer-sp

169 Erasmus Breast Cancer Cohort, 5-year distant-metastasis-free survival was longer in patients with hig

170 Metastasis-free survival was significantly longer in pat

171 on-free survival, local failure, and distant metastasis-free survival were not different between IMRT

172 nd points included overall survival, distant metastasis-free survival, freedom from relapse, and safe

173 ll survival, local and regional PFS, distant metastasis-free survival, quality of life, adverse event

174 on bone quality using a mouse model of bone metastasis from mammary tumor.

175 signature discriminated cases that developed metastasis from those that did not.

176 stases; as well as tumor microenvironment of metastasis function, the hallmark of hematogenous dissem

177 ression and clinically relevant invasion and metastasis gene signatures.

178 d p-EMT as an independent predictor of nodal metastasis, grade, and adverse pathologic features.

179 cess of triple-negative breast cancer (TNBC) metastasis has not been addressed.

180 lysis of their specific association with HCC metastasis has not been conducted.

181 a result, CRC tumorigenesis, progression and metastasis have been heavily studied, especially with re

182 sible tumour cell plasticity is required for metastasis, however, in vivo steps and molecular mechani

183 old in cancer patients, promotes blood-borne metastasis in an animal cancer model.

184 in multiple cancer cell systems and reduced metastasis in an experimental mouse model of lung metast

185 that hypoxia-regulated autophagy suppresses metastasis in breast cancer by preventing tumor fibrosis

186 uture treatment strategies to prevent cancer metastasis in breast cancer cases.

187 for OGT-mediated regulation of invasion and metastasis in breast cancer cells.

188 utor to the complex mechanisms that underlie metastasis in colorectal cancer and a potential novel bi

189 tic link between EPHB receptor mutations and metastasis in colorectal cancer.

190 ic accuracy in the detection of abdominal LN metastasis in high-risk endometrial cancer.

191 of human cancers and loss of OTUD1 increases metastasis in intracardial xenograft and orthotopic tran

192 e main cause of local recurrence and distant metastasis in lung cancer.

193 rs from MAN2A1-FER cells and prevented their metastasis in mice.

194 rresponding enzymes associated with melanoma metastasis in patient samples.

195 edicts disease recurrence and progression to metastasis in patients choosing radical prostatectomy.

196 erall survival after detection of intestinal metastasis in patients receiving systemic treatment was

197 lesterol biosynthesis, significantly reduces metastasis in relevant animal models of cancer.

198 transcriptional reprogramming that supports metastasis in response to mTOR inhibition.

199 survival, anoikis resistance, invasion, and metastasis in several cancers.

200 tion of one 3q driver gene FXR1 with distant metastasis in TNBC (P = 0.01) was further validated by i

201 that LOXL2 is a key driver of breast cancer metastasis in two conditional transgenic mouse models of

202 se data reveal a late-dissemination model of metastasis in two CRC patients and provide an unpreceden

203 expression of XRN2 induced EMT and promoted metastasis in vitro and in vivo.

204 and invasion in vitro and drove experimental metastasis in vivo Gene expression profiling revealed a

205 that vimentin has an important role in tumor metastasis in vivo in the setting of pre-diabetes and en

206 /TAZ was sufficient to inhibit neuroblastoma metastasis in vivo Overall, we identify gene expression

207 NT2 also promotes tumor growth, invasion and metastasis in vivo.

208 stimulates tumor cell motility in vitro and metastasis in vivo.

209 colony formation, and in vivo promoted lung metastasis independent of tumor growth.

210 Metastasis is a complex biological process that has been

211 Bone metastasis is a prominent cause of morbidity and mortali

212 Metastasis is responsible for most cancer-related deaths

213 the role of GOF mutant p53 in promoting lung metastasis is shown to be critically dependent on the tr

214 Metastasis is the leading cause of death for cancer pati

215 Since liver metastasis is the main cause of death in cancer patients

216 ic and pathological processes such as cancer metastasis, its underlying mechanism and connections to

217 ated in vivo tumor angiogenesis, growth, and metastasis, largely by stimulating tumor cell proliferat

218 in CSF, a remarkably acellular, mitogen-poor metastasis microenvironment.

