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1 igh doses can augment the development of the neovasculature.
2 he RESDECs participated in forming the tumor neovasculature.
3 s in prostate cancer and in tumor-associated neovasculature.
4 cated in the successful development of tumor neovasculature.
5  human prostate tissues, and the surrounding neovasculature.
6 eceptors expressed selectively in angiogenic neovasculature.
7 t PSMA is also expressed in tumor-associated neovasculature.
8 owing endothelium and limit establishment of neovasculature.
9 expression, enhancing apoptosis, or reducing neovasculature.
10 g circulation time and leakage through tumor neovasculature.
11 ors and is required for development of tumor neovasculature.
12 ents and oxygen supplied by tumor-associated neovasculature.
13 yze sequential gene expression in developing neovasculature.
14 umor cells and indirect effects on the tumor neovasculature.
15 on is associated with the development of the neovasculature.
16 s for immunotherapy as well as inhibit tumor neovasculature.
17 ere mainly on the smooth muscle cells of the neovasculature.
18 e a loss of angiotensin II receptor on tumor neovasculature.
19 es targeted to molecular signatures on tumor neovasculature.
20 cell adhesion protein overexpressed in tumor neovasculature.
21 tly affect the architecture of the ingrowing neovasculature.
22 n can be contributors to all lineages of the neovasculature.
23 are supported in their growth by a dedicated neovasculature.
24 are highly expressed on tumors and the tumor neovasculature.
25  glioma stem cells, vasculogenic mimicry and neovasculature.
26 ules with antivascular activity selective to neovasculature.
27  during angiogenesis on the tumor associated neovasculature.
28 tiation between tip cells and stalk cells of neovasculature.
29  on the surface of tumor cells and the tumor neovasculature.
30 e the morphology and function of postinfarct neovasculature.
31 dicine," for which the ideal target is tumor neovasculature.
32 n experimental in vivo representation of the neovasculature.
33  of fibronectin expressed in disease ECM and neovasculature.
34 I protein was localized selectively to tumor neovasculature.
35 mors previously shown to express PSMA on the neovasculature.
36  enabling detailed small-animal PET of tumor neovasculature.
37 itates the homing of progenitor cells to the neovasculature.
38 , which are expressed on actively remodeling neovasculature.
39  COX-2 expression is restricted to the tumor neovasculature.
40 and endothelial cells in areas of developing neovasculature after focal cerebral ischemia in adult ra
41  identified in corpus luteal and endometrial neovasculature after inductive ovulation.
42 toxin, has been shown to target pathological neovasculature and activate complement (C3), thereby ind
43 endothelial precursor cells incorporate into neovasculature and have been successfully used as vehicl
44        Importantly, RNAi-MMP-9 reduces tumor neovasculature and increases tumor cell death.
45 int suppression of angiogenesis in the tumor neovasculature and induction of tumor cell apoptosis.
46 llin nanoparticles were used to suppress the neovasculature and inhibit Vx-2 adenocarcinoma developme
47 te cancer cells and nonprostatic solid tumor neovasculature and is a target for anticancer imaging an
48 xpression on many solid tumors and the tumor neovasculature and its role in metastasis and angiogenes
49 rexpressed in hepatocellular carcinoma (HCC) neovasculature and may serve as a useful imaging biomark
50 oliferation, diffuse invasion, and prominent neovasculature and necrosis.
51 othelium cadherin that is expressed in tumor neovasculature and on endothelial progenitor cells in th
52 tegrins present in both the tumor-associated neovasculature and on the surface of ovarian cancer cell
53 ressed on endothelial cells lining the tumor neovasculature and on tumor cells; the active site of fa
54 vitro and in vivo as well as their homing to neovasculature and outgrowth into differentiated cell ty
55  for prospectively studying the link between neovasculature and plaque vulnerability.
56 nation of GSC-derived pericytes disrupts the neovasculature and potently inhibits tumor growth.
57 ust neoplastic cells but also stromal cells, neovasculature, and a gamut of immune cells.
58      MAbs directed toward tumor cells, tumor neovasculature, and host negative immunoregulatory eleme
59 enograft tumors expressing human Thy1 on the neovasculature, and on the neovasculature of a genetic m
60 ue formation, including the establishment of neovasculature, and the formation of fibrotic scar tissu
61 cellular elements such as stromal cells, the neovasculature, and the full gamut of immune cells.
62 tides that recognize CD13 receptors in tumor neovasculature are of high interest, in particular due t
63 , and cancers (tumor cells, as well as tumor neovasculature) are key targets.
64  is expressed by multiple tumor types and on neovasculature, are likewise effective in delaying tumor
65        COX-2 is expressed within human tumor neovasculature as well as in neoplastic cells present in
66  of donor endothelial cells into the newborn neovasculature as well as tissue vascularity were signif
67 cinar epithelium and the prostate and in the neovasculature associated with tumors, prostate-specific
68 d from inflammatory cells at 3 days and from neovasculature at 7 days after operation.
