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1 at BMP4 interfered with the stabilization of tumor angiogenesis.
2 l cells and mesenchymal mural-like cells for tumor angiogenesis.
3 providing new information on its key role in tumor angiogenesis.
4 as a master transcription factor, modulates tumor angiogenesis.
5 proangiogenic factor VEGF-A and by increased tumor angiogenesis.
6 study has focused on the role of SFN in HCC tumor angiogenesis.
7 ctivity, VEGF production, tumor hypoxia, and tumor angiogenesis.
8 w that depletion of all microRNAs suppresses tumor angiogenesis.
9 blood facilitates tumor growth by promoting tumor angiogenesis.
10 mor blood vessels, and its blockade inhibits tumor angiogenesis.
11 Twist, a transcription factor that promotes tumor angiogenesis.
12 r 2 (VEGFR2) and stimulates VEGF-independent tumor angiogenesis.
13 contribute to tumor development by promoting tumor angiogenesis.
14 lls of the tumor microenvironment to promote tumor angiogenesis.
15 upus erythematosus, and basal cell carcinoma tumor angiogenesis.
16 5 is important in vascular remodeling during tumor angiogenesis.
17 etion by normoxic tumor cells and stimulated tumor angiogenesis.
18 y constitute a novel strategy for inhibiting tumor angiogenesis.
19 lls to produce and secrete VEGF-A augmenting tumor angiogenesis.
20 d offer a novel rational strategy to inhibit tumor angiogenesis.
21 the stromal tissue, where it contributes to tumor angiogenesis.
22 lucidate a novel function for soluble CEA in tumor angiogenesis.
23 umor microenvironment and, thereby, promotes tumor angiogenesis.
24 ing antibodies displayed opposing effects on tumor angiogenesis.
25 cantly inhibited tumor growth by suppressing tumor angiogenesis.
26 in a S100A8/A9-dependent manner and promotes tumor angiogenesis.
27 ning as a signaling molecule that stimulates tumor angiogenesis.
28 tumor protein laminin-411 in order to block tumor angiogenesis.
29 ity, suggesting a role for endogenous H2S in tumor angiogenesis.
30 l cells attenuated CEA-induced signaling and tumor angiogenesis.
31 of PI3K, contributes in an unexpected way to tumor angiogenesis.
32 inase domain of VEGFR-1 resulted in enhanced tumor angiogenesis.
33 atically hindered tumor growth and inhibited tumor angiogenesis.
34 y present a therapeutic opportunity to block tumor angiogenesis.
35 l proliferation, survival, invasiveness, and tumor angiogenesis.
36 a key feature of inflammatory disorders and tumor angiogenesis.
37 ding in tumor cells was highly correlated to tumor angiogenesis.
38 o-angiogenic genes, as well as the degree of tumor angiogenesis.
39 he identification of new targets involved in tumor angiogenesis.
40 cell mobilization and myeloid cell-dependent tumor angiogenesis.
41 gating and targeting the events that control tumor angiogenesis.
42 fy PRAK as a novel host factor essential for tumor angiogenesis.
43 to unlock the complex mechanisms regulating tumor angiogenesis.
44 eloid cells is critical for VEGF-independent tumor angiogenesis.
45 1/NF-kappaB/CXCL8: a new regulatory axis for tumor angiogenesis.
46 essential for endothelial cell motility and tumor angiogenesis.
47 d vessel development as well as pathological tumor angiogenesis.
48 lar endothelial growth factor (VEGF)-induced tumor angiogenesis.
49 isoform of TF also affects tumor growth and tumor angiogenesis.
50 in tumor stroma and may, thus, contribute to tumor angiogenesis.
51 c growth factors that play a pivotal role in tumor angiogenesis.
52 egs make significant direct contributions to tumor angiogenesis.
53 the effect of the BRAF inhibitor PLX4720 on tumor angiogenesis.
54 d alpha(V)beta(5)-integrin play key roles in tumor angiogenesis.
