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1 vent resistance could fulfill the promise of antiangiogenic therapy.
2 rtance, VEGF has been at the center stage of antiangiogenic therapy.
3 may mediate a mesenchymal-type resistance to antiangiogenic therapy.
4 ng for improvements in blood perfusion after antiangiogenic therapy.
5 vasculature, similar to that occurring with antiangiogenic therapy.
6 biomarkers exist to image tumor responses to antiangiogenic therapy.
7 sessing the response of vascularized PEDs to antiangiogenic therapy.
8 out-or before-angiogenesis or in response to antiangiogenic therapy.
9 GBM) to characterize the response of rGBM to antiangiogenic therapy.
10 patient care and monitoring the response to antiangiogenic therapy.
11 and 28 days after combined chemotherapy and antiangiogenic therapy.
12 ggesting COUP-TFII as a candidate target for antiangiogenic therapy.
13 n after 28 days of combined chemotherapy and antiangiogenic therapy.
14 in pancreatic tumors can predict response to antiangiogenic therapy.
15 -catenin, this may provide a good target for antiangiogenic therapy.
16 ontribute in inherent/acquired resistance to antiangiogenic therapy.
17 act as a surrogate marker of the benefit of antiangiogenic therapy.
18 s not been considered an important target in antiangiogenic therapy.
19 could be an effective approach for enhancing antiangiogenic therapy.
20 se-2 (MetAP2) represents a novel approach to antiangiogenic therapy.
21 tification of potential rational targets for antiangiogenic therapy.
22 o have a reduced growth response to targeted antiangiogenic therapy.
23 redict which mRCC patients will benefit from antiangiogenic therapy.
24 tors or markers for tumor vessel response to antiangiogenic therapy.
25 ing and monitoring tumor vessel responses to antiangiogenic therapy.
26 cusses promising avenues of investigation in antiangiogenic therapy.
27 cancer, suggesting possible new targets for antiangiogenic therapy.
28 ls and interstitium that are associated with antiangiogenic therapy.
29 essiveness and thus enhances the efficacy of antiangiogenic therapy.
30 ting both DLL4 and VEGF pathways may improve antiangiogenic therapy.
31 ibitors and that ATRs are useful targets for antiangiogenic therapy.
32 ring the tumor vasculature more resistant to antiangiogenic therapy.
33 se for monitoring tumor vascular response to antiangiogenic therapy.
34 tions for their development as biomarkers of antiangiogenic therapy.
35 rrently evaluated as potential biomarkers of antiangiogenic therapy.
36 rins on tumor blood vessels before and after antiangiogenic therapy.
37 etriotic growth and the efficacy of systemic antiangiogenic therapy.
38 flow in mouse tumors engineered to simulate antiangiogenic therapy.
39 ls but not changes in microvessel density in antiangiogenic therapy.
40 umor types that shows a clinical response to antiangiogenic therapy.
41 human tumors may represent a potential novel antiangiogenic therapy.
42 ctor and modulator of endostatin efficacy in antiangiogenic therapy.
43 uggest its usefulness in angioprevention and antiangiogenic therapy.
44 with implications for the rational design of antiangiogenic therapy.
45 target to endothelial cells for efficacious antiangiogenic therapy.
46 wide have received some form of experimental antiangiogenic therapy.
47 xamined potential surrogates for response to antiangiogenic therapy.
48 gnaling could serve as a marker of effective antiangiogenic therapy.
49 ly neovascularized and so may be amenable to antiangiogenic therapy.
50 o dynamic balance, which can be modulated by antiangiogenic therapy.
51 presents a promising strategy for delivering antiangiogenic therapy.
52 d could be helpful in selecting patients for antiangiogenic therapy.
53 umor progression can be restricted solely by antiangiogenic therapy.
54 pilimumab, 93 of whom had not received prior antiangiogenic therapy.
55 g responses to anticancer therapy, including antiangiogenic therapy.
56 herapies, especially for tumors treated with antiangiogenic therapy.
57 ted negative effects following withdrawal of antiangiogenic therapy.
58 th treatment-naive BCVA and BCVA outcomes in antiangiogenic therapy.
59 with clear-cell mRCC previously treated with antiangiogenic therapy.
60 inhibited tumor rebound after withdrawal of antiangiogenic therapy.
61 atic renal cell carcinoma (RCC) treated with antiangiogenic therapy.
62 nal measurement of ovarian tumor response to antiangiogenic therapy.
