ライフサイエンスコーパス: tumor vessel

1 93.6% (nodules), 93.2% (masses), and 78.1% (tumor vessels).

2 ually increased when expressed per surviving tumor vessel.

3 proach restored blood flow in non-functional tumor vessels.

4 eased RCA I binding and internalization into tumor vessels.

5 e necessary to suppress VEGFR3 expression on tumor vessels.

6 isplatin-loaded nanoparticles (F3-Cis-Np) to tumor vessels.

7 fibrin-associated clotted plasma proteins in tumor vessels.

8 morphologic and functional abnormalities of tumor vessels.

9 followed by increased activated caspase-3 in tumor vessels.

10 lular effects of VEGF and PDGF inhibitors on tumor vessels.

11 f platelet adhesion receptors in stabilizing tumor vessels.

12 nable target for specific destabilization of tumor vessels.

13 ls and decreased numbers of medium and large tumor vessels.

14 r bed while improving perfusion in surviving tumor vessels.

15 r the surface area per unit tissue volume of tumor vessels.

16 sement membrane left behind after pruning of tumor vessels.

17 s a tool to differentiate between normal and tumor vessels.

18 uited GFP-positive cells that organized into tumor vessels.

19 ics can gain access to tumor cells via leaky tumor vessels.

20 on of the integrin on the luminal surface of tumor vessels.

21 ibody-dependent cellular cytotoxicity toward tumor vessels.

22 eting and potentially eliminating neoplastic tumor vessels.

23 hat S1P(1) expression is strongly induced in tumor vessels.

24 the cellular effects of these inhibitors on tumor vessels.

25 angiogenesis or cause regression of existing tumor vessels.

26 unoreactivities were similarly ubiquitous on tumor vessels.

27 suggesting that these agents target immature tumor vessels.

28 ely to sites of active angiogenesis, notably tumor vessels.

29 mor vessels, and therapeutic manipulation of tumor vessels.

30 42 degrees C led to hemorrhage and stasis in tumor vessels.

31 ot increase leukocyte rolling or adhesion in tumor vessels.

32 in-1, may modulate adhesion of leukocytes to tumor vessels.

33 inflammation, could explain the leakiness of tumor vessels.

34 e metastasis ischemia by the embolization of tumor vessels.

35 ilar to the fenestrated endothelium found in tumor vessels.

36 X-irradiation occurs selectively within the tumor vessels.

37 ammatory/angiostatic milieu coexisted around tumor vessels.

38 e show that S1PR1 is expressed and active in tumor vessels.

39 s and formed a continuous sheet wrapping the tumor vessels.

40 of the three-dimensional micromorphology of tumor vessels.

41 lecule endocan (ESM1) was highly elevated on tumor vessels.

42 as well as the diameter and permeability of tumor vessels.

43 ressure does not cause vessel compression of tumor vessels.

44 eins are upregulated on endothelial cells of tumor vessels.

45 or EC JAM-C in the development of functional tumor vessels.

46 significantly increases the number of human tumor vessels.

47 enetic modifications in endothelial cells of tumor vessels.

48 ill need to be identified on these resistant tumor vessels.

49 more homogeneous distribution of functional tumor vessels.

50 rasound imaging showed reduced blood flow in tumor vessels.

51 Tumor vessels abundantly express receptors for vascular

52 as endothelial cells, and those on surviving tumor vessels acquired a more normal phenotype.

53 The permeability of the tumor vessels affects the blood clearance of the cytokin

54 The reduction in integrin expression on tumor vessels after antiangiogenic therapy raises the po

55 antibody transport increases from surviving tumor vessels after normalization by inhibition of VEGF

56 The heterogeneous vascular permeability in tumor vessels, along with several other factors, creates

57 not of Ang1, was up-regulated in angiogenic tumor vessels already in early stages of skin carcinogen

58 ility of macromolecules to extravasate leaky tumor vessels and accumulate in the tumor tissue.

59 d (NR) "activators" that populate the porous tumor vessels and act as photothermal antennas to specif

60 ar permeability is a landmark feature of the tumor vessels and an important driver of the EPR.

