ライフサイエンスコーパス: tumor metastasis

1 modulate the immune response to promote lung tumor metastasis.

2 al transition (EMT) occurs frequently during tumor metastasis.

3 in various human cancers and is involved in tumor metastasis.

4 tent microenvironmental factor that promotes tumor metastasis.

5 epithelial-mesenchymal transition (EMT) and tumor metastasis.

6 lates lung homeostasis, immune response, and tumor metastasis.

7 rocesses, including inflammatory disease and tumor metastasis.

8 epithelial-mesenchymal transition, and lung tumor metastasis.

9 l process for both embryonic development and tumor metastasis.

10 typically house primary breast carcinoma or tumor metastasis.

11 tial implication in cancer cell invasion and tumor metastasis.

12 s, identifying a crucial regulatory axis for tumor metastasis.

13 inases (TIMP)-1 has been thought to suppress tumor metastasis.

14 impairs platelet-tumor cell interaction and tumor metastasis.

15 ascular invasion provides a direct route for tumor metastasis.

16 mor cells in vivo and inhibit development of tumor metastasis.

17 ymal transition (EMT) during development and tumor metastasis.

18 ism, liver homeostasis, immune response, and tumor metastasis.

19 CNL could be used to prevent and treat solid tumor metastasis.

20 g that TAMs may contribute to HOXB7-promoted tumor metastasis.

21 d iNKT cells effectively protected mice from tumor metastasis.

22 gical processes like cell differentiation or tumor metastasis.

23 back regulatory loop between anaphylaxis and tumor metastasis.

24 ch as lymphedema, inflammatory diseases, and tumor metastasis.

25 -C motif) receptor 4 (CXCR4) is critical for tumor metastasis.

26 and increased cell motility-all mediators of tumor metastasis.

27 t in cell migration, lymphatic invasion, and tumor metastasis.

28 eedback relationship between anaphylaxis and tumor metastasis.

29 talk between endocytic pathway, hypoxia, and tumor metastasis.

30 reover, TGF-beta blockade reduced postpartum tumor metastasis.

31 that postpartum involution increases mammary tumor metastasis.

32 sembly to drive malignant transformation and tumor metastasis.

33 egulation of EC barrier function controlling tumor metastasis.

34 DNase I treatment was sufficient to suppress tumor metastasis.

35 and contributes to cancer cell invasion and tumor metastasis.

36 g miR-204 levels therapeutically to suppress tumor metastasis.

37 extracellular matrix degradation to promote tumor metastasis.

38 ation of HMGA2 and its effector functions in tumor metastasis.

39 ell migration and plays an important role in tumor metastasis.

40 critical process in normal morphogenesis and tumor metastasis.

41 trolling both local tumor growth and distant tumor metastasis.

42 indicating that host A2A receptors enhanced tumor metastasis.

43 latory loop plays important roles in EMT and tumor metastasis.

44 new actin-based mechanism that can suppress tumor metastasis.

45 ent may be an effective strategy to suppress tumor metastasis.

46 y resistance, cancer stem cell survival, and tumor metastasis.

47 sm (EPLIN), a putative suppressor of EMT and tumor metastasis.

48 helial plasticity implicated in fibrosis and tumor metastasis.

49 to specifically inhibit processes that drive tumor metastasis.

50 o establish a favorable microenvironment for tumor metastasis.

51 ion is available regarding their function in tumor metastasis.

52 inding proteins that is directly involved in tumor metastasis.

53 rrow-derived cells was necessary for optimal tumor metastasis.

54 l, suggesting the involvement of V-ATPase in tumor metastasis.

55 ssing SOX18 function is sufficient to impede tumor metastasis.

56 is commonly known as a central regulator of tumor metastasis.

57 signaling, cell adhesion, wound healing, and tumor metastasis.

58 at hijacks the Met signal pathway to promote tumor metastasis.

59 pithelial-to-mesenchymal transition (EMT) in tumor metastasis.

60 inase has been reported in human cancers and tumor metastasis.

61 a specific NK killer receptor in preventing tumor metastasis.