55 ed EPC homing to tumor tissue, and increased tumor angiogenesis.
56 mediated induction of IL-13(+) Th2 cells and tumor angiogenesis.
57 ndothelial cells, which is also required for tumor angiogenesis.
58 ay significantly inhibit melanoma growth and tumor angiogenesis.
59 Notch signaling has been implicated in tumor angiogenesis.
60 ligands for VEGFR-1, has been implicated in tumor angiogenesis.
61 significantly increases melanoma growth and tumor angiogenesis.
62 ltiple human malignancies, where it promotes tumor angiogenesis.
63 n, epithelial to mesenchymal transition, and tumor angiogenesis.
64 to suppress tumor growth through inhibiting tumor angiogenesis.
65 ein methylation and other PTMs in regulating tumor angiogenesis.
66 diminished VEGF-induced ear angiogenesis and tumor angiogenesis.
67 ack multiple myeloma tumor cell survival and tumor angiogenesis.
68 eduction in tumor size and the inhibition of tumor angiogenesis.
69 es endothelial cell proliferation to promote tumor angiogenesis.
70 igating the influence of therapies affecting tumor angiogenesis.
71 doppel as a potential therapeutic target for tumor angiogenesis.
72 ogenesis, VEGF-induced ear angiogenesis, and tumor angiogenesis.
73 GF signaling in TECs and selectively inhibit tumor angiogenesis.
74 ocesses, including inflammation, cancer, and tumor angiogenesis.
75 apping and high-resolution quantification of tumor angiogenesis.
76 could have implications for alcohol-induced tumor angiogenesis.
77 been implicated in VEGF-A regulation during tumor angiogenesis.
78 e variant of fibronectin (FN), a hallmark of tumor angiogenesis.
79 investigate the potential role of miR-497 in tumor angiogenesis.
80 s copper chelators have been used to inhibit tumor angiogenesis.
81 gands for cancer therapeutics by controlling tumor angiogenesis.
82 nontranscriptional mechanism, thus affecting tumor angiogenesis.
83 ppresses tumor growth in part by restraining tumor angiogenesis.
84 y tumor growth and metastasis by suppressing tumor angiogenesis.
85 essels, indicating that serglycin may affect tumor angiogenesis.
87 MDA PCa 118b, also significantly suppressed tumor angiogenesis accompanied with decreased tumor grow
88 these cells was suppressed via reductions in tumor angiogenesis after intraperitoneal treatment with
89 as also been shown to be capable of limiting tumor angiogenesis, although its underlying mechanism re
90 GBM effect of Ang-4 is mediated by promoting tumor angiogenesis and activating Erk1/2 kinase in GBM c
91 etic Tie-2 positive cells), which normalizes tumor angiogenesis and allows an adaptation of blood sup
92 was accompanied by a significant decrease in tumor angiogenesis and an increase in apoptosis index.
97 with autoimmune disease rapidly accelerates tumor angiogenesis and consequent tumor progression, par
98 vivo growth of human GBM cells by promoting tumor angiogenesis and directly activating extracellular
99 ults establish the novel effects of Ang-4 on tumor angiogenesis and GBM progression and suggest that
100 collagen structure in the tumor and inhibits tumor angiogenesis and glioblastoma multiforme growth in
101 l properties of extracellular matrix control tumor angiogenesis and glioblastoma progression is not c
102 and HIF-transcriptional targets involved in tumor angiogenesis and glycolysis, but did not affect HI
103 from the endothelium of adult mice inhibits tumor angiogenesis and growth by decreasing endothelial
104 ed with miR-497 mimic and applied to monitor tumor angiogenesis and growth by in vivo bioluminescent
107 ies demonstrated that the effects of aPLs on tumor angiogenesis and growth were dependent on tumor ce
110 EGFR-2 blocking antibodies similarly reduced tumor angiogenesis and growth; however, no additive inhi
111 finger protein 24), as a novel inhibitor of tumor angiogenesis and have demonstrated that ZNF24 exer
112 sults provide insight into the regulation of tumor angiogenesis and highlight ELTD1 as key player in
113 ion of ovarian cancer through enhancement of tumor angiogenesis and immunosuppressive networks that r
114 lizing microvasculature dynamics involved in tumor angiogenesis and in inflammatory joint diseases.