61 ration of cell-cell junction proteins in the tumor vessels and astrocyte-endothelium interactions in

62 sion construct localized selectively to PC-3 tumor vessels and caused thrombotic damage to tumor vess

63 ed with the uniform CD31 immunoreactivity of tumor vessels and contrasted sharply with the patchy acc

64 specifically promoted mural cell coverage of tumor vessels and decreased vascular leakiness.

65 nesis chemotherapeutic drug, can cutdown the tumor vessels and delay tumor growth obviously.

66 as monotherapy, reduced pericyte coverage of tumor vessels and enhanced efficacy in combination with

67 However, cytokines are cleared via tumor vessels and escape from the tumor periphery into t

68 telet count selectively induces leakiness of tumor vessels and favors the delivery of chemotherapy to

69 leolin antibodies selectively accumulated in tumor vessels and in angiogenic vessels of implanted "ma

70 its complexes are expressed on the walls of tumor vessels and in tumor stroma.

71 Tumor-infiltrating DCs migrated to tumor vessels and independently assembled neovasculature

72 poietin-2 (Ang-2), is produced by angiogenic tumor vessels and is a chemoattractant for TEMs.

73 beta1 is among the proteins overexpressed on tumor vessels and is a potential target for diagnostics

74 (1) is overexpressed on endothelial cells of tumor vessels and is uniformly and rapidly accessible to

75 pid accessibility of alpha5beta1 integrin on tumor vessels and may prove useful in assessing other po

76 e observed real-time targeting of this NP to tumor vessels and noted selective apoptosis in regions o

77 re used at high doses in the clinic to prune tumor vessels and paradoxically may compromise various t

78 resulting peptide (CRNGRGPDC, iNGR) homed to tumor vessels and penetrated into tumor tissue more effe

79 vasculature induces expression of CLEC14A on tumor vessels and pro-angiogenic phenotypes.

80 one marrow-derived cells to the formation of tumor vessels and stroma, tumor cells were implanted in

81 We investigated whether platelets stabilize tumor vessels and studied the underlying mechanisms.

82 mor cells with nuclear EZH2 is larger around tumor vessels and the invasive front, suggesting that nu

83 s should be initially cationic to target the tumor vessels and then change to neutral charge after ex

84 ould specifically bind to fibronectin in the tumor vessels and tumor stroma.

85 rsely, enforced Zbtb46 expression normalized tumor vessels and, by suppressing Cebpb, skewed bone mar

86 ysis of vascular targets, targeting drugs to tumor vessels, and therapeutic manipulation of tumor ves

87 d tumor growth and metastasis by normalizing tumor vessels, and this was abrogated by p53 haploinsuff

88 Tumor vessels are characterized by abnormal morphology a

89 Not all tumor vessels are equal.

90 atients develop vascular neurofibromas where tumor vessels are invested in a dense pericyte sheath.

91 Specific markers in tumor vessels are particularly well suited for targeting

92 emotherapeutics, accompanied by increases in tumor vessel area and intratumoral drug delivery.

93 ted mouse bones, positively correlating with tumor vessel area.

94 or angiogenesis, contravening the dogma that tumor vessels arise exclusively from postcapillary venul

95 EM5, and mTEM8) were abundantly expressed in tumor vessels as well as in the vasculature of the devel

96 The injected antibody strongly labeled tumor vessels at all time points but did not label most

97 the reduction in vascular permeability, the tumor vessels became smaller in diameter and less tortuo

98 This conjugate accumulated selectively in tumor vessels because of the enhanced permeability and r

99 indicate that basement membrane covers most tumor vessels but has profound structural abnormalities,

100 conclude that pericytes are present on most tumor vessels but have multiple abnormalities, including

101 travenous injection, RCA I bound strongly to tumor vessels but not to normal blood vessels.

102 f PDGF-B signaling can lead to regression of tumor vessels, but the magnitude is tumor specific and d

103 ceptors has allowed selective destruction of tumor vessels by administration of a chimeric protein co

104 for enhancing revascularization or targeting tumor vessels by exploiting CXCR4 agonists and antagonis

105 y via the intraperitoneal route, even though tumor vessels can act as sinks during the dissemination

106 m-sized (>20 micro m in diameter) and larger tumor vessels compared with normal choroidal vessels.

107 lso exhibited increased expression in breast tumor vessels compared with that in normal tissues.