63 t to Nck as an emergent target for effective antiangiogenic therapy.
64 ve outcomes of patients with GBM who receive antiangiogenic therapy.
65 assessment of early treatment response after antiangiogenic therapy.
66 with Angpt/Tie2 has the potential to improve antiangiogenic therapy.
67 e an antitumor agent and open a new field of antiangiogenic therapy.
68 es is not necessarily decreased by effective antiangiogenic therapy.
69 2 followed tumor volume in studies featuring antiangiogenic therapy.
70 ectively block tumor progression and improve antiangiogenic therapy.
71 orafenib might be a ceiling for single-agent antiangiogenic therapy.
72 oit this seminal pathway and improve current antiangiogenic therapies.
73 oma has lent support to the increased use of antiangiogenic therapies.
74 which may represent a target for innovative antiangiogenic therapies.
75 implications for the design of both pro- and antiangiogenic therapies.
76 sensitive reporter of the hypoxic effects of antiangiogenic therapies.
77 hronic kidney disease and patients receiving antiangiogenic therapies.
78 s of patients with cancer who are undergoing antiangiogenic therapies.
79 one of the most potent cytokines targeted in antiangiogenic therapies.
80 intrinsic hormone resistance may respond to antiangiogenic therapies.
81 on is critically involved in the response to antiangiogenic therapies.
82 of both IL-8 and VEGF signaling may improve antiangiogenic therapies.
83 suggests indications for clinical trials of antiangiogenic therapies.
84 sis-related diseases and provide a guide for antiangiogenic therapies.
85 nificant implications for the development of antiangiogenic therapies.
86 s, and the potential activity of alternative antiangiogenic therapies.
87 allow for an improved response assessment to antiangiogenic therapies.
88 cells is critical for developing appropriate antiangiogenic therapies.
89 genic factors has important implications for antiangiogenic therapies.
90 creatic islets, and demonstrated efficacy of antiangiogenic therapies.
91 es attractive targets for the development of antiangiogenic therapies.
92 s that affect vascular permeability, such as antiangiogenic therapies.
93 ad previously received immune checkpoint and antiangiogenic therapies.
94 sent in GSC and are resistant to traditional antiangiogenic therapies.
95 condition associated with antiresorptive and antiangiogenic therapies.
96 , age, tumor type and involvement, and prior antiangiogenic therapies.
98 nd its cognate ligand apelin in VEGFA/VEGFR2 antiangiogenic therapy against distinct subtypes of GBM.
100 dentify novel targets for the development of antiangiogenic therapies aimed at the treatment of Kapos
102 to the application of immunotherapy alone or antiangiogenic therapy alone, which delayed the tumor gr
105 uation of the effectiveness of commonly used antiangiogenic therapies and determination of their opti
106 erlying mechanisms of resistance specific to antiangiogenic therapy and develop strategies to overcom
107 nism by which neuroblastoma can partly evade antiangiogenic therapy and may explain why experimental
108 gs challenge both the original rationale for antiangiogenic therapy and our understanding of the phys
110 a suggest mitochondria as a novel target for antiangiogenic therapy and provide mechanistic insights
111 -Met pathway in development of resistance to antiangiogenic therapy and suggests a potential strategy
112 dy tested the hypothesis that combination of antiangiogenic therapy and tumor immunotherapy of cancer
113 onse and nonenhancing tumor progression from antiangiogenic therapies, and pseudoprogression from rad
114 discuss successes and challenges of current antiangiogenic therapy, and highlight emerging antiangio
116 ased approaches to antifibrinolytic therapy, antiangiogenic therapy, and iron deficiency anemia manag
117 infiltration into tumors after withdrawal of antiangiogenic therapy, and lowering platelet counts mar
118 CC as an important candidate target gene for antiangiogenic therapy, and PDGF-CC inhibition may be of
119 on factors were selected chemotherapy, prior antiangiogenic therapy, and platinum-free interval.
120 num-free interval, residual tumour, previous antiangiogenic therapy, and study group language, and we
121 ikely reflects an onset of hypoxia caused by antiangiogenic therapy, and that beta1 inhibition is wel
123 umors were implanted, mice were treated with antiangiogenic therapy (anti-VEGFR-2 mAb, 1.4 mg/30 g bo
126 ly improved vascular function as a result of antiangiogenic therapy are explored, as are the implicat
127 nexpected finding is that repeated cycles of antiangiogenic therapy are followed by prolonged tumour
129 an be uniquely exploited in combination with antiangiogenic therapy as a promising new biologic appro
130 naling remains a major challenge for current antiangiogenic therapies, as these antiangiogenic agents
131 ivo appears to be crucial for the success of antiangiogenic therapy based on integrin antagonism.
