ライフサイエンスコーパス: tumor invasion

1 lications for development, inflammation, and tumor invasion.

2 ite and elicited leukocytic infiltration and tumor invasion.

3 mily genes are significantly associated with tumor invasion.

4 al oncogenic signaling pathways that promote tumor invasion.

5 This leads, in turn, to decreased tumor invasion.

6 a, creating a microenvironment permissive to tumor invasion.

7 role of the tumor microenvironment in brain tumor invasion.

8 itically involved in HIF1alpha signaling and tumor invasion.

9 in HNSCC where they suppress invadopodia and tumor invasion.

10 igenesis, cancer cell survival and regulates tumor invasion.

11 and actin dynamics are modulated for EMT and tumor invasion.

12 EB1 sufficient for repression of miR-200 and tumor invasion.

13 plex and stimulates actin polymerization for tumor invasion.

14 lls rescued the aggressive 3D phenotypes and tumor invasion.

15 ous diseases such as cardiac hypertrophy and tumor invasion.

16 adherin on non-tumorigenic cells and promote tumor invasion.

17 y correlated with histological parameters of tumor invasion.

18 mined the role of HNK-1 glycan in astrocytic tumor invasion.

19 Cartilage is resistant to tumor invasion.

20 yrosination occurs at the earliest stages of tumor invasion.

21 talloproteinases, which are known to promote tumor invasion.

22 utic target for prevention of EMT-associated tumor invasion.

23 mitotic somal translocation and glioblastoma tumor invasion.

24 itical for the initiation and progression of tumor invasion.

25 the epithelial phenotype and a suppressor of tumor invasion.

26 ding stromal collagen at the leading edge of tumor invasion.

27 volume and surface area but had no effect on tumor invasion.

28 olecular explanation of how Pdcd4 suppresses tumor invasion.

29 ing proteinases, that play critical roles in tumor invasion.

30 l-appreciated role in matrix degradation and tumor invasion.

31 low avidity for tumor Ag were inefficient in tumor invasion.

32 somes to efficiently deposit ECM and promote tumor invasion.

33 signal-induced activation of PIKE-A/Akt and tumor invasion.

34 BM remodeling occurs during development and tumor invasion.

35 ion of BM is essential for developmental and tumor invasion.

36 that inhibits neoplastic transformation and tumor invasion.

37 ance of biophysical parameters in regulating tumor invasion.

38 ronan/CD44s signaling in underpinning breast tumor invasion.

39 by both TIMP and RECK are required to block tumor invasion.

40 lular structures that are thought to mediate tumor invasion.

41 nce of any one of these three genes impaired tumor invasion.

42 ses may have on ICP levels and the extent of tumor invasion.

43 ugh disruption of cell growth, survival, and tumor invasion.

44 on of adherent cells during wound repair and tumor invasion.

45 s junctions contributes to cell motility and tumor invasion.

46 edded in collagen that provide a lattice for tumor invasion.

47 rate specificity in collagen proteolysis and tumor invasion.

48 lly explaining their differential effects on tumor invasion.

49 tions with the extracellular matrix regulate tumor invasion.

50 cytoskeleton remodeling, cell adhesion, and tumor invasion.

51 unclear how collagen organization influences tumor invasion.

52 of hypoxic stimulation that is important for tumor invasion.

53 ialylation likely plays a role in colorectal tumor invasion.

54 lating mechanism of Wingless (Wg) pathway in tumor invasion.

55 n by promoting angiogenesis, metastasis, and tumor invasion.

56 activity and matrix degradation facilitates tumor invasion.

57 n of ESRPs can suppress AR-antagonist-driven tumor invasion.

58 een Arm and Ras(V12) is sufficient to induce tumor invasion.

59 synergy with androgen receptor in mediating tumor invasion.

60 corresponded with the onset of seizures and tumor invasion.

61 ion of ribosomal protein S6 kinase A1 drives tumor invasion.

62 ceptor, which can promote cell migration and tumor invasion.

63 ne kinase promotes invadopodia formation for tumor invasion.

64 g, tumor dissemination, cell co-culture, and tumor invasion.

65 ing embryonic development, wound repair, and tumor invasion.