62 this interaction is involved in hematogenous tumor metastasis.

63 f understanding of the mechanisms leading to tumor metastasis.

64 lariasis, transplant rejection, obesity, and tumor metastasis.

65 bits ezrin protein as an approach to prevent tumor metastasis.

66 studies with respect to the role of SPDEF in tumor metastasis.

67 may contribute in part to hypoxia-stimulated tumor metastasis.

68 ent in the pathogenesis of lung fibrosis and tumor metastasis.

69 but also functionally involved in enhancing tumor metastasis.

70 s, a process essential for wound healing and tumor metastasis.

71 ould play a central role in TGFbeta-promoted tumor metastasis.

72 nto how miR-155 modulates the development of tumor metastasis.

73 giogenic switch during tumor development and tumor metastasis.

74 tion of C/EBP-delta in lymphangiogenesis and tumor metastasis.

75 nt issue given that EMT is an early event in tumor metastasis.

76 1 and Snail2 act together to promote EMT and tumor metastasis.

77 es to prevent ensuing tumor angiogenesis and tumor metastasis.

78 nce for a master regulatory role of FoxM1 in tumor metastasis.

79 (EMTs) during both embryonic development and tumor metastasis.

80 is lung carcinoma (LLC) s.c. tumors and lung tumor metastasis.

81 target therapeutics and processes underlying tumor metastasis.

82 lung colonization in vitro, a final stage in tumor metastasis.

83 nt efficacy on both primary solid tumors and tumor metastasis.

84 applied in in vivo brain vessel imaging and tumor metastasis.

85 able development of chronic inflammation and tumor metastasis.

86 MET, pEMT, and plasticity in the context of tumor metastasis.

87 regulates PI4KIIIalpha activity and mediate tumor metastasis.

88 nd collective behaviors likely contribute to tumor metastasis.

89 okine signaling regulates cell migration and tumor metastasis.

90 -7Ralpha are promising targets of inhibiting tumor metastasis.

91 e prevention and/or treatment of PAR1-driven tumor metastasis.

92 e in cell proliferation, cell migration, and tumor metastasis.

93 further supporting the PI4KIIIalpha role in tumor metastasis.

94 n tissue fluid balance, graft rejection, and tumor metastasis.

95 olished increased neutrophil recruitment and tumor metastasis.

96 ganelles, is essential for platelet-mediated tumor metastasis.

97 ence that these two genes are suppressors of tumor metastasis.

98 al transition (EMT) occurs frequently during tumor metastasis.

99 upporting TNFalpha-activated MSCs to promote tumor metastasis.

100 ma tissues was significantly associated with tumor metastasis.

101 NX)-we showed that mtDNA could alter mammary tumor metastasis.

102 singly recognized for their contributions to tumor metastasis.

103 hat VEGFA induction of Sox2 promotes EMT and tumor metastasis.

104 ng processes and also strongly implicated in tumor metastasis.

105 ly decreased IL-6-meditated tumor growth and tumor metastasis.

106 scriptional activity of RelA and facilitates tumor metastasis.

107 that plays crucial roles in inflammation and tumor metastasis.

108 l resection of the tumors, by suppression of tumor metastasis.

109 ential drug target and prognostic marker for tumor metastasis.

110 at p90 ribosomal S6 kinase 2 (RSK2) promotes tumor metastasis.

111 ZNF367 promoted tumor metastasis accompanied with increase of CTC number

112 struction in cystic fibrosis, and facilitate tumor metastasis after dormancy.

113 CD73 also enhances tumor metastasis, although the nature of the immune subs

114 g the miR-23b/27b/24 cluster might influence tumor metastasis, although the precise nature of this re

115 As (miRNAs), but their roles in KSHV-induced tumor metastasis and angiogenesis remain largely unclear

116 To determine whether it has a role in breast tumor metastasis and angiogenesis, its levels were measu

117 ctivity that has been implicated strongly in tumor metastasis and angiogenesis.

118 Here, we report that transgenic GLK promotes tumor metastasis and cell migration through the scaffold

119 metalloenzymes with well-documented roles in tumor metastasis and fibrotic diseases.