69 newborn mice, and osteoblasts and associated neovasculature at sites of endochondrial ossification in
70 anoparticles penetrated into the leaky tumor neovasculature but did not appreciably migrate into the
71 enovirus could prevent or regress tumor-free neovasculature, but it was progressively less effective
72 s identified as a specific biomarker of PDAC neovasculature by proteomic analysis.
73 re are two distinct processes by which tumor neovasculature can be built: angiogenesis is the formati
74 y, and pericyte recruitment into the growing neovasculature can be rescued by local intramuscular del
75 of the formation of a pathological choroidal neovasculature (CNV) that damages the macular region of
76 ake of TRC105 (which binds to CD105 on tumor neovasculature) conjugated HMSN in the 4T1 murine breast
77 ncreased histopathology, suggesting that the neovasculature contributes to tissue damage during colit
78 pha(v)beta(3) integrin receptor expressed on neovasculature, could increase systemic RIT efficacy of
79  Histologic analysis revealed specific tumor neovasculature damage after treatment with 4 doses of VE
80                        However, the level of neovasculature did not translate into significant improv
81 f tumors such as physicochemical properties, neovasculature, elasticity, surface electrical charge, a
82 tolytic immune response against the targeted neovasculature endothelial cells and tumor cells.
83 SMA has been reported exclusively within the neovasculature endothelial cells of nonprostatic cancers
84 II immunoconjugate bound to tissue factor on neovasculature endothelial cells.
85                                              Neovasculature enhancement was dependent on the relaxivi
86 ene glycol (PEG), as a means to target tumor neovasculature expressing integrins and used to deliver
87 ival, reduces infarct expansion, and induces neovasculature formation.
88 promoted the establishment of well-organized neovasculature formation.
89 lly, we assessed the extent and character of neovasculatures formed by freshly isolated and cultured
90 prostate-specific membrane antigen (PSMA) in neovasculature has been described in glioblastoma multif
91 y, the presence of PSMA on nonprostate tumor neovasculature has opened the possibility of PSMA-target
92                    We assessed the impact of neovasculature imaging by (68)Ga-PSMA-11 PET/CT on disea
93               Capillary endothelial cells of neovasculature in 137 malignant tumors (non-brain) obtai
94 cells, inhibits cell invasion, and decreases neovasculature in HUVEC and also tumor volume in EAT mou
95 can be effectively used to image mouse tumor neovasculature in lesions as small as several millimeter
96               We searched for new markers of neovasculature in PDAC and assessed their potential for
97 ility of 2ME2 to target both tumor cells and neovasculature in preclinical models led to ongoing eval
98 h had been shown to destroy the pathological neovasculature in solid tumors, on the formation of lase
99 bbits in comparison with sparse incidence of neovasculature in the control animals.
100  we undertook studies to examine whether the neovasculature in tumors also differed depending upon tu
101 s technique can be used to directly identify neovasculature in vivo and to facilitate gene therapy by
102 to tumor vessels and independently assembled neovasculature in vivo.
103  marrow-derived cells incorporating into the neovasculature, indicating that recruitment and/or reten
104 ization of solid tumors and their supporting neovasculature is a fundamental prerequisite for effecti
105                                    The tumor neovasculature is also characterized by an abnormal vasc
106 cancer is a highly vascular tumor, where the neovasculature is unique in that it arises only from the
107 f plaque composition, including macrophages, neovasculature, necrotic core, calcification, loose matr
108 genic therapy, the factors controlling tumor neovasculature need to be systemically maintained at sta
109            Despite expression of PSMA in CRC neovasculature, none of the patients exhibited tumor avi
110 human Thy1 on the neovasculature, and on the neovasculature of a genetic mouse model of PDAC.
111 ive anti-PSMA mAbs reacted strongly with the neovasculature of a wide spectrum of malignant neoplasms
112       PSMA was consistently expressed in the neovasculature of a wide variety of malignant neoplasms
113 ntigen is also expressed in tumor-associated neovasculature of a wide variety of malignant neoplasms.
114             It is concluded that even in the neovasculature of brain tumors, Pgp has the facility to
115 lignant prostate epithelial cells and by the neovasculature of many tumor types; however, it is not e
116              However, P-gp expression in the neovasculature of metastatic brain tumors is similar to
117 mmunohistochemical expression of P-gp in the neovasculature of metastatic tumors, as well as our rece
118 n the surface of prostate carcinomas and the neovasculature of most other solid tumors.
119 r marker associated with prostate cancer and neovasculature of most solid tumors.
120  membrane antigen (PSMA) is expressed in the neovasculature of multiple solid tumors, including renal
121 dent growth, cell invasion, and formation of neovasculature of NSCLC.
