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1 ually increased when expressed per surviving tumor vessel.
2 s a tool to differentiate between normal and tumor vessels.
3 followed by increased activated caspase-3 in tumor vessels.
4 lular effects of VEGF and PDGF inhibitors on tumor vessels.
5 f platelet adhesion receptors in stabilizing tumor vessels.
6 nable target for specific destabilization of tumor vessels.
7 ls and decreased numbers of medium and large tumor vessels.
8 r bed while improving perfusion in surviving tumor vessels.
9 r the surface area per unit tissue volume of tumor vessels.
10 sement membrane left behind after pruning of tumor vessels.
11 uited GFP-positive cells that organized into tumor vessels.
12 ics can gain access to tumor cells via leaky tumor vessels.
13 on of the integrin on the luminal surface of tumor vessels.
14 ibody-dependent cellular cytotoxicity toward tumor vessels.
15 eting and potentially eliminating neoplastic tumor vessels.
16 hat S1P(1) expression is strongly induced in tumor vessels.
17 the cellular effects of these inhibitors on tumor vessels.
18 angiogenesis or cause regression of existing tumor vessels.
19 s and formed a continuous sheet wrapping the tumor vessels.
20 unoreactivities were similarly ubiquitous on tumor vessels.
21 suggesting that these agents target immature tumor vessels.
22 ely to sites of active angiogenesis, notably tumor vessels.
23 mor vessels, and therapeutic manipulation of tumor vessels.
24 42 degrees C led to hemorrhage and stasis in tumor vessels.
25 ot increase leukocyte rolling or adhesion in tumor vessels.
26 in-1, may modulate adhesion of leukocytes to tumor vessels.
27 inflammation, could explain the leakiness of tumor vessels.
28 e metastasis ischemia by the embolization of tumor vessels.
29 ilar to the fenestrated endothelium found in tumor vessels.
30 X-irradiation occurs selectively within the tumor vessels.
31 of the three-dimensional micromorphology of tumor vessels.
32 lecule endocan (ESM1) was highly elevated on tumor vessels.
33 as well as the diameter and permeability of tumor vessels.
34 ressure does not cause vessel compression of tumor vessels.
35 eins are upregulated on endothelial cells of tumor vessels.
36 or EC JAM-C in the development of functional tumor vessels.
37 significantly increases the number of human tumor vessels.
38 enetic modifications in endothelial cells of tumor vessels.
39 ill need to be identified on these resistant tumor vessels.
40 more homogeneous distribution of functional tumor vessels.
41 rasound imaging showed reduced blood flow in tumor vessels.
42 eased RCA I binding and internalization into tumor vessels.
43 e necessary to suppress VEGFR3 expression on tumor vessels.
44 isplatin-loaded nanoparticles (F3-Cis-Np) to tumor vessels.
45 fibrin-associated clotted plasma proteins in tumor vessels.
46 morphologic and functional abnormalities of tumor vessels.
50 antibody transport increases from surviving tumor vessels after normalization by inhibition of VEGF
51 The heterogeneous vascular permeability in tumor vessels, along with several other factors, creates
52 not of Ang1, was up-regulated in angiogenic tumor vessels already in early stages of skin carcinogen
54 d (NR) "activators" that populate the porous tumor vessels and act as photothermal antennas to specif
55 ration of cell-cell junction proteins in the tumor vessels and astrocyte-endothelium interactions in
56 sion construct localized selectively to PC-3 tumor vessels and caused thrombotic damage to tumor vess
57 ed with the uniform CD31 immunoreactivity of tumor vessels and contrasted sharply with the patchy acc
60 as monotherapy, reduced pericyte coverage of tumor vessels and enhanced efficacy in combination with
61 telet count selectively induces leakiness of tumor vessels and favors the delivery of chemotherapy to
62 leolin antibodies selectively accumulated in tumor vessels and in angiogenic vessels of implanted "ma
66 beta1 is among the proteins overexpressed on tumor vessels and is a potential target for diagnostics
67 (1) is overexpressed on endothelial cells of tumor vessels and is uniformly and rapidly accessible to
68 pid accessibility of alpha5beta1 integrin on tumor vessels and may prove useful in assessing other po
69 e observed real-time targeting of this NP to tumor vessels and noted selective apoptosis in regions o
70 re used at high doses in the clinic to prune tumor vessels and paradoxically may compromise various t
71 resulting peptide (CRNGRGPDC, iNGR) homed to tumor vessels and penetrated into tumor tissue more effe
73 one marrow-derived cells to the formation of tumor vessels and stroma, tumor cells were implanted in
75 mor cells with nuclear EZH2 is larger around tumor vessels and the invasive front, suggesting that nu
76 s should be initially cationic to target the tumor vessels and then change to neutral charge after ex
78 ysis of vascular targets, targeting drugs to tumor vessels, and therapeutic manipulation of tumor ves
81 atients develop vascular neurofibromas where tumor vessels are invested in a dense pericyte sheath.