115 agents have often been successful in halting tumor angiogenesis and in regressing rapidly growing mou
116 M1 inhibited primary tumor growth, inhibited tumor angiogenesis and inflammatory cell recruitment and
117 mitogen-activated protein kinase signaling, tumor angiogenesis and inflammatory cell recruitment.
119 resulted in the coordinated diminishment of tumor angiogenesis and intravasation, both of which were
124 t on the mechanisms by which YKL-40 promotes tumor angiogenesis and malignancy, and thus provide a th
125 tte smoking; it simultaneously inhibits lung tumor angiogenesis and metastasis by catalyzing the form
126 dicated that AZD1480 can effectively inhibit tumor angiogenesis and metastasis mediated by STAT3 in s
127 In cancer, KISS1R has been implicated in tumor angiogenesis and metastasis, but a broader evaluat
134 thelial cells and showed severe reduction of tumor angiogenesis and metastatic growth, with minimal e
137 physical microenvironment has a key role in tumor angiogenesis and progression, the mechanism by whi
139 nal and hepatocellular carcinoma, suppresses tumor angiogenesis and promotes autophagy in tumor cells
140 Ron promotes prostate tumor growth, prostate tumor angiogenesis and prostate cancer cell survival in
141 e attempted to find the associations between tumor angiogenesis and radiomic imaging features from PE
142 , decreased orthotopic tumor growth, reduced tumor angiogenesis and recruitment of inflammatory cells
143 tronomic gemcitabine significantly inhibited tumor angiogenesis and reduced tumor perfusion and infla
144 TRPV4 channels to be critical regulators of tumor angiogenesis and represent a novel target for anti
148 MMP-14 have been reported to be crucial for tumor angiogenesis and the formation of metastasis, thus
149 that KOR agonists play an important role in tumor angiogenesis and this knowledge could lead to a no
150 nct proMMP-9 in the coordinate regulation of tumor angiogenesis and tumor cell dissemination, however
151 that tumor-derived PlGF negatively modulates tumor angiogenesis and tumor growth and may potentially
152 cental growth factor (PlGF) in modulation of tumor angiogenesis and tumor growth remains an enigma.
156 nction of effector T cells and a decrease in tumor angiogenesis and tumor infiltration by Treg cells.
158 ptor potential vanilloid 4 (TRPV4) regulates tumor angiogenesis and tumor vessel maturation via modul
159 nesis in an in vivo Matrigel plug assay, and tumor angiogenesis and tumorigenesis in a B16F10 melanom
161 ation between PlGF and VEGF in modulation of tumor angiogenesis and vascular remodeling is less under
162 mplicate AQP1 as an important determinant of tumor angiogenesis and, hence, as a potential drug targe
163 h endothelial cells induced by YKL-40 during tumor angiogenesis, and also enhance our understanding o
164 s overexpressed in many tumors, required for tumor angiogenesis, and blockade of RLIP76 results in tu
165 , e.g. wound healing, macrophage chemotaxis, tumor angiogenesis, and cancer invasion/metastasis.
166 tly inhibited SDF-1alpha-induced EPC homing, tumor angiogenesis, and decreased melanoma growth in viv
168 been associated with increased tumor growth, tumor angiogenesis, and metastatic potential in many mal
169 action of progranulin in cancer progression, tumor angiogenesis, and perhaps neurodegenerative diseas
170 s essential for embryonic vasculogenesis and tumor angiogenesis, and provides the proof-of-concept ev
172 proliferation, chemotaxis, homing, adhesion, tumor angiogenesis, and resistance to conventional and t
174 he enhancement of myeloid cell accumulation, tumor angiogenesis, and suppression of tumor immunity.