66 ession as new hallmarks of CAFs that promote tumor invasion.

67 rity induces JNK-mediated cell migration and tumor invasion.

68 nderstanding development, wound healing, and tumor invasion.

69 ed MMP2, a secreted proteinase key for brain tumor invasion.

70 the degradation of extracellular matrix and tumor invasion.

71 umor microenvironment and is correlated with tumor invasion.

72 or of matrix metalloproteinase 2 (TIMP2) and tumor invasion.

73 ective treatment of choroid and ocular nerve tumor invasion (1 of 20 animals with invasive disease in

74 but increased significantly with submucosal tumor invasion (22%)[P = 0.0003].

75 5) versus a less invasive (worst pattern of tumor invasion 3) pattern of invasion, we identified a t

76 umors with a more invasive (worst pattern of tumor invasion 5) versus a less invasive (worst pattern

77 ed accelerated tumor development, aggressive tumor invasion and a decreased survival rate in Ctnnb1(L

78 t, constitutively active ALK5-T204D enhances tumor invasion and angiogenesis by stimulating expressio

79 mediators of our defense system, to promote tumor invasion and angiogenesis remain incompletely unde

80 post-EMT cells were supportive in promoting tumor invasion and angiogenesis.

81 at3 in tumor cells has been shown to promote tumor invasion and angiogenesis.

82 ion of beta-catenin plays a critical role in tumor invasion and development.

83 lly, Prkd1 knockdown in vivo blocked primary tumor invasion and distant metastasis in a mouse model o

84 asive molecules that ultimately induce local tumor invasion and distant metastasis in PanNETs.

85 Expression of kinase-inactive ALK5 reduces tumor invasion and formation of new blood vessels within

86 ar adhesion, with potential implications for tumor invasion and keratinopathies, settings in which di

87 ntiated phenotype and showed increased local tumor invasion and lymph node metastasis.

88 reased PTEN transcription, likely germane in tumor invasion and metastases but not initiation.

89 ged with various stresses and contributes to tumor invasion and metastases, whereas its deregulation

90 lial-Mesenchymal Transition (EMT) to promote tumor invasion and metastasis and can also inhibit apopt

91 It is widely believed to play a role in tumor invasion and metastasis and therefore to represent

92 Tumor invasion and metastasis are strongly regulated by

93 Tumor invasion and metastasis are the main causes of dea

94 nd angiogenic growth factors and facilitates tumor invasion and metastasis by degrading the ECM.

95 TGF-beta promotes tumor invasion and metastasis by inducing an epithelial-

96 rming growth factor-beta (TGF-beta) promotes tumor invasion and metastasis by inducing epithelial-mes

97 ncer cells into adipocytes repressed primary tumor invasion and metastasis formation in mouse models

98 d survival, the roles of the PI3K pathway in tumor invasion and metastasis have not been well delinea

99 re associated with an increased frequency of tumor invasion and metastasis in certain cancers.

100 ntestinal epithelial cells markedly enhances tumor invasion and metastasis in Trp53DeltaIEC mice (Trp

101 between angiopoietin 2 (Ang2) expression and tumor invasion and metastasis in various human cancers,

102 l inhibition of this pathway prevents breast tumor invasion and metastasis in vivo.

103 Whether and how FBXW2 regulates tumor invasion and metastasis is previously unknown.

104 otein, confers metabolic plasticity to drive tumor invasion and metastasis of non-small cell lung can

105 he standard form of CD44 in promoting breast tumor invasion and metastasis to the liver.

106 inding proteins that is directly involved in tumor invasion and metastasis via interactions with spec

107 Cholinergic-induced tumor invasion and metastasis were inhibited by pharmaco

108 pendent vessel normalization by CQ restrains tumor invasion and metastasis while improving chemothera

109 icroenvironment by stromal caveolin-1 favors tumor invasion and metastasis' (Goetz et al., 2011).