108 he chemokine receptor CXCR4 was decreased in tumor vessels, consistent with defective homing of vascu

109 was associated with a reduced leakiness from tumor vessels, consistent with induction of a vascular n

110 Immune cells and tumor vessels constitute important elements in tumor tis

111 Partial regression of tumor-vessel contact indicates suitability for surgical

112 Notably, endocan expression on tumor vessels correlated strongly with staging and invas

113 Anionic phospholipids on tumor vessels could potentially provide markers for tumo

114 ated the role of the BRAF(V600E) oncogene in tumor/vessel crosstalk and analyzed the effect of the BR

115 companied by a simultaneous 50% reduction in tumor vessel density and a 5-fold increase in inflammato

116 signaling in ccRCC tumor xenografts reduced tumor vessel density and growth under the renal capsule.

117 Combination therapy reduced the tumor vessel density and plasma volume in tumors to a gr

118 We detected an increase in tumor vessel density and size in VEGF-overexpressing tum

119 is, as there is no significant difference in tumor vessel density between wild-type tumors and tumors

120 this was not associated with alterations in tumor vessel density or immune cell infiltration.

121 trations of angiogenic chemokines, increased tumor vessel density, and greatly augmented prostate tum

122 /-) mice had decreased tumor size, decreased tumor vessel density, and reduced tumor invasiveness com

123 TSR2+RFK and TSR2 reduce tumor vessel density, but TSR2+RFK has a greater effect

124 Therapy reduced tumor vessel density, which was attributable to a decrea

125 srupting vascular function despite increased tumor vessel density.

126 ntly increased tumor growth independently of tumor vessel density.

127 inistration of hNSC-aaTSP-1 markedly reduces tumor vessel-density that results in inhibition of tumor

128 vessels derived from the brain compared with tumor vessels derived from subcutaneous tissues.

129 ssion of both Flk-1 and Flt-1 was greater in tumor vessels derived from the brain compared with tumor

130 LT relies on tumor-vessel detachment, and the presence of communicati

131 O donor (spermine NO, 100 mumol/L) increased tumor vessel diameter and flow rate, whereas systemic in

132 In both models, tumor vessel diameter, length/surface area density, and

133 nd TF(DeltaCT)/PAR2(-/-) mice, and increased tumor vessel diameters of TF(DeltaCT) mice were partiall

134 ormed larger hemorrhagic pools and increased tumor vessel dilation consistent with CEUS observations

135 Tumor vessel dysfunction is a pivotal event in cancer pr

136 iogenesis is important, STAT5 is detected in tumor vessel EC nuclei, consistent with STAT5 activation

137 cacy of cancer therapeutics, but the role on tumor vessel efficiency and drug delivery is unclear.

138 xpression in two ways: 1) acting directly on tumor vessel endothelial cells, and 2) acting on the tum

139 Targeting tumor vessel endothelium therefore should serve as an ef

140 oidal endothelial cells, the origin of liver tumor vessel endothelium, are known to be fenestrated an

141 t that in the presence of tumor cells, hESCT tumor vessels express human TVMs.

142 Human tumor vessels express tumor vascular markers (TVM), prot

143 xpression, angiogenic factor expression, and tumor vessel findings, including vessels encapsulating t

144 ablished between IL-6-dependent licensing of tumor vessels for Tem trafficking and apoptosis of tumor

145 with Mekk3(Deltaflox/-) BM were impaired for tumor vessel formation.

146 e almost ubiquitous presence of pericytes on tumor vessels found in the present study may be attribut

147 ized to concurrently image and differentiate tumor vessels from both the perivascular cells and the m

148 racterize the endothelial cell morphology in tumor vessels from either the periphery or the core of t

149 cessful when administered at early stages of tumor vessel growth but is less effective when administe

150 The tumor microenvironment contributes to tumor vessel growth, and distinct myeloid cells recruite

151 ated MPhi toward M1 polarization, suppressed tumor vessel growth, and enhanced survival (metastasis m

152 Jagged1 has been recently shown to restrict tumor vessel growth.

153 RBC flux was higher in larger tumor vessels (>30 micro m in diameter) compared with si

154 After inhibition of Ang2, tumor vessels had many features of normal blood vessels

155 We conclude that some tumor vessels have a defective cellular lining composed

156 growth factor (VEGF) mechanisms to normalize tumor vessels have offered limited therapeutic efficacie