175 r E-selectin profoundly inhibits EPC homing, tumor angiogenesis, and tumor growth in human melanoma x
178 , endothelial cell-specific contributions to tumor angiogenesis are muddied by the use of a global kn
180 -FDG PET/CT is significantly associated with tumor angiogenesis as evaluated by immunohistochemistry
181 hts into the inhibitory effect of SFN on HCC tumor angiogenesis as well as tumor growth, and indicate
182 egulates integrin function, which facilitate tumor angiogenesis both in vitro and in mouse models.
183 therapeutic target for controlling not only tumor angiogenesis but also osteolytic bone metastasis i
184 tion, migration, invasion, tumor growth, and tumor angiogenesis, but also suppressed the mTOR-HIF pat
185 s a key regulator of HIF1alpha/VEGF-mediated tumor angiogenesis by antagonizing the crosstalk between
186 a2beta1 in mice results in reduced wound and tumor angiogenesis by cell-autonomous and extrinsic mech
187 Our experiments show that PKM2 promotes tumor angiogenesis by increasing endothelial cell prolif
188 ulates Gr1(+)CD11b(+) myeloid cell-dependent tumor angiogenesis by inhibiting the G-CSF-Bv8 signaling
189 tion of the microtubule cytoskeleton impairs tumor angiogenesis by inhibiting the hypoxia-inducible f
190 Furthermore, MMP9 enhances PKD2-mediated tumor angiogenesis by releasing extracellular matrix-bou
191 r results demonstrate that hTERT facilitates tumor angiogenesis by up-regulating VEGF expression thro
192 ant role of GAB2 overexpression in promoting tumor angiogenesis by upregulating expression of multipl
194 reased proliferation and remarkably enhanced tumor angiogenesis compared with those in wild type mice
195 tinct myeloid cell populations contribute to tumor angiogenesis, discuss current approaches in the cl
196 TEPA administration significantly inhibited tumor angiogenesis, down-regulated hypoxia-induced trans
197 reduced primary and metastatic NSCLC growth, tumor angiogenesis, endothelial Cyp2c44 expression, and
198 ar permeability factor VEGF-A as the primary tumor angiogenesis factor prompted the development of a
200 report that lal(-/-) ECs facilitated in vivo tumor angiogenesis, growth, and metastasis, largely by s
202 In vivo, ALK regulated VEGFA production and tumor angiogenesis in ALCL and NSCLC, and the treatment
203 To our surprise, atypical E2Fs suppressed tumor angiogenesis in all three cancer models, which is
205 otransplants showed reductions in growth and tumor angiogenesis in Bmx gene-deleted ((-/-)) mice, whe
206 t3 have opposite effects on tumor growth and tumor angiogenesis in both B16 melanoma and Lewis Lung C
208 ity on angiogenesis, and shows that impaired tumor angiogenesis in caveolin-1-null mice is, at least
212 e evidence that GAB2 is a novel regulator of tumor angiogenesis in NRAS-driven melanoma through regul
213 vascularization after hind limb ischemia and tumor angiogenesis in oncogene-induced mammary cancer, r
214 has been identified as a promising target in tumor angiogenesis in preclinical studies, and Dll4 inhi
217 ulation of cancer-associated fibroblasts and tumor angiogenesis in the ovarian cancer microenvironmen
218 the BMP4/TSP1 loop paracrinically suppressed tumor angiogenesis in the tumor microenvironment, which
220 , temsirolimus, but not Ku0063794, decreased tumor angiogenesis in vivo, and decreased the viability
224 r both tumor cell proliferation/survival and tumor angiogenesis, in both normal and malignant myeloid
225 ese three miRs is involved in the control of tumor angiogenesis, indicating an option in the treatmen
228 ) receptor system controls developmental and tumor angiogenesis, inflammatory vascular remodeling, an
231 olid tumors, and its expression is linked to tumor angiogenesis, invasion, metastasis, and prognosis.