110 icroenvironment by stromal caveolin-1 favors tumor invasion and metastasis' by Goetz and colleagues,

111 Known to be vital for tumor invasion and metastasis, accumulating evidence als

112 trix by proteolytic enzymes is a hallmark of tumor invasion and metastasis, and aspartyl proteinase c

113 ased activity of SRC family kinases promotes tumor invasion and metastasis, and overexpression of the

114 se transcriptase (hTERT) plays a key role in tumor invasion and metastasis, but the mechanism of its

115 an cancers and significantly correlated with tumor invasion and metastasis, but the mechanisms involv

116 MUC1 plays crucial roles in tumor invasion and metastasis, especially in opposing ce

117 t of beta-catenin and a key regulator during tumor invasion and metastasis, was also decreased.

118 l transition (EMT) is an important driver of tumor invasion and metastasis, which causes many cancer

119 mplantation of mammary fibroblasts inhibited tumor invasion and metastasis, which was reversed by Tia

120 the EMT transcription factor ZEB1 to trigger tumor invasion and metastasis.

121 ng the roles of both TGF-beta and seprase in tumor invasion and metastasis.

122 opodia that have been uniquely implicated in tumor invasion and metastasis.

123 roteinase-2 (MMP-2) is a protease related to tumor invasion and metastasis.

124 binding inhibitory protein), towards driving tumor invasion and metastasis.

125 n of miR-200, which is thought to facilitate tumor invasion and metastasis.

126 the potential to disrupt the role of FAP in tumor invasion and metastasis.

127 f EMT in cervical cancer and associated with tumor invasion and metastasis.

128 n about the underlying mechanisms that drive tumor invasion and metastasis.

129 -9, which have been previously implicated in tumor invasion and metastasis.

130 atocyte growth factor c-Met, which can drive tumor invasion and metastasis.

131 clear factor kappaB signaling that represses tumor invasion and metastasis.

132 MDSCs infiltrate into tumors and promote tumor invasion and metastasis.

133 ily kinase (SFK) activity is associated with tumor invasion and metastasis.

134 ion through genes (i.e., TSP-1) important in tumor invasion and metastasis.

135 en postulated as an absolute requirement for tumor invasion and metastasis.

136 ht into the mechanism by which Ubc9 promotes tumor invasion and metastasis.

137 n, specifically their functions in mediating tumor invasion and metastasis.

138 induces functions that are also required for tumor invasion and metastasis.

139 Matrix degradation is a pivotal step in tumor invasion and metastasis.

140 lar hyperacetylated hsp90alpha may undermine tumor invasion and metastasis.

141 atrix metalloproteinase (MMP)-2, involved in tumor invasion and metastasis.

142 cell lines may be relevant to mechanisms of tumor invasion and metastasis.

143 erine proteases, which play crucial roles in tumor invasion and metastasis.

144 the mechanisms by which telomerase promotes tumor invasion and metastasis.

145 ErbB2 (HER2, Neu) and Ras play key roles in tumor invasion and metastasis.

146 KLF6 and KLF6-SV1 can directly alter ovarian tumor invasion and metastasis.

147 e deregulated in many solid tumors and drive tumor invasion and metastasis.

148 skeletal development but also implicated in tumor invasion and metastasis.

149 o, ATDC is required for TP63-induced bladder tumor invasion and metastasis.

150 s highly correlated with cell proliferation, tumor invasion and metastasis.

151 ocalization on the cell surface is linked to tumor invasion and metastasis.

152 -RAS activates TGF-beta signaling to promote tumor invasion and metastasis.

153 r matrix (ECM), which serves as a barrier to tumor invasion and metastasis.

154 romising therapeutic strategy for preventing tumor invasion and metastasis.

155 ial for primary tumor growth and facilitates tumor invasion and metastasis.

156 telomere length, which significantly reduced tumor invasion and metastatic potential.

157 expression on tumor cells has been linked to tumor invasion and metastatic spread, the contribution o

158 In the current work, tumor invasion and peritumoral pH were monitored over ti

159 ogen-independent impact of adipose tissue on tumor invasion and progression needs to be elucidated.

160 ithin the epithelial microenvironment impact tumor invasion and progression.

161 the tumor microenvironment is important for tumor invasion and progression.

162 activation of MAPK signaling, which promotes tumor invasion and progression.

163 at RNAi-mediated silencing of NEMO increased tumor invasion and progression.