120 These discoveries suggest novel paradigms in tumor metastasis and identify new opportunities for ther

121 ication potential in the early monitoring of tumor metastasis and in individualized treatment.

122 Reduced ASPP2 expression associates with tumor metastasis and increased p63 expression in human h

123 tasis, osteoclastogenesis, immune functions, tumor metastasis and infections such as osteonecrosis of

124 wound healing and plays an important role in tumor metastasis and inflammatory diseases.

125 hatic vasculature provides a major route for tumor metastasis and inhibiting neolymphangiogenesis ind

126 Developing tumor metastasis and invasion is the most important caus

127 LRIG1 is acting as a critical suppressor of tumor metastasis and is an early clinical indicator of r

128 Tumor metastasis and lack of NKG2D ligand (NKG2DL) expre

129 ect of the PPARgamma agonist pioglitazone on tumor metastasis and liver injury following IRI in a mou

130 vivo the requirement of "reversible EMT" in tumor metastasis and may resolve the controversy on the

131 Angiogenesis, a hallmark step in tumor metastasis and ocular neovascularization, is drive

132 Despite strong correlations with tumor metastasis and poor patient prognosis, there is ve

133 nd sarcomas, often associating with enhanced tumor metastasis and poor prognosis.

134 men, and increased collagen density promotes tumor metastasis and progression.

135 considered as a well-established marker for tumor metastasis and recurrence.

136 unctional blood vessels, which contribute to tumor metastasis and reduce the efficacy of therapeutic

137 e tetraspanin CD82 is a potent suppressor of tumor metastasis and regulates several processes includi

138 loid cell expression of EGFR associated with tumor metastasis and shorter patient survival time.

139 amples, lower levels of ATG5 associated with tumor metastasis and shorter survival time.

140 tor of ATF4-dependent anoikis resistance and tumor metastasis and suggest ATF4 and HO-1 as potential

141 between PI4KIIIalpha and CXCR4 in promoting tumor metastasis and suggests that PI4KIIIalpha pharmaco

142 show that beta1 integrin activation promotes tumor metastasis and that activated beta1 integrin may s

143 tumoral hypoxia caused an unexpected rise in tumor metastasis and the accumulation of cancer stem cel

144 Furthermore, SOX9 knockdown suppressed tumor metastasis and the expression of the stem cell mar

145 or formation, yet its function in regulating tumor metastasis and the underlying mechanisms remain co

146 f nonclassical, patrolling monocytes in lung tumor metastasis and their functional relationships with

147 inflammation and related diseases to prevent tumor metastasis and to increase tumor sensitivity to ch

148 ceptors, which play important roles in human tumor metastasis and tumor-induced angiogenesis.

149 os, (iv) inhibited tumor growth, (v) blocked tumor metastasis, and (vi) improved overall survival wit

150 n of biomarkers associated with persistence, tumor metastasis, and autoimmunity, such as soluble CD16

151 nduced immunosuppressive phenotypes, blocked tumor metastasis, and caused tumor regression in 60% of

152 may be responsible for treatment resistance, tumor metastasis, and disease recurrence.

153 nflammation, bacterial and viral infections, tumor metastasis, and genetic disorders.

154 ntrols cell cycle, apoptosis, autophagy, and tumor metastasis, and its expression is frequently down-

155 promotes cancer cell migration/invasion and tumor metastasis, and its expression is upregulated in m

156 role in blood-lymphatic vessel development, tumor metastasis, and prevention of inflammatory bleedin

157 associated with increased expression of MET, tumor metastasis, and shorter patient survival times.

158 nhibit cell proliferation, angiogenesis, and tumor metastasis, and the biological activity of the HK

159 ssociated with advanced tumor stage, greater tumor metastasis, and worse survival.

160 biological processes, such as morphogenesis, tumor metastasis, and wound healing.

161 ing the stages of cancer progression-primary tumor, metastasis, and at the metastatic site.