219 Employing a lung metastasis model of murine breast cancer, we found that

220 pression were observed in a PCa experimental metastasis model.

221 on away from the M2 phenotype in spontaneous metastasis models of 4T1 breast cancer and B16F10 melano

222 ell as more clinically relevant, spontaneous metastasis models, we visualize all stages of metastatic

223 large-scale study by creating breast cancer metastasis network and equipped it with different confor

224 ontrast, the calculated pore size of a brain metastasis of breast cancer was approximately 10-fold sm

225 n mediating tumor-stroma interactions during metastasis of cancer to different target organs.

226 Knocking down Elmo1 impairs metastasis of carcinoma cells to the lung, thereby provi

227 The contribution of somatic mutations to metastasis of colorectal cancers is currently unknown.

228 odels showed that the lung extravasation and metastasis of FOXC1-overexpressing TNBC cells were atten

229 nd stable overexpression of miR-194 enhanced metastasis of intravenous and intraprostatic tumor xenog

230 In addition to its inhibitory effect on bone metastasis of Jagged1-expressing tumor cells, 15D11 dram

231 hat DOCK5 inhibition attenuates invasion and metastasis of MDA-MB-231 cells and prolongs life span of

232 ne mechanism that leads to osteoblastic bone metastasis of PCa.

233 , is reported to be involved in invasion and metastasis of some cancers, but the role of FPR2 in gast

234 the MET proto-oncogene, promote invasion and metastasis of tumor cells and have been considered poten

235 one patient had colon cancer with a hepatic metastasis, one patient had a hepatic angioma, one patie

236 fied for the GEP NET patients, not even bone metastasis or estimated BM dose.

237 gnificantly higher detection rate of distant metastasis or synchronous cancer than strategies in curr

238 (local recurrence, nodal metastasis, distant metastasis, or disease-specific death) of CSCCs with CPN

239 Because LH2 promotes fibrosis and cancer metastasis, our findings suggest that pharmacologic stra

240 infiltration was positively associated with metastasis, pre-metastatic niche formation and poor prog

241 n acquire oncogenic properties that increase metastasis, proliferation, and cell survival.

242 Taken together, our studies uncover a new metastasis-promoting pathway in Ewing Sarcoma, with ther

243 m cooperated with Pten deletion to produce a metastasis-prone tumor.

244 2 patients, subsequent resection of a brain metastasis proved HER2-positive disease, confirming that

245 tations, especially their enrichment in bone metastasis, raised even more provocative questions on th

246 e features that include increased lymph node metastasis, reduced responsiveness to neoadjuvant therap

247 11q22.1-q22.2 amplification with lymph node metastasis, reduced survival, and increased cancer recur

248 kappaB target gene expression, including the metastasis-related proteins intercellular adhesion molec

249 , the role of TNFalpha-treated MSCs in tumor metastasis remains elusive.

250 his altered metabolism contributes to tumour metastasis remains elusive.

251 Thus, the use of SRS after brain metastasis resection could be an alternative to whole-br

252 e cell migration in wound closure and cancer metastasis, respectively.