164 s as a 3D physicotactic agent during sarcoma tumor invasion and propose the O2-controllable hydrogels

165 r and ErbB2 strongly implicated in mediating tumor invasion and spreading.

166 mine the role of endogenous c-Jun in mammary tumor invasion and stem cell function.

167 n lung squamous cell carcinoma and increases tumor invasion and survival through activation of focal

168 s, but absent in normal brain, that promotes tumor invasion and survival.

169 ure that invasive TAMs link angiogenesis and tumor invasion and that Wnt-signaling plays a role in me

170 obtain an accurate diagnosis and assess for tumor invasion and the extent of the disease.

171 that polysialic acid facilitates astrocytic tumor invasion and thereby tumor progression.

172 l periostin as an important mediator of ESCC tumor invasion and they indicate that organotypic (three

173 lass of matrix-degrading enzymes involved in tumor invasion and tissue remodeling, have yet to be lin

174 04D cells by RNA interference (RNAi) reduces tumor invasion and tumor growth.

175 elial cells and cooperate with Met to induce tumor invasion and vascularization.

176 se) proteins RhoA and RhoC are essential for tumor invasion and/or metastasis in breast carcinomas.

177 nase-9 (MMP-9) is associated with human lung tumor invasion and/or metastasis.

178 nd metastasis by stimulating cell migration, tumor invasion, and angiogenesis.

179 xenografts prevents in vivo SG formation and tumor invasion, and completely blocks lung metastasis in

180 gnaling suppressed lgl(-/-)/Ras(V12)-induced tumor invasion, and cooperation between Arm and Ras(V12)

181 aggressive human cancers, with rapid growth, tumor invasion, and development of distant metastases.

182 he astrogliotic capsule can directly inhibit tumor invasion, and its absence from GBM presents an env

183 chemotactic loop drives collagen remodeling, tumor invasion, and metastasis and could be an important

184 ith downregulation of genes involved in EMT, tumor invasion, and metastasis.

185 positive role of Wnt/beta-catenin pathway in tumor invasion, and provide a conserved mechanism that c

186 promoting cell growth, differentiation, and tumor invasion, and represent attractive targets for ant

187 hat N-cadherin expression is associated with tumor invasion, and that some cancer cells respond to sp

188 cy by increasing angiogenesis, tumor growth, tumor invasion, and tumor metastasis.

189 Tetraspanin CD82 suppresses cell migration, tumor invasion, and tumor metastasis.

190 olved in tumor cell survival, proliferation, tumor invasion, and/or immunosuppression.

191 ly inhibited tumor invasiveness in vitro and tumor invasion, angiogenesis, and metastasis in vivo.

192 tro, suggesting that the effects of SPDEF on tumor invasion are mediated, in part, through the suppre

193 dulating cell force balance and subsequently tumor invasion are understudied.

194 7 has previously been shown to inhibit local tumor invasion as well as lymph node and pulmonary metas

195 here an EMT-independent action of Snail1 on tumor invasion, as it is required for the activation of

196 on is important for therapeutic targeting of tumor invasion, as key regulatory pathways for intrinsic

197 Our microfluidic model advances current tumor invasion assays towards a more physiologically rea

198 POE protein plays a significant role in OSCC tumor invasion because of its effects on cellular choles

199 ction inhibitors does not appreciably reduce tumor invasion, because these pathways are redundant; bl

200 chondrial dysfunction, stress signaling, and tumor invasion by a mechanism similar to that described

201 tory signaling cascades in gliomas, blocking tumor invasion by directly targeting myosin II remains e

202 Stimulation of glutamine-driven epithelial tumor invasion by fibroblasts required previous CAF acti

203 is a potential tumor suppressor and inhibits tumor invasion by inducing suppressive cell microenviron

204 mechanism by which 14-3-3sigma guides breast tumor invasion by integrating cytoskeletal dynamics: it

205 Finally, TAMs can directly facilitate tumor invasion by recruiting tumor cells nearby vessels

206 TbetaRIII appeared to inhibit tumor invasion by undergoing ectodomain shedding and pro

207 rain but upregulated in gliomas and promotes tumor invasion by unknown mechanisms.