132 RC-52 xenografts after treatment with either antiangiogenic therapy (bevacizumab or sorafenib) or tum
134 enal cell carcinoma (ccRCC) after failure of antiangiogenic therapies, but its activity on brain meta
136 e effect and to potentiate responsiveness to antiangiogenic therapy by concomitantly targeting ECM-mo
139 lioblastoma tumors, and the effectiveness of antiangiogenic therapy can be enhanced when combined wit
140 m between two angiostatic molecules and that antiangiogenic therapy can be used to inhibit ovarian ca
142 nd IFV profiles in tumors, we show here that antiangiogenic therapy can decrease IFP by decreasing th
145 ndings offer strong evidence that short-term antiangiogenic therapy can promote a transient vessel no
147 g laser photocoagulation, vitrectomy, and/or antiangiogenic therapy confirmed by an external adjudica
150 asiveness, paradoxically induced by the very antiangiogenic therapy designed to destroy the tumor.
153 om clinical trials of both proangiogenic and antiangiogenic therapies does not suggest that inhibitio
154 fied PDGF-DD as an important target gene for antiangiogenic therapy due to its pleiotropic effects on
158 r SK-RC-52 xenografts was not affected after antiangiogenic therapy, except in head and neck squamous
159 r reviews the evidence supporting the use of antiangiogenic therapies for adult soft tissue sarcomas.
162 tion would have a dose-sparing effect on rK5 antiangiogenic therapy for brain tumors and further sugg
164 Phase I clinical trials of endostatin as an antiangiogenic therapy for cancer, the protein was admin
165 ctions of RAC exosomes, we might improve the antiangiogenic therapy for CNV in age-related macular de
167 plications of alteration of Sp1 signaling in antiangiogenic therapy for pancreatic cancer and other c
168 ew challenge for uninterrupted and sustained antiangiogenic therapy for treatment of human cancers.
170 rker synaptophysin expression indicated that antiangiogenic therapy given at an early-stage disease r
178 istic of metastatic disease, and clinically, antiangiogenic therapies have shown value in the setting
179 Tumor-bearing mice treated with combined antiangiogenic therapy (IM862 or EMAP-II) and PDT had im
181 ma is a highly vascularized brain tumor, and antiangiogenic therapy improves its progression-free sur
184 ntal mechanisms that explain the efficacy of antiangiogenic therapies in retinal vascular disease.
185 r in advanced breast cancer, yet response to antiangiogenic therapies in this disease remains highly
186 r knowledge, this is the first evaluation of antiangiogenic therapy in a spontaneous autochthonous tu
187 jor role for Gal-1 as a tractable target for antiangiogenic therapy in advanced stages of the disease
195 c (CT) images, and predict tumor response to antiangiogenic therapy in patients with metastatic renal
196 s comparable to post-surgical treatment with antiangiogenic therapy in patients with mRCC, but it may
197 elucidate a novel mechanism of resistance to antiangiogenic therapy in which hypoxia-mediated autopha
198 to which their net extraction is improved by antiangiogenic therapy, in turn, depends on the extent t
199 e accurate monitoring of patient response to antiangiogenic therapies (including treatment suspension
201 plored the hypothesis that hypoxia caused by antiangiogenic therapy induces tumor cell autophagy as a
206 tion of continuous low-dose chemotherapy and antiangiogenic therapy is predicted to have the most sig
209 teration of Sp1 signaling on the efficacy of antiangiogenic therapy is unclear, yet understanding the
210 inflammatory agents, or other non-VEGF-based antiangiogenic therapies, is actively investigated.
211 rapy in certain hormone-dependent tumors and antiangiogenic therapy lead to vessel regression and hav
212 in the tumor microenvironment in response to antiangiogenic therapy, leading to drug resistance.