122 K1 reduced the proliferation Ki-67 index and neovasculature of orthotopic xenografts.
123  protein enriched in prostate cancer and the neovasculature of other solid tumors, including CRC.
124  expressed in prostate cancer and within the neovasculature of other solid tumors.
125  we could demonstrate PSMA expression in the neovasculature of several PSMA PET-positive lung cancers
126 ent murine bone marrow incorporated into the neovasculature of subsequently transplanted syngeneic ne
127 irectly related to VEGFR-2 expression in the neovasculature of the angiogenic rim.
128 y permits direct, real-time visualization of neovasculature of the atherosclerotic plaque and associa
129 ons stained with X-gal demonstrated that the neovasculature of the developing tumor frequently compri
130 ved endothelial cells were found only in the neovasculature of the newborn recipients.
131 ors is similar to the P-gp expression in the neovasculature of the primary, extracranial tumor.
132 quely or highly expressed in tumor cells and neovasculature of tumors of various origins.
133 n expressed in prostate cancer cells and the neovasculature of various solid tumors.
134  on PET is based on PSMA-specific binding to neovasculature or aspecific uptake in tumor.
135 gly activated (>300-fold) in response to the neovasculature or to the low extracellular pH in tumours
136 , these preliminary studies suggest that the neovasculature originates by sprouting from larger, host
137 resented to predict the development of tumor neovasculature over time and the specific, vascular accu
138 )beta(3)-GNBs homed specifically to immature neovasculature (PECAM(+), Tie-2(-)) along the immediate
139 ation was to determine whether the amount of neovasculature present in advanced carotid plaques can b
140 There was extensive destruction of the tumor neovasculature, presumably mediated by the factor VII im
141                           PSMA expression in neovasculature provides a possible explanation for this
142 eraction between tumors and their associated neovasculature provides an explanation for the focal eff
143 elated with macrophage (r = 0.54, P = .004), neovasculature (r = 0.68, P < .001), and loose matrix (r
144 elated with macrophage (r = 0.75, P < .001), neovasculature (r = 0.71, P < .001), and loose matrix (r
145 ow and shear rates increase within the tumor neovasculature, reaching values comparable with those me
146 n the intracranial cTVT, suggesting that its neovasculature represented an interruption of the normal
147 dings indicate that generation of functional neovasculature requires close titration of NO-Tie2 signa
148                             In addition, the neovasculature resulting from ZFP-induced expression of
149 xtent to which Pgp expression in brain tumor neovasculature retains its capacity to limit drug penetr
150  and quantitatively with the amount of leaky neovasculature seen on T1Gd.
151 gliomas have higher P-gp expression in their neovasculature, similar to the greater intrinsic express
152 ntegrin alphavbeta3 is expressed only on the neovasculature, such as in the HNSCC tumors.
153 ation with phosphorylated TF specifically on neovasculature, suggesting that phosphorylation of the T
154 led significantly higher VAP-1 expression in neovasculature than in the preexisting vessels.
155 useful for characterizing tumors with sparse neovasculature that are unlikely to have a reduced growt
156 like 4 can restrict tumor growth and disrupt neovasculature, the effect of inhibiting Notch receptor
157 nscription factor that promotes formation of neovasculature through activation of target genes, such
158 t for attacking tumor cells as well as tumor neovasculature to facilitate immunotherapeutic treatment
159 )beta(3))-fumagillin nanoparticles decreased neovasculature to negligible levels relative to control;
160 revealed as functionally important for tumor neovasculature, using kinase inhibitors targeting their
161 on of the anti-PSMA mAbs to tumor-associated neovasculature was confirmed by CD34 immunohistochemistr
162                                          The neovasculature was temporally responsive to VEGFR2 immun
163 Three stages in the development of the tumor neovasculature were characterized by intravital microsco
164 1 and FaDu) that induce alphavbeta3-positive neovasculature when transplanted into nude mice.
165 nd procoagulant activity on tumor-associated neovasculature when used in isolation perfusion, the lat
166  we hypothesize that E4G10 can only bind the neovasculature, where VE-cadherin has not yet engaged in
167  TMV and demonstrate that stimulation of the neovasculature with cytokines and chemoattractants can r
168                             The formation of neovasculature with functionally defective blood vessels
169    Superfusion of the lymphotoxin-stimulated neovasculature with leukotriene B4 (LTB4) resulted in st
170 ously and provided specific detection of the neovasculature within 2 hours by routine magnetic resona
171                                              Neovasculature within atherosclerotic plaques is believe
172  MRI provides an indication of the extent of neovasculature within carotid atherosclerotic plaque.
173 -1 is up-regulated in the small, angiogenic, neovasculature within the fibrotic septa of cirrhotic li
174 oscopically evident perfusion of the corneal neovasculature without affecting macroscopic measurement

 
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