208 Our results also suggest that inhibiting tumor invasion can enhance tumor proliferation and that

209 and heterogeneous and the regions of highest tumor invasion corresponded to areas of lowest pH.

210 Tumor invasion did not occur into regions with normal or

211 novel model where the EMT that occurs during tumor invasion downregulates tubulin tyrosine ligase, in

212 ar staining of pSTAT3-Y705 identified at the tumor invasion front in ductal breast carcinomas correla

213 The analysis of invading leader cells at the tumor invasion front is of significant interest as these

214 nal tumoroid culture which recapitulated the tumor invasion front, allowing for both quantification o

215 /ECM compositions, with a clearly demarcated tumor invasion front, thus allowing us to quantitatively

216 The acid-mediated tumor invasion hypothesis proposes altered glucose metab

217 Current models of this acid-mediated tumor invasion hypothesis, however, do not account for i

218 ER-negative breast cancer cells in vitro and tumor invasion in a co-transplant xenograft mouse model.

219 STAT3 was recently reported to suppress tumor invasion in Apc(min)(/+) mice.

220 mental tissue invasion for disc eversion and tumor invasion in Drosophila and modulate BM integrity w

221 modification of the extracellular matrix and tumor invasion in HGSOC.

222 results in significant inhibition of glioma tumor invasion in Matrigel and spheroid invasion assay m

223 hance AXL-dependent downstream signaling and tumor invasion in PDAC.

224 ient PMo into Nr4a1-deficient mice prevented tumor invasion in the lung.

225 n-regulation of LRP and inhibited astrocytic tumor invasion in vitro.

226 cantly decreased melanoma xenograft size and tumor invasion in vivo.

227 nd a candidate therapeutic target to inhibit tumor invasion in vivo.

228 egradation completely blocks both tissue and tumor invasion, indicating that modulation of BM is esse

229 diated activation of c-Src was important for tumor invasion induced by oncogenic Ras.

230 are not always surgically achievable due to tumor invasion into adjacent tissues or involvement of c

231 Tumor invasion into surrounding stromal tissue is a hall

232 Increased tumor invasion into the smooth muscle layer and aberrant

233 hat obesity promotes EMT in cancer cells and tumor invasion into the surrounding fat tissue.

234 points during metastasis, including primary tumor invasion, intravasation, and extravasation.

235 Tumor invasion is a critical step in the spread of cance

236 apability of human or murine CAFs to promote tumor invasion is dependent on Snail1 expression.

237 The effect of PEA-15 on tumor invasion is mediated by its interaction with ERK1/

238 of cell surface carbohydrates in astrocytic tumor invasion is not known.

239 sults demonstrate that the role of Snail1 in tumor invasion is not limited to EMT, but it is also dep

240 Collectively, our results demonstrate that tumor invasion is subject to polymorphic genetic control

241 while targeting just myosin IIA also impairs tumor invasion, it surprisingly increases tumor prolifer

242 Brain tumor invasion leads to recurrence and resistance to tre

243 dian survival included presence and depth of tumor invasion, margin-positive resection, and expressio

244 cule and is essential for active AKT-induced tumor invasion, metastasis and anoikis resistance in lun

245 que opportunity to study the early events of tumor invasion, metastasis and drug responses.

246 expression of KLF8 and MMP9 with the patient tumor invasion, metastasis and poor survival.

247 Articles on tumor invasion, metastasis, and angiogenesis in normal a

248 trix metalloproteinases in the regulation of tumor invasion, metastasis, and angiogenesis was recogni

249 nase-2 (COX-2) expression is associated with tumor invasion, metastasis, and poor prognosis in non-sm

250 andin E2 (PGE2)- and Akt/GSK-3beta-dependent tumor invasion/metastasis.

251 The acid-mediated tumor invasion model provides a simple mechanism linking

252 0.59, 0.80; P = .0004) for massive choroidal tumor invasion (n = 219).

253 motes tumor progression through induction of tumor invasion, neoangiogenesis, and immunosuppression.