157 Approximately 85% of tumor vessels have uniform CD31 and/or CD105 immunoreact

158 Endothelial cells of tumor vessels have well-documented alterations, but it i

159 ity, as their depletion selectively rendered tumor vessels highly permeable and caused massive intrat

160 sues analyzed, in cultured ECs and in breast tumor vessels; however, ANTXR2/CMG2 expression was not r

161 bly by attenuating incorporation of VMC into tumor vessels, impairing endothelial survival, and raise

162 is-Np led to near complete loss of all human tumor vessels in a murine model of human tumor vasculatu

163 termed "dynamic control." Dynamic control of tumor vessels in C57BL/6 mice bearing B16 melanoma was p

164 d blood vessels, we measured the diameter of tumor vessels in HSTS-26T tumors implanted in transparen

165 vasive visualization of VEGFR2 expression in tumor vessels in mice.

166 everely impaired the maturation processes of tumor vessels in mice.

167 Poor functionality of tumor vessels in NG2 null brain is reflected by reduced

168 at resembled the radiosensitive phenotype of tumor vessels in SCID mice.

169 Tumor vessels in the Ang-1 group developed a significant

170 Tumor vessels in the FAK CKO mice displayed reduced VP c

171 which can be used to localize tTF to occlude tumor vessels in two diversely different murine tumor mo

172 nimals for their ability to incorporate into tumor vessels in vivo, as well as to migrate in response

173 umor endothelial cells in vitro and to human tumor vessels in vivo.

174 d tumor microenvironment in the induction of tumor vessel injury in thrombocytopenic mice.

175 lets, stroma-infiltrating leukocytes induced tumor vessel injury.

176 to the challenges associated with observing tumor-vessel interactions deep within tumors in real-tim

177 ows real-time and quantitative assessment of tumor-vessel interactions under conditions that recapitu

178 No tumor-vessel interface was noted at the superior mesente

179 on after extravasation of nanoparticles from tumor vessels into the extravascular fluid space.

180 s and tumors, the selected phage spread from tumor vessels into the perivascular tumor parenchyma.

181 s, and report here that improved function of tumor vessels is a key determinant of benefit from metro

182 rtment of genes that are expressed in breast tumor vessels is needed to facilitate the development of

183 The leakiness of tumor vessels is well documented in experimental tumor m

184 ess, which greatly exceeds blood pressure in tumor vessels, is sufficient to induce the collapse of v

185 Do tumor vessels lack the signals to mature or, instead, is

186 Openings between these cells contribute to tumor vessel leakiness and may permit access of macromol

187 participants discussed the cellular basis of tumor vessel leakiness, endothelial barrier function of

188 rs of endothelial leakiness, consequences of tumor vessel leakiness, genomic analysis of vascular tar

189 arrier function of blood vessels, monitoring tumor vessel leakiness, mediators of endothelial leakine

190 , NPs tend to accumulate mostly at the inlet tumor vessels leaving the inner and outer vasculature de

191 for 14 days increased the number of perfused tumor vessels marked by lectin in the bloodstream by 50%

192 ar distribution of RGD-4C phage in surviving tumor vessels matched the alpha(5)beta(1) integrin expre

193 From these data the authors hypothesize that tumor vessel maturation in RB initiates in central regio

194 d 4 (TRPV4) regulates tumor angiogenesis and tumor vessel maturation via modulation of TEC mechanosen

195 ight represent an exploitable tool to induce tumor vessel maturation.

196 Strategies to enhance S1PR1 signaling in tumor vessels may be an important adjunct to standard ca

197 normal vessels and proteins present only on tumor vessels may serve as biomarkers or targets for ant

198 g delivery framework that relies on advanced tumor/vessel models, high-throughput NC libraries, nano-

199 .Egr-TNF and X-irradiation were specific for tumor vessels, non-tumor-bearing mice were irradiated af

200 Hence, tumor vessel normalization (TVN) is emerging as an anti-

201 s that, once inoculated into a tumor, induce tumor vessel normalization and inhibit tumor growth.

202 Tumor vessel normalization has been proposed as a therap

203 n of a cytotoxic treatment in this window of tumor vessel normalization resulted in increased efficac

204 Ang2 inhibitor, the Ang1 inhibitor prevented tumor vessel normalization, but not the reduction in tum

205 As a consequence of the observed N6L-induced tumor vessel normalization, pre-treatment with N6L effic

206 extensive areas of necrosis and by decreased tumor vessel number and size.

