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1 tasis initiation with immune suppression and neoangiogenesis.
2 scular endothelial growth factor protein and neoangiogenesis.
3 raft growth in mice while markedly impairing neoangiogenesis.
4 l components of the earliest phases of tumor neoangiogenesis.
5 al neoplasia, stimulating cell migration and neoangiogenesis.
6 ment of VEGF in MDSC transplantation-induced neoangiogenesis.
7 Ps may be clinically effective in augmenting neoangiogenesis.
8 how bone marrow derived cells contribute to neoangiogenesis.
9 entify PML as a novel suppressor of mTOR and neoangiogenesis.
10 ciated with an osteoblast bone formation and neoangiogenesis.
11 ith the expression of osteoblast markers and neoangiogenesis.
12 earch to identify factors that support tumor neoangiogenesis.
13 activity constitutes a barrier to effective neoangiogenesis.
14 cancer progression, presumably by preventing neoangiogenesis.
15 d inflammation was associated with increased neoangiogenesis.
16 Tumor growth requires neoangiogenesis.
17 tions in the hosts, including stimulation of neoangiogenesis.
18 of NO formation resulted in reduced retinal neoangiogenesis.
19 ed by hypoxia-inducible factor signaling and neoangiogenesis.
20 retion, extracellular matrix stiffening, and neoangiogenesis.
21 ne tumor (pNET) model commonly used to study neoangiogenesis.
22 endowed with protumoral activities, such as neoangiogenesis.
23 ng of AMCs into areas of MM tumor growth and neoangiogenesis.
24 proliferation and invasiveness coupled with neoangiogenesis.
25 stromal endothelial cells that mediate tumor neoangiogenesis.
26 g to the degree of vascular inflammation and neoangiogenesis.
27 solid tumors one had to target the inherent neoangiogenesis.
28 sites of ischemic injury where they promote neoangiogenesis.
29 ritical role in vascular tone regulation and neoangiogenesis.
30 nic liver diseases associated with increased neoangiogenesis.
31 emained mostly intact and showed very little neoangiogenesis.
32 on of Angiopoietin-1 in pericytes to enhance neoangiogenesis.
33 n, result in vision loss because of aberrant neoangiogenesis.
34 ial progenitor cells in the process of tumor neoangiogenesis.
35 ecreased beta8 expression leads to defective neoangiogenesis.
38 RII) are the predominant regulators of tumor neoangiogenesis, a key element for tumor growth and prog
39 Artery tertiary lymphoid organs show marked neoangiogenesis, aberrant lymphangiogenesis, and extensi
41 on, exhibit a decrease in glioma volumes and neoangiogenesis and an increase in antitumorigenic GAM i
45 tion of Cxcl9 led to a strong attenuation of neoangiogenesis and experimental liver fibrosis in vivo.
47 c-Cbl deletion was associated with enhanced neoangiogenesis and increased expression of vascular end
49 oproteinase (MMP)-2 has been associated with neoangiogenesis and it has been proposed that the levels
50 tumor microenvironment severely compromised neoangiogenesis and lymphangiogenesis during pancreatic
52 onstitute a favorable environment to support neoangiogenesis and may explain why vascular insults syn
53 rmalities in the pancreas included fibrosis, neoangiogenesis and mild macrophage infiltration, and th
54 ees of cellularity, mitoses, hypoxia-induced neoangiogenesis and necrosis, features that characterize
55 type), which is accompanied by inflammation, neoangiogenesis and neoinnervation, resulting in shoulde
57 factors did not have any benefit in terms of neoangiogenesis and perfusion and had minimal effect on
58 coordinates stemness with immune evasion and neoangiogenesis and point to the potential clinical util
60 tch receptor signaling is required for tumor neoangiogenesis and provides a new target for tumor ther
61 dent remodeling of the myofibers may promote neoangiogenesis and restoration of blood perfusion in sk
62 ransmural inflammation induces microvascular neoangiogenesis and results in lumen-occlusive intimal h
64 of COUP-TFII in adults severely compromised neoangiogenesis and suppressed tumor growth in xenograft
65 ly following treatment, suggesting increased neoangiogenesis and T-cell infiltration upon treatment o
66 uggest that JNK1 plays a key role in retinal neoangiogenesis and that it represents a new pharmacolog
67 iseased mouse and human arteries in areas of neoangiogenesis and that these cells constitute a main c
71 r3(-/-) mice was strongly linked to enhanced neoangiogenesis and VEGF/VEGFR2 expression compared with
72 an important protumorigenic role by favoring neoangiogenesis and/or by suppressing antitumor immune r
73 ltered production of inflammatory cytokines, neoangiogenesis, and autoreactive T lymphocytes have all
76 tegrin beta3 is critical for tumor invasion, neoangiogenesis, and inflammation, making it a promising
82 (+) effector T cells developed microvascular neoangiogenesis as well as hyperplasia of the intimal la
83 This vascular pattern is not suggestive for neoangiogenesis, as arteriovenous shunts from malignant
86 etastasis, concomitant with a suppression of neoangiogenesis at secondary sites, while leaving primar
87 nhibitors p130 and p27 show defects in tumor neoangiogenesis, both in xenografts and spontaneously ar
88 ssels, suggesting that VEGF is essential for neoangiogenesis but not survival of mature vessels in th
89 novial hypertrophy, macrophage infiltration, neoangiogenesis, cartilage degeneration, and chondrocyte
90 is ameliorative effect is linked to enhanced neoangiogenesis (CD31 staining and microfil perfusion) b
92 espiration in vascular endothelial cells for neoangiogenesis during development, tissue repair and ca
93 ating that VEGF is essential for endometrial neoangiogenesis during postmenstrual/postpartum repair.