254 Integrin beta3 is critical for tumor invasion, neoangiogenesis, and inflammation, makin

255 e 3-4 vs. grade 1; HR, 2.42; P < 0.001), and tumor invasion of adjacent structures (HR, 1.37; P < 0.0

256 Perineural tumor invasion of intrapancreatic nerves, neurogenic inf

257 gnificantly larger xenografts with increased tumor invasion of surrounding tissue in vivo.

258 ale sex, tumor site on the scalp or neck, or tumor invasion of the entire papillary dermis each indep

259 ry papillomatosis had progressive, bilateral tumor invasion of the lung parenchyma.

260 Tumor invasion of the otic capsule was associated with l

261 carcinoma, may reflect tumor proximity to or tumor invasion of the pterygoid process.

262 In order to model tumor invasion of the stroma, we find it necessary to do

263 o-vasculature TKIs are delivered to decrease tumor invasion; on the other hand, the neo-vasculature c

264 idation set, RRM2B was negatively related to tumor invasion (OR = 0.45, 95% CI = 0.19-0.99, P = 0.040

265 most common etiology of cancer pain is local tumor invasion (primary or metastatic), involving inflam

266 brain metastases is not a surrogate of local tumor invasion, primary cancer type, or aggressive pheno

267 ession, are shared by both disc eversion and tumor invasion processes.

268 ression of an alternative splicing-dependent tumor invasion program.

269 s correlated with elevated mTORC1 signaling, tumor invasion, progression, and poor prognosis.

270 ACTH secretion, cellular proliferation, and tumor invasion rates in vitro.

271 mbryonal development, tissue homeostasis and tumor invasion relies on invadosomes, a collective term

272 sms underlying interleukin-7 (IL-7)-mediated tumor invasion remain unclear.

273 but the role of this receptor in astrocytic tumor invasion remains poorly understood.

274 he precise role and mechanism of Notch-1 for tumor invasion remains unclear.

275 er cell-intrinsic functions of CtsZ, whereas tumor invasion required contributions from both macropha

276 Tumor invasion requires efficient cell migration, which

277 neoplasia in murine prostate and stimulated tumor invasion, similarly to ERG.

278 n is associated with increased angiogenesis, tumor invasion, suppression of host immunity and promote

279 Programmed cell death 4 (Pdcd4), a tumor invasion suppressor, is frequently downregulated i

280 rcellular adhesion and repulsion and acts as tumor/invasion suppressor in colorectal cancer.

281 , these data implicate Rap1GAP as a putative tumor/invasion suppressor in the thyroid.

282 racrine invasion loop, resulting in enhanced tumor invasion that is independent of macrophage signali

283 er of studies have implicated CD44 in breast tumor invasion, the evidence is still circumstantial.

284 y a novel mechanism by which IFs can promote tumor invasion through an influence on cell-cell adhesio

285 most patients with T3 or T4 disease without tumor invasion through cartilage into soft tissues, a la

286 s found to have a critical role in promoting tumor invasion, through both macrophage and cancer cell

287 rrelates lymph node metastases with depth of tumor invasion, tumor size, presence of lymphovascular i

288 this study, we will investigate multispecies tumor invasion, tumor-induced angiogenesis, and focus on

289 ma driver whose levels can be tuned to favor tumor invasion, ultimately defining metastatic risk.

290 Tumor invasion was limited to the mucosa (T1a) in 75 pat

291 heterogeneity that may illuminate drivers of tumor invasion, we created a glioblastoma tumor cell atl

292 To analyze tumor invasion, we used O2-controllable hydrogels to rec

293 pecificity, and accuracy of MRI in detecting tumor invasion were determined.

294 Upfront resection and microvascular tumor invasion were poor prognostic factors for both OS

295 3 cm or more on histology, and microvascular tumor invasion were poor prognostic factors for OS and R

296 ist and the presence of LNM and the depth of tumor invasion were recorded.

297 s effective in cell-based in vitro models of tumor invasion, where it significantly abrogated invasio

298 -type PDGFRA decreases latency and increases tumor invasion, while ATRX knockdown is associated with

299 Tumor invasion within the interstitial space is critical

300 ment, during wound healing, and in cancerous tumor invasion, yet most detailed knowledge of cell migr