83 or angiogenesis, contravening the dogma that tumor vessels arise exclusively from postcapillary venul
84 EM5, and mTEM8) were abundantly expressed in tumor vessels as well as in the vasculature of the devel
86 the reduction in vascular permeability, the tumor vessels became smaller in diameter and less tortuo
87 This conjugate accumulated selectively in tumor vessels because of the enhanced permeability and r
88 indicate that basement membrane covers most tumor vessels but has profound structural abnormalities,
89 conclude that pericytes are present on most tumor vessels but have multiple abnormalities, including
91 f PDGF-B signaling can lead to regression of tumor vessels, but the magnitude is tumor specific and d
92 ceptors has allowed selective destruction of tumor vessels by administration of a chimeric protein co
93 for enhancing revascularization or targeting tumor vessels by exploiting CXCR4 agonists and antagonis
94 y via the intraperitoneal route, even though tumor vessels can act as sinks during the dissemination
95 m-sized (>20 micro m in diameter) and larger tumor vessels compared with normal choroidal vessels.
97 he chemokine receptor CXCR4 was decreased in tumor vessels, consistent with defective homing of vascu
98 was associated with a reduced leakiness from tumor vessels, consistent with induction of a vascular n
102 ated the role of the BRAF(V600E) oncogene in tumor/vessel crosstalk and analyzed the effect of the BR
103 companied by a simultaneous 50% reduction in tumor vessel density and a 5-fold increase in inflammato
106 is, as there is no significant difference in tumor vessel density between wild-type tumors and tumors
108 trations of angiogenic chemokines, increased tumor vessel density, and greatly augmented prostate tum
113 inistration of hNSC-aaTSP-1 markedly reduces tumor vessel-density that results in inhibition of tumor
115 ssion of both Flk-1 and Flt-1 was greater in tumor vessels derived from the brain compared with tumor
116 O donor (spermine NO, 100 mumol/L) increased tumor vessel diameter and flow rate, whereas systemic in
118 nd TF(DeltaCT)/PAR2(-/-) mice, and increased tumor vessel diameters of TF(DeltaCT) mice were partiall
120 iogenesis is important, STAT5 is detected in tumor vessel EC nuclei, consistent with STAT5 activation
121 cacy of cancer therapeutics, but the role on tumor vessel efficiency and drug delivery is unclear.
122 xpression in two ways: 1) acting directly on tumor vessel endothelial cells, and 2) acting on the tum
124 oidal endothelial cells, the origin of liver tumor vessel endothelium, are known to be fenestrated an
127 ablished between IL-6-dependent licensing of tumor vessels for Tem trafficking and apoptosis of tumor
129 e almost ubiquitous presence of pericytes on tumor vessels found in the present study may be attribut
130 ized to concurrently image and differentiate tumor vessels from both the perivascular cells and the m
131 racterize the endothelial cell morphology in tumor vessels from either the periphery or the core of t
132 cessful when administered at early stages of tumor vessel growth but is less effective when administe
133 The tumor microenvironment contributes to tumor vessel growth, and distinct myeloid cells recruite
134 ated MPhi toward M1 polarization, suppressed tumor vessel growth, and enhanced survival (metastasis m
141 sues analyzed, in cultured ECs and in breast tumor vessels; however, ANTXR2/CMG2 expression was not r
142 bly by attenuating incorporation of VMC into tumor vessels, impairing endothelial survival, and raise
143 is-Np led to near complete loss of all human tumor vessels in a murine model of human tumor vasculatu
144 d blood vessels, we measured the diameter of tumor vessels in HSTS-26T tumors implanted in transparen
151 which can be used to localize tTF to occlude tumor vessels in two diversely different murine tumor mo
152 nimals for their ability to incorporate into tumor vessels in vivo, as well as to migrate in response
158 s and tumors, the selected phage spread from tumor vessels into the perivascular tumor parenchyma.
159 s, and report here that improved function of tumor vessels is a key determinant of benefit from metro
160 rtment of genes that are expressed in breast tumor vessels is needed to facilitate the development of
162 ess, which greatly exceeds blood pressure in tumor vessels, is sufficient to induce the collapse of v
164 Openings between these cells contribute to tumor vessel leakiness and may permit access of macromol
165 participants discussed the cellular basis of tumor vessel leakiness, endothelial barrier function of
166 rs of endothelial leakiness, consequences of tumor vessel leakiness, genomic analysis of vascular tar
167 arrier function of blood vessels, monitoring tumor vessel leakiness, mediators of endothelial leakine
168 , NPs tend to accumulate mostly at the inlet tumor vessels leaving the inner and outer vasculature de
169 for 14 days increased the number of perfused tumor vessels marked by lectin in the bloodstream by 50%
170 ar distribution of RGD-4C phage in surviving tumor vessels matched the alpha(5)beta(1) integrin expre
171 From these data the authors hypothesize that tumor vessel maturation in RB initiates in central regio
172 d 4 (TRPV4) regulates tumor angiogenesis and tumor vessel maturation via modulation of TEC mechanosen
174 normal vessels and proteins present only on tumor vessels may serve as biomarkers or targets for ant
175 .Egr-TNF and X-irradiation were specific for tumor vessels, non-tumor-bearing mice were irradiated af
177 s that, once inoculated into a tumor, induce tumor vessel normalization and inhibit tumor growth.