207 ificantly reduced tumor growth and decreased tumor vessel number, as compared with controls, addition

208 Reduced tumor vessel numbers and function following antiangiogen

209 From all of the peripheral tumor vessels observed, fenestrated endothelium was obse

210 diffusion coefficient and flow speed within tumor vessels of 4T1 murine mammary adenocarcinomas impl

211 CD13 was expressed in tumor vessels of all cases.

212 vestibular schwannomas and VEGFR-2 in 32% of tumor vessels on immunohistochemical analysis.

213 othesize that because of the leaky nature of tumor vessels, oncotic pressure in tumor interstitium sh

214 IGF-2 protein was localized primarily to tumor vessels or vascular channels.

215 The CNN's performance in detecting tumor vessels, papillary projections, nodules, and masse

216 d in pancreatic tumor endothelium and alters tumor vessel parameters through a VEGF-independent mecha

217 scopy that cediranib significantly decreased tumor vessel permeability and diameter.

218 responses were associated with high baseline tumor vessel permeability and elevated blood levels of v

219 hows that antiangiogenic agents can decrease tumor vessel permeability and interstitial fluid pressur

220 Thus, medulloblastoma genotype dictates tumor vessel phenotype, explaining in part the disparate

221 ich tumor-infiltrating immune cells regulate tumor vessel phenotype.

222 Tumor vessels possess unique physiological features that

223 before neoplastic cells, and rarefaction of tumor vessels precedes the decrease in tumor size.

224 Tumor vessel presence, vascular patterns and vascular de

225 ctin was localized within the endothelium of tumor vessels prior to treatment.

226 e tumor site by altering the permeability of tumor vessels producing tumor:normal organ ratios of 420

227 Abnormal tumor vessels promote metastasis and impair chemotherapy

228 We hypothesized that VWF fibers in tumor vessels promote tumor-associated thromboembolism a

229 e excision showed induction of E-selectin on tumor vessels, recruitment of CLA(+) CD8(+) T cells, and

230 n of PDGF in LLC reduced pericytes, and then tumor vessels regressed because pericytes were the main

231 inhibition is not required for Ang-2-induced tumor vessel regression and growth delay.

232 The sequence of events that leads to tumor vessel regression and the functional characteristi

233 ression of Ang-2 leads to unexpected massive tumor vessel regression within 24 h, even without concom

234 D8 T- and NK-cell activation, IFNy-dependent tumor vessel regression, and ischemic tumor necrosis/apo

235 D8 T and NK cells led to efficient and rapid tumor vessel regression, intratumoral ischemia, and tumo

236 he latter finding reveals a new mechanism of tumor vessel regression-i.e., blocking the interactions

237 -regulation, endothelial cell apoptosis, and tumor vessel regression.

238 les of Ang-2-induced pericyte dropout during tumor vessel regression.

239 ribute to different cellular compartments in tumor vessels, reinforcing the vascular architecture.

240 ogenesis and the maintenance of integrity of tumor vessels require the presence of VEGF/VPF in the ti

241 , and alpha nu beta 3 on the luminal side of tumor vessels, respectively, were developed and tested f

242 Together, these data show that the extent of tumor vessel response to angiogenic inhibition could be

243 This order markedly influenced tumor vessel response to anti-vascular therapy with reco

244 re are no reliable predictors or markers for tumor vessel response to antiangiogenic therapy.

245 linical trials for predicting and monitoring tumor vessel responses to antiangiogenic therapy.

246 roliferation, and the presence of pericytes, tumor vessels segregated into three categories.

247 hown to have a key role in the regulation of tumor vessel size.

248 By normalizing tumor vessel structure and function and increasing perfu

249 levels have profound pleiotropic effects on tumor vessel structure, perfusion, oxygenation, and apop

250 l % doubled the accumulation of liposomes in tumor vessels, suggesting a change in intratumor distrib

251 injection of picogram amounts of NGR-TNF, a tumor vessel-targeted TNFalpha derivative currently in p

252 essels could potentially provide markers for tumor vessel targeting and imaging.