162 em to be involved in initiation, growth, and tumor metastasis, as well as in radio- and chemotherapy

163 ymal transition, a critical step that drives tumor metastasis, as well as proliferation of carcinoma

164 ECM in CRLM and help explain the finding of tumor metastasis-associated proteins and peptides in uri

165 TIAM1 is well known for its role in tumor metastasis, but it also possesses overlapping cell

166 EVs have been implicated in promoting tumor metastasis, but the molecular composition of tumor

167 ic growth factors and later shown to promote tumor metastasis, but their effects on carcinogenesis ar

168 ha-driven remodeling of lymph nodes promotes tumor metastasis by activating integrin alpha4beta1 on l

169 er, our results suggest that PELP1 regulates tumor metastasis by controlling the expression and funct

170 mmary, TGF-beta-induced TG2 enhances ovarian tumor metastasis by inducing EMT and a cancer stem cell

171 correlated with advanced cancer and promotes tumor metastasis by influencing tumor cell migration and

172 It is believed that fascin facilitates tumor metastasis by promoting the formation of invasive

173 ssociated platelets in the blood facilitates tumor metastasis by relaxing endothelial barrier functio

174 TNFalpha-activated MSCs strikingly enhanced tumor metastasis compared with normal MSCs.

175 In patients with distant tumor metastasis, deaths per 1000 person-years were 87.7

176 ZEB1 axis, defines a novel mechanism driving tumor metastasis, delineates collagen as a prognostic ma

177 cell lung cancer (NSCLC) and correlates with tumor metastasis, disease recurrence, and poor survival

178 ssue sarcomas were associated with grade III tumors, metastasis-free survival, and overall survival.

179 lation between the parabiosed mice, to study tumor metastasis from one parabiont to another, or to in

180 angiogenic regulator stimulates MCF-7 breast tumor metastasis from their orthotopic sites to distant

181 and its potential involvement in controlling tumor metastasis has been lacking.

182 including breast cancer, and its role(s) in tumor metastasis has been studied on a very limited basi

183 ll migration, extracellular matrix assembly, tumor metastasis, hemostasis, and thrombosis.

184 herapy currently in phase II trials, reduced tumor metastasis in a murine model of prostate cancer.

185 argets to predict and inhibit, respectively, tumor metastasis in carcinoma patients.

186 major mediator of cancer cell migration and tumor metastasis in cell culture and in intact mice.

187 ignant cell proliferation, angiogenesis, and tumor metastasis in many cancers.

188 his study identifies a negative regulator of tumor metastasis in MDSCs, NGP, which is down-regulated

189 Tumor metastasis in mice was monitored for 30 d by biolu

190 of the epithelial isoform of Exo70 inhibits tumor metastasis in mice.

191 ared with control cells, but miR-28 promoted tumor metastasis in mice.

192 Targeting GDH1 with R162 attenuated tumor metastasis in patient-derived xenograft model and

193 ory mesenchymal state has been implicated in tumor metastasis in preclinical models.

194 from RUNX3 mutation is associated with more tumor metastasis in the lung.

195 nce that extracellular AGR2 (eAGR2) promotes tumor metastasis in various in vivo models.

196 ed evidence that IL-37 inhibited effectively tumor metastasis in vitro and in vivo.

197 show that vimentin has an important role in tumor metastasis in vivo in the setting of pre-diabetes

198 cts as a potent tumor suppressor, inhibiting tumor metastasis in vivo when systemically delivered.

199 attenuated cancer cell invasion in vitro and tumor metastasis in vivo, whereas expression of Fascin-1

200 we further show that FoxA1 inhibits prostate tumor metastasis in vivo.

201 cer cell migration and invasion in vitro and tumor metastasis in vivo.

202 pithelial-mesenchymal transition, and abated tumor metastasis in vivo.

203 function in vitro and hamper CXCR4-dependent tumor metastasis in vivo.