94 h as macrophages, have been shown to promote neoangiogenesis during tumor growth and wound healing.
95 ation of these systems may minimise both the neoangiogenesis essential for tumour growth and associat
96 ed to the ability of breast tumors to induce neoangiogenesis, even in the face of cytotoxic chemother
97 l, we determined that heart regeneration and neoangiogenesis following MI depends on neonatal macroph
98 rived growth factors and cytokines stimulate neoangiogenesis from surrounding capillaries to support
99 e show that venous endothelial cells express neoangiogenesis gene signatures and show increased proli
101 b, an inhibitor of key molecules involved in neoangiogenesis, has an established role in the treatmen
103 ritis patients with and without up-regulated neoangiogenesis identified interferon-gamma and vascular
104 induce impressive reversal of skin fibrosis, neoangiogenesis, improved functionality and quality of l
109 ibited the sprouts of mouse aortic rings and neoangiogenesis in chick embryo chorioallantoic membrane
110 that venous endothelial cells contribute to neoangiogenesis in demyelinating neuroinflammatory condi
114 mediated endothelial cell proliferation and neoangiogenesis in human Matrigel and placental angiogen
115 from hypoxia-treated tumor cells results in neoangiogenesis in human umbilical vein endothelial cell
117 in parameters, EPC numbers and function, and neoangiogenesis in lupus-prone mice, independent of dise
120 s studies of APN-null mice revealed impaired neoangiogenesis in model systems without cancer cells an
121 ings show that the A2 system enables retinal neoangiogenesis in OIR by enhancing perivascular activat
123 ility is accompanied by reduced pathological neoangiogenesis in oxygen-induced retinopathy, similarly
126 be attributed, at least in part, to enhanced neoangiogenesis in the infarcted region via upregulation
127 erleukin-6, infiltration of macrophages, and neoangiogenesis in the synovium following hemarthrosis.
130 mature endothelial cells, and contribute to neoangiogenesis in vivo during tumor angiogenesis and wo
131 ated levels of endoglin (CD105), a marker of neoangiogenesis, in BSIII-IV, coinciding with altered ex
133 lated by sera of patients with TAK supported neoangiogenesis (increased human umbilic vein endothelia
134 lated by sera of patients with TAK supported neoangiogenesis (increased human umbilic vein endothelia
135 ch co-opts vessels in a VEGF-independent and neoangiogenesis-independent manner, was upregulated in n
136 cific and hypoxia-inducible VEGF expression, neoangiogenesis, infarct-size reduction, and cardiac fun
137 inantly of vascular endothelial cell origin, neoangiogenesis, inflammatory cell infiltration, and ede
138 ve response to injury, leading to intramural neoangiogenesis, intimal hyperplasia, and luminal occlus
143 uitously expressed TPCs include VEGF-induced neoangiogenesis, LDL-cholesterol trafficking and degrada
144 Inhibition of Tie2 resulted in impaired neoangiogenesis, leading to a delay in hematopoietic rec
146 VE-cadherin angiogenic complexes, levels of neoangiogenesis marker Endoglin, vascular density, and c
149 lial progenitor cell (EPC) function, in vivo neoangiogenesis, plaque development, and occlusive throm
154 HIF-1alpha pathway as a critical mediator of neoangiogenesis required for skeletal regeneration and s
156 ta also implicate DCs in regulation of tumor neoangiogenesis, suggesting a novel role of DCs in tumor
157 ERRgamma is a hypoxia-independent inducer of neoangiogenesis that can promote reparative revasculariz
160 owth by inducing newly formed blood vessels (neoangiogenesis) that sustain tumor cell viability and g
161 e we identify PML as a critical inhibitor of neoangiogenesis (the formation of new blood vessels) in
162 or and further production of VEGF to support neoangiogenesis, thereby favoring the development of the
163 F may provide a novel mechanism for inducing neoangiogenesis through both direct actions on local Trk
164 ic synergy correlates with the inhibition of neoangiogenesis through the downregulation of COX-2, iNO
165 vity to growth inhibitory signals, sustained neoangiogenesis, tissue invasiveness and migration capab
167 ting strategies that reduce inflammation and neoangiogenesis to reduce the incidence of restenosis.
168 cell proliferation, collagen deposition, and neoangiogenesis to the levels observed in control animal
170 cts that are preferentially expressed during neoangiogenesis: vascular endothelial growth factor rece
171 y stimulating podosome nucleation, motility, neoangiogenesis, vasculogenic mimicry, and osteoclastoge
172 ls play a key role in both tumorigenesis and neoangiogenesis via the production of matrix metalloprot
178 growth difference of tumor xenografts or in neoangiogenesis were found in beta3KOP mice, in contrast
179 erial inflammatory infiltrates and increased neoangiogenesis were observed in apoE(-/-) IFNAR(-/-) mi
180 non-ischemic ears or ischemic limbs induced neoangiogenesis, with a 2-fold increase in the capillary
181 cells of the newly formed capillaries during neoangiogenesis within malignant human brain tumors expr