253 By increasing hypoxia in tumors, vessel-targeting agents can be combined with gly

254 reatment of mice increased the percentage of tumor vessels that expose anionic phospholipids from 35%

255 Thus, most regions of tumor vessels that lack CD31 and CD105 immunoreactivity

256 Murine tumor vessels that lack S1PR1 in the vascular endotheliu

257 Most tumor vessels that lacked pericytes at 7 days subsequent

258 t developmental cues to promote formation of tumor vessels that sustain their growth, but these angio

259 est vessel blood flow; and (4) well-perfused tumor vessels that were hypoxic and, consequently, large

260 d significantly less microvessel density but tumor vessels that were more functional as lectin inject

261 east in part by downregulating E-selectin on tumor vessels, thereby restricting entry of skin-homing

262 nterface method, onset and aging of discrete tumor vessels through angiogenesis, and incorporation of

263 lation between the collagen content around a tumor vessel to the permeability of that vessel permeabi

264 Due to the high permeability of tumor vessels to fluids and plasma proteins, the microva

265 The hyperpermeability of tumor vessels to macromolecules, compared with normal ve

266 As tumor vessels transitioned from the initial dense regula

267 col coated liposomes to optimize delivery to tumor vessels using biodistribution studies and intravit

268 argeted HAuNS and are quickly dispersed from tumor vessels via receptor-mediated endocytosis and subs

269 is shows that malignant ovaries have greater tumor vessel volume, length and number of segments, as c

270 o enable the passage of the drug through the tumor vessel wall and enhance its interaction with liver

271 le in tissues on both cellular components of tumor vessel wall: CD31(bright)CD45- endothelial cells a

272 n vivo video imaging of whole mouse body and tumor vessels was achieved using a ~6-fold lower injecte

273 ation of blood clots (thrombosis) within the tumor vessels was initiated by targeting the cell surfac

274 At 6 minutes, RCA I fluorescence of tumor vessels was largely diffuse, but over the next hou

275 CLEC14A overexpression in tumor vessels was seen in a wide range of solid tumor ty

276 8 and 96 h after paclitaxel, the diameter of tumor vessels was significantly increased.

277 vessels and pericytes, and functionality of tumor vessels were all lower in mice lacking Cd248 (Cd24

278 Pathological tumor vessels were closed using particles filling the en

279 reas surrounding skin and muscle, from which tumor vessels were derived, had fenestrated endothelium

280 Tumor vessels were identified by immunohistochemical sta

281 The majority of the tumor vessels were instead recruited from tissue adjacen

282 In untreated animals, both MCaIV and LS174T tumor vessels were leaky to albumin.

283 tumors, and both the density and the size of tumor vessels were significantly reduced, although tumor

284 Between 15 and 40% of endothelial cells in tumor vessels were stained.

285 with this tumor-homing peptide accumulate in tumor vessels, where they induce additional local clotti

286 geted nanoworms caused extensive clotting in tumor vessels, whereas no clotting was observed in the v

287 induced thrombosis in small and medium sized tumor vessels, whereas the chTNT-3/tTF induced clotting

288 Both experimental settings showed that tumor vessels, which are resistant to anti-VEGF therapy,

289 e particles can cause additional clotting in tumor vessels, which creates more binding sites for the

290 intravasation, and metastasis by normalizing tumor vessels, which improved vessel maturation and perf

291 tion indicated normalization of the residual tumor vessels, which was also implied by low levels of a

292 mplete understanding of the basic biology of tumor vessels will be necessary to fully appreciate the

293 segmentally dilated, architecturally erratic tumor vessels with decreased nascent pericytes and scant

294 erin knockdown in PDAC xenografts results in tumor vessels with decreased radii and tortuosity.

295 umor vessels and caused thrombotic damage to tumor vessels with extravasation of red blood cells into

296 On the other hand, tumor vessels with high expression of S1PR1 (S1pr1 ECTG)

297 depletion led to a rapid destabilization of tumor vessels with intratumor hemorrhage starting as soo

298 thout back-flux to the vasculature, Model-3: tumor vessels with leakage and back-flux.

299 h by decreasing endothelial cell survival in tumor vessels, without affecting normal vasculature.

300 ent viscosity, abnormally high HCT(m) in the tumor vessels would increase vascular resistance and dec