204 ghlight the critical role of nuclear MIIP in tumor metastasis.In colorectal cancer, EGFR signalling i

205 of genes critical for cell proliferation and tumor metastasis, including Cdc25b, Cyclin B1, Plk-1, Lo

206 identified upregulation of genes involved in tumor metastasis, including the G protein-coupled recept

207 2A(-/-) mice were strongly protected against tumor metastasis, indicating that host A2A receptors enh

208 More than 90% of cancer patients died from tumor metastasis, instead of primary tumor growth.

209 al analysis of several genes associated with tumor metastasis, invasion, and the epithelial-mesenchym

210 Organogenesis and tumor metastasis involve the transformation of epithelia

211 Solid tumor metastasis is a complex biology, impinged upon by

212 Tumor metastasis is a hallmark of cancer.

213 Tumor metastasis is a highly complex, dynamic, and ineff

214 l role of hypoxia-induced Notch signaling in tumor metastasis is as yet poorly understood.

215 driving stromal activation and their role in tumor metastasis is critical to furthering research with

216 Understanding mechanisms mediating tumor metastasis is crucial for diagnostic and therapeut

217 te a novel molecular mechanism through which tumor metastasis is endowed by the hnRNPM-mediated splic

218 Tumor metastasis is mainly caused by somatic genomic alt

219 Epithelial tumor metastasis is preceded by an accumulation of colla

220 Tumor metastasis is the leading cause of death among bre

221 Tumor metastasis is the major cause of death among cance

222 Tumor metastasis is the primary cause of death due to ca

223 g receptors is involved in the prevention of tumor metastasis is unknown.

224 ular program associated with development and tumor metastasis, is fueled by upregulation of ribosome

225 in addition to being an initiating event for tumor metastasis, is implicated in conferring several cl

226 ion and signaling, immune cell function, and tumor metastasis, it is of interest to determine how the

227 hological lymphangiogenesis, particularly in tumor metastasis, making it an attractive therapeutic ta

228 Here, by using an experimental tumor metastasis model and in vitro studies, we further

229 ely detected small disseminated lesions in a tumor metastasis model, complementing the current clinic

230 tations activate enhancers using a xenograft tumor metastasis model, where mutations are induced natu

231 issemination in a syngeneic mouse 4T1 breast tumor metastasis model.

232 response was observed in both bilateral and tumor metastasis models.

233 emain suboptimal, suggesting that AKT-driven tumor metastasis needs to be further understood.

234 ssays revealed that WISP1 knockout represses tumor metastasis of B16F10 and YUMM1.7 melanoma cells in

235 OPN is associated with tumor metastasis of several tumors and is overexpressed

236 dundant functions that cooperatively promote tumor metastasis or limit EGFR-inhibitor response.

237 ke gene signature and were unable to control tumor metastasis or viral infection.

238 rapeutic transplants, migrating cells during tumor metastasis, or cell populations induced by an immu

239 maging treatments and instead with different tumor metastasis potential.

240 Thus, our studies suggest a paradigm of tumor metastasis: primary epithelial carcinoma cells tha

241 Tumor metastasis refers to spread of a tumor from site o

242 methylation affects immune surveillance and tumor metastasis remains ambiguous.

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

244 The role of neutrophils in solid tumor metastasis remains largely controversial.

245 Tumor metastasis remains the major cause of cancer-relat

246 However, the role of this lipid kinase in tumor metastasis remains unclear.

247 ymph node microenvironment actively promotes tumor metastasis remains unknown.

248 eceptors RPTPbeta/zeta and Syndecan-3 during tumor metastasis remains unknown.

249 It has been implicated in tumor metastasis, renal tubular acidosis, and osteoporos

250 eseeding), and (iii) reseeding of metastatic tumors (metastasis reseeding).

251 the PyMT mouse model, which enhances mammary tumor metastasis, results in selective inhibition of Akt

252 In 2 independent murine models of breast tumor metastasis, stable shRNA-based SRPK1 knockdown sup

253 ogical process that plays important roles in tumor metastasis, "stemness," and drug resistance.

254 the GLK-IQGAP cascade in cell migration and tumor metastasis, suggesting it as a potential biomarker

255 ethylation and transcriptional repression of tumor metastasis suppressor gene BRMS1, highlights a new

256 cer G-protein-coupled-receptor-1 (OGR1) is a tumor metastasis suppressor in prostate cancer (PCa).