253 distal oesophageal cancer with coeliac node metastasis seem to have a similarly poor survival as pat

254 d SOX9 is associated with stem cell-like and metastasis signatures, and their depletion impairs the m

255 alignant process); (iii) ROI area size; (iv) metastasis site; and (v) entropy in the psoas muscle (re

256 the clinical setting for the development of metastasis-specific drugs and for patient stratification

257 acrovascular invasion; and showed the lowest metastasis-specific gene expression levels and TP53 muta

258 Whether metastasis-specific genetic alterations exist remains co

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

260 of the Liver Italian Program, and tumor-node-metastasis staging systems; had no macrovascular invasio

261 Candidate lncRNAs related to metastasis, such as HAND2-AS1, were further validated us

262 Furthermore, SNAI2 transduction rescues metastasis suppression by miR-452.

263 have been shown to have potent antitumor and metastasis-suppressive effects in multiple animal models

264 tic genes identified the scaffolding protein metastasis suppressor 1 (MTSS1) as a novel Akt2-regulate

265 Additionally, an iron-regulated metastasis suppressor interacts with the epidermal growt

266 The iron-regulated metastasis suppressor N-myc downstream-regulated gene 1

267 RNA editing hotspot in miR-200b, a key tumor metastasis suppressor, we found that the miR-200b editin

268 ated affecting the reliability of tumor node metastasis system classification.

269 ryocytes, yet they developed more aggressive metastasis than wild-type hosts.

270 to be an adverse factor in tumor growth and metastasis, the role of G9a in regulating gene expressio

271 to endothelial cells is a key step in cancer metastasis; therefore, identifying the key molecules inv

272 t driver of breast carcinoma progression and metastasis, these results lay the groundwork for future

273 Cs to stimulate tumor cell proliferation and metastasis through stimulation of lysosome-anchored Rab7

274 lls-mechanisms critical to tumorigenesis and metastasis-through a TLR4/nuclear factor kappa-light-cha

275 subpopulations with a higher propensity for metastasis to bone and the central nervous system.

276 or cells, 15D11 dramatically sensitizes bone metastasis to chemotherapy, which induces Jagged1 expres

277 During metastasis to distant sites, tumor cells migrate to bloo

278 ase-expressing LV12 cells reduced attachment/metastasis to liver to the same level as that observed w

279 l PPP1R11 associated with TP53 mutations and metastasis to the liver.

280 on CD8(+) T cells and limited B16 pulmonary metastasis to the same degree as PD-1 gene deficiency.

281 iscuss new avenues of investigation for bone metastasis treatment based on current knowledge.

282 fferences in survival for patients with bone metastasis versus soft-tissue or no metastasis for both

283 vated mTORC2 promotes cancer cell growth and metastasis via Akt(S437) phosphorylation mediated signal

284 potential and is involved in prostate cancer metastasis via direct regulation of CD44, a ubiquitous m

285 Although STAT4 mediated EOC metastasis via inducing epithelial-to-mesenchymal transi

286 ggest that ECs enhance EMT-induced TNBC cell metastasis via PAI-1 and CCL5 signaling and illustrate t

287 Overall prevalence of distant metastasis was 13.7% (21 of 153) for cervical cancer and

288 ated that the inhibition of tumor growth and metastasis was associated with activation of Bax, cleave

289 However, hepatic metastasis was present.

290 ced CXCL12, an important chemokine in tumour metastasis, was markedly inhibited by TGFbeta.

291 y profile secreted proteins involved in lung metastasis, we applied quantitative mass spectrometry-ba

292 genotypic alterations before and after bone metastasis, we conducted genome-wide mRNA profiling and

293 molecular mechanisms mediating neuroblastoma metastasis, we developed a mouse model using intracardia

294 esis that reducing megakaryocytes may reduce metastasis, we found that thrombopoietin-deficient mice

295 Plau, and Wsb1 that promote invasiveness and metastasis, were enriched in mouse and human angiosarcom

296 mary tumor cells dramatically decreased lung metastasis, whereas LOXL2 overexpression promoted metast

297 ired ES cell proliferation, tumor growth and metastasis, which was rescued by the constitutively acti

298 had prolonged time to death, recurrence and metastasis, while CD44 was a promising biomarker predict

299 ginsenoside Ro significantly prevented lung metastasis with downregulation of integrin alphavbeta6 a

300 that promote cancer cell invasive growth and metastasis, yet the mechanisms mediating these functions