179 n of a cytotoxic treatment in this window of tumor vessel normalization resulted in increased efficac
180 Ang2 inhibitor, the Ang1 inhibitor prevented tumor vessel normalization, but not the reduction in tum
181 As a consequence of the observed N6L-induced tumor vessel normalization, pre-treatment with N6L effic
183 ificantly reduced tumor growth and decreased tumor vessel number, as compared with controls, addition
186 diffusion coefficient and flow speed within tumor vessels of 4T1 murine mammary adenocarcinomas impl
188 othesize that because of the leaky nature of tumor vessels, oncotic pressure in tumor interstitium sh
190 d in pancreatic tumor endothelium and alters tumor vessel parameters through a VEGF-independent mecha
192 responses were associated with high baseline tumor vessel permeability and elevated blood levels of v
193 hows that antiangiogenic agents can decrease tumor vessel permeability and interstitial fluid pressur
194 Thus, medulloblastoma genotype dictates tumor vessel phenotype, explaining in part the disparate
199 e tumor site by altering the permeability of tumor vessels producing tumor:normal organ ratios of 420
202 e excision showed induction of E-selectin on tumor vessels, recruitment of CLA(+) CD8(+) T cells, and
203 n of PDGF in LLC reduced pericytes, and then tumor vessels regressed because pericytes were the main
206 ression of Ang-2 leads to unexpected massive tumor vessel regression within 24 h, even without concom
207 he latter finding reveals a new mechanism of tumor vessel regression-i.e., blocking the interactions
210 ogenesis and the maintenance of integrity of tumor vessels require the presence of VEGF/VPF in the ti
211 , and alpha nu beta 3 on the luminal side of tumor vessels, respectively, were developed and tested f
212 Together, these data show that the extent of tumor vessel response to angiogenic inhibition could be
219 levels have profound pleiotropic effects on tumor vessel structure, perfusion, oxygenation, and apop
220 l % doubled the accumulation of liposomes in tumor vessels, suggesting a change in intratumor distrib
221 injection of picogram amounts of NGR-TNF, a tumor vessel-targeted TNFalpha derivative currently in p
224 reatment of mice increased the percentage of tumor vessels that expose anionic phospholipids from 35%
227 t developmental cues to promote formation of tumor vessels that sustain their growth, but these angio
228 est vessel blood flow; and (4) well-perfused tumor vessels that were hypoxic and, consequently, large
229 east in part by downregulating E-selectin on tumor vessels, thereby restricting entry of skin-homing
230 nterface method, onset and aging of discrete tumor vessels through angiogenesis, and incorporation of
231 lation between the collagen content around a tumor vessel to the permeability of that vessel permeabi
234 col coated liposomes to optimize delivery to tumor vessels using biodistribution studies and intravit
235 argeted HAuNS and are quickly dispersed from tumor vessels via receptor-mediated endocytosis and subs
236 o enable the passage of the drug through the tumor vessel wall and enhance its interaction with liver
237 le in tissues on both cellular components of tumor vessel wall: CD31(bright)CD45- endothelial cells a
238 n vivo video imaging of whole mouse body and tumor vessels was achieved using a ~6-fold lower injecte
239 ation of blood clots (thrombosis) within the tumor vessels was initiated by targeting the cell surfac
244 reas surrounding skin and muscle, from which tumor vessels were derived, had fenestrated endothelium
248 tumors, and both the density and the size of tumor vessels were significantly reduced, although tumor
250 with this tumor-homing peptide accumulate in tumor vessels, where they induce additional local clotti
251 geted nanoworms caused extensive clotting in tumor vessels, whereas no clotting was observed in the v
252 induced thrombosis in small and medium sized tumor vessels, whereas the chTNT-3/tTF induced clotting
254 e particles can cause additional clotting in tumor vessels, which creates more binding sites for the
255 intravasation, and metastasis by normalizing tumor vessels, which improved vessel maturation and perf
256 tion indicated normalization of the residual tumor vessels, which was also implied by low levels of a
257 mplete understanding of the basic biology of tumor vessels will be necessary to fully appreciate the
258 segmentally dilated, architecturally erratic tumor vessels with decreased nascent pericytes and scant
260 umor vessels and caused thrombotic damage to tumor vessels with extravasation of red blood cells into
261 depletion led to a rapid destabilization of tumor vessels with intratumor hemorrhage starting as soo
262 h by decreasing endothelial cell survival in tumor vessels, without affecting normal vasculature.
263 ent viscosity, abnormally high HCT(m) in the tumor vessels would increase vascular resistance and dec
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