257 me, in any system, that SPDEF functions as a tumor metastasis suppressor in vivo.

258 l migration and invasion in vitro and acts a tumor metastasis suppressor in vivo.

259 also upregulated the expression of KISS1, a tumor metastasis suppressor, and attenuated metastasis i

260 To determine how tetraspanin KAI1/CD82, a tumor metastasis suppressor, inhibits cell migration, we

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

262 Elucidating targets of physiological tumor metastasis suppressors can highlight key signaling

263 trolling the expression and functions of the tumor metastasis suppressors miR-200a and miR-141.

264 ta expression, and a reduction of postpartum tumor metastasis that was similar to the metastasis freq

265 al antibodies that inhibit cell invasion and tumor metastasis, the hallmark of heparanase activity.

266 at loss of E-cadherin is a central tenant in tumor metastasis, the results of our studies, by providi

267 cell migration, cytoskeletal remodeling and tumor metastasis, the tumor-derived mutants (L(71)P, L(9

268 ily controversial role of SH3BGRL in driving tumor metastasis through c-Src activation, and suggests

269 atency and size, but significantly decreased tumor metastasis through inhibition of tumor cell intrav

270 Our results thus revealed that CD73 promotes tumor metastasis through multiple mechanisms, including

271 of the MYC oncogene, which in turn regulates tumor metastasis through specific effects on cancer cell

272 t NGF blockade immediately upon detection of tumor metastasis to bone may help preserve the integrity

273 the recruitment of molecules that facilitate tumor metastasis to integrin-based adhesions.

274 otential therapeutic strategy for mitigating tumor metastasis to LNs.

275 the microvasculature of the lung and reduce tumor metastasis to lung in multiple mouse metastatic tu

276 MM is the most common solid tumor metastasis to the breast.

277 Tumor metastasis to the draining lymph nodes is critical

278 excised avian embryonic organs revealed that tumor metastasis to the liver was significantly reduced

279 in liver architecture significantly enhance tumor metastasis to the liver.

280 ll proliferation and migration in vitro, and tumor metastasis to the lung in vivo.

281 tatic potential in a setting of experimental tumor metastasis to the lung.

282 e (247 mg/m(3) TSP), P=0.02) and significant tumor metastasis to various distant organs in the CS-exp

283 ion, on generation of a primary subcutaneous tumor, metastasis to regional lymph nodes was clearly re

284 For many tumors, metastasis to the LNs is predictive of poor prog

285 significant roles in disease progression and tumor metastasis toward secondary sites.

286 nstrate that TNFalpha-activated MSCs promote tumor metastasis via CXCR2(+) neutrophil recruitment.

287 ytes play a critical role in preventing lung tumor metastasis via NK cell recruitment and activation.

288 ant function of IL-33 and ILC2s in promoting tumor metastasis via their capacity to suppress innate t

289 f GAS5-AS1 in NSCLC and subsequently promote tumor metastasis via upregulation of several key EMT mar

290 Unexpectedly, tumor metastasis was observed in 77% of the subjects tre

291 ntribution of N-cadherin and HER2 in mammary tumor metastasis, we targeted N-cadherin expression in t

292 chanism through which pleiotrophin regulates tumor metastasis, we used two different prostate carcino

293 ression is of utmost importance for blocking tumor metastasis; we have identified that semaphorin 7a

294 omoting epithelial to mesenchymal transition/tumor metastasis were activated.

295 These effects on tumor metastasis were not a result of the effect of SPDE

296 We focus in particular on tumor metastasis, which is the greatest impediment to cl

297 essed the growth of CCA tumor xenografts and tumor metastasis while displaying low toxicity levels.

298 rapies targeting hematologic cancer or solid tumors metastasis with bone tropism.

299 5) can lead to heterotypic cell adhesion and tumor metastasis within the pleural and peritoneal cavit

300 Lymph nodes are initial sites of tumor metastasis, yet whether the lymph node microenviro