215 detected changes in tumor uptake after acute antiangiogenic therapy markedly earlier than any signifi
216 e with suppression of tumor growth, and that antiangiogenic therapies may be ineffective for melanoma
217 gimens, targeted molecular agents, and other antiangiogenic therapies may have activity in recurrent
218 ing strategies of combinations of immune and antiangiogenic therapies may lead to further advancement
219 bitors from a single tumor and suggests that antiangiogenic therapies may provide an avenue for futur
220 tumor vessel numbers and function following antiangiogenic therapy may also affect intratumoral deli
221 tic that complements and improves concurrent antiangiogenic therapy may be a promising treatment stra
222 In conclusion, tumor perfusion changes after antiangiogenic therapy may distinguish responders vs. no
226 s, whereas current treatment, and especially antiangiogenic therapy, may trigger spatial heterogeneit
227 -switch" model to explain how the targets of antiangiogenic therapy might change as a function of tum
229 eflects the viability of tumor tissue during antiangiogenic therapy more reliably than contrast-enhan
231 s of their growth and dissemination, optimal antiangiogenic therapy necessitates inhibition of multip
232 molecular aspects of tumor angiogenesis and antiangiogenic therapy of cancer in combination with con
234 e as an "unconventional" MMP-9 inhibitor for antiangiogenic therapy of cervical cancer and potentiall
236 ation of the blood-brain barrier (BBB) after antiangiogenic therapy of gliomas with bevacizumab may r
243 prior lines of therapy, including 1 or more antiangiogenic therapies or nivolumab plus ipilimumab.
244 decade and propose strategies for improving antiangiogenic therapy outcomes for malignant and nonmal
245 and whether IRE1alpha inhibition can enhance antiangiogenic therapy-previously found to be ineffectiv
247 munotherapy in simultaneous combination with antiangiogenic therapy provides a more efficient strateg
248 n integrin expression on tumor vessels after antiangiogenic therapy raises the possibility that integ
249 eted therapy (radiation/chemo) together with antiangiogenic therapies reduced GBM tumor size but incr
251 g force for tumor growth and metastasis, and antiangiogenic therapy represents one of the most promis
254 junctive CXCR4 antagonists may help overcome antiangiogenic therapy resistance, benefiting GBM patien
256 this time period of improved oxygenation by antiangiogenic therapy resulted in a synergistic delay i
257 city of the tumor vasculature in the face of antiangiogenic therapy (see the related article beginnin
260 paid to the microvascular endothelium and to antiangiogenic therapies, specific studies on the lympha
261 However, rapid emergence of resistance to antiangiogenic therapies, such as bevacizumab, greatly l
263 etabolic traits of tumors can be selected by antiangiogenic therapy suggests insights into the evolut
264 ailing hypotheses on how these tumors escape antiangiogenic therapy: switch to VEGF-independent angio
266 endometrium is a major limitation for use of antiangiogenic therapy targeting endometrial vessels.
267 herefore be a potential target for nontoxic, antiangiogenic therapy that could prevent tumor recurren
268 about unexpected complications arising from antiangiogenic therapy that may potentially involve TF.
269 owever, for long-term tumor-free survival by antiangiogenic therapy, the factors controlling tumor ne
270 reasing the growth rate of the tumor with an antiangiogenic therapy, the low-avidity repertoire of ne
271 Thus, beta1 integrins promote resistance to antiangiogenic therapy through potentiation of multiple
272 ective inhibition of antiapoptotic pathways, antiangiogenic therapy, tissue-selective therapy (includ
277 ncer that responds to checkpoint blockade or antiangiogenic therapy, uncovering a protective role by
280 ugh many ccRCC patients initially respond to antiangiogenic therapies, virtually all develop progress
284 e absence of VEGF, following radiotherapy or antiangiogenic therapy, we documented an increase in Ang
285 ve of this study was to evaluate alternative antiangiogenic therapies, which target multiple VEGF fam
286 ifferently to hypoxia and, as a consequence, antiangiogenic therapies will not be suitable for both s
288 yeloid cells contribute to refractoriness to antiangiogenic therapy with an anti-VEGF-A antibody.
292 nitor response of colon cancer xenografts to antiangiogenic therapy with functional and molecular US
293 perimental animals have shown that combining antiangiogenic therapy with radiation can enhance tumor
295 f disease manifestations and is a target for antiangiogenic therapy with the monoclonal antibody beva
296 tient management and monitor the response to antiangiogenic therapy with the optimum noninvasive imag
297 sized that immunotherapy in combination with antiangiogenic therapy would be a more efficient strateg
298 rgeting pBMDC influx along with radiation or antiangiogenic therapy would be critical to prevent vasc
299 t phase of human cancer may be vulnerable to antiangiogenic therapy years before symptoms, or before
300 ently been implicated in tumor resistance to antiangiogenic therapy, yet their precise involvement in