232 d HIF-2alpha), transcriptional regulators of tumor angiogenesis, invasion, survival, and glucose util
243 ngiogenesis assays show that B cell-mediated tumor angiogenesis is mainly dependent on the induction
250 ew blood vessels in tumors, a process termed tumor angiogenesis, is a crucial step during oncogenic p
251 low-dose Cilengitide and Verapamil increases tumor angiogenesis, leakiness, blood flow, and Gemcitabi
252 umorigenesis through its TSR1 by suppressing tumor angiogenesis, likely by down-regulating pro-angiog
253 n of hypoxia-inducible factor 1 (HIF-1) with tumor angiogenesis, metastasis, and patient mortality.
255 udy we discovered that atypical E2Fs control tumor angiogenesis, one of the hallmarks of cancer.
256 ology, provides a model for diseases such as tumor angiogenesis or thrombosis and serves as a startin
257 ing axis that promotes GBM cell survival and tumor angiogenesis, particularly in necrotic mesenchymal
260 ing tumors and are believed to contribute to tumor angiogenesis, possibly through secretion of CSF-2
263 pathologies, including ischemia/reperfusion, tumor angiogenesis, pulmonary edema, sepsis, and acute l
267 exhibited defects in both developmental and tumor angiogenesis, responses that require endothelial c
268 ance of VEGFR2 signaling toward uncontrolled tumor angiogenesis, resulting in dysfunctional tumor vas
269 s are part of a balance mechanism regulating tumor angiogenesis, serving as intrinsic microenvironmen
270 ulation, leading to excessive stimulation of tumor angiogenesis, suppression of tumor immune response
271 ough telomerase is thought to be involved in tumor angiogenesis, the evidence and underlying mechanis
272 a role in embryonic vascular development and tumor angiogenesis, the molecular mechanisms that underl
273 been established as a critical regulator of tumor angiogenesis, the role of mechanical signaling in
274 damage response, metastasis, immune escape, tumor angiogenesis, the Warburg effect and oncogene addi
276 Here we demonstrate that TAp73 regulates tumor angiogenesis through repression of proangiogenic a
277 We also found that activated PAR-2 enhanced tumor angiogenesis through the release of vascular endot
278 tresses and play critical roles in promoting tumor angiogenesis, tissue remodeling, and immunosuppres
280 d tumor growth is correlated with diminished tumor angiogenesis, together with reduced tumor cell pro
281 ce, UPI peptide markedly impaired functional tumor angiogenesis, tumor growth, and metastasis, result
282 novel duality for decorin as a suppressor of tumor angiogenesis under normoxia by simultaneously down
283 mTORC1/2 dual inhibition on VEGF production, tumor angiogenesis, vascular regression, and vascular re
284 , e.g. wound healing, macrophage chemotaxis, tumor angiogenesis, vascular repair, and cancer invasion
285 ession of ENOX1 impairs surrogate markers of tumor angiogenesis/vasculogenesis, providing support for
286 ry tumor growth and metastasis by inhibiting tumor angiogenesis via selective inhibition of endotheli
287 we showed that BMP4 paracrinically inhibited tumor angiogenesis via the induction of Thrombospondin-1
288 epsins--proteins involved in endocytosis--in tumor angiogenesis via their modulation of VEGF signalin
291 migration (microinvasion), tumor growth, and tumor angiogenesis was higher compared with Pak6 knockdo
294 molecular mechanisms underlying Hh-mediated tumor angiogenesis, we established an Hh-sensitive angio
296 whether ligand-driven Hh signaling promotes tumor angiogenesis, we found that Hh antagonism reduced
297 Consistent with roles for IL6 in promoting tumor angiogenesis, we found that MEDI5117 inhibited the
298 ells markedly reduced tumor take, growth and tumor angiogenesis, whereas reexpression of integrin bet
299 meric PKM2 possess the activity in promoting tumor angiogenesis, which is consistent with the observa
300 n feature in a variety of cancers, targeting tumor angiogenesis with scVEGF/(177)Lu warrants further
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