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1 ies, nitric oxide synthetase inhibitors, and antiangiogenic agents).
2 lite of estradiol, is a potent antitumor and antiangiogenic agent.
3 t a specific inhibitor of Ang2 can act as an antiangiogenic agent.
4 C1 domain contains endostatin (ES), a potent antiangiogenic agent.
5  (and not a possible contaminant) acts as an antiangiogenic agent.
6 ential applicability in cancer therapy as an antiangiogenic agent.
7 C single-arm studies that did not include an antiangiogenic agent.
8 during tumorigenesis and its potential as an antiangiogenic agent.
9 D was also observed after treatment with the antiangiogenic agent.
10  form of syntaxin 6 has good potential as an antiangiogenic agent.
11 gment of plasminogen, is a potent endogenous antiangiogenic agent.
12 -escalating protocol for endostatin, a novel antiangiogenic agent.
13 ck of tumor-homing capability of the current antiangiogenic agents.
14 nts for thyroid cancers, acting primarily as antiangiogenic agents.
15 ast cancer treated with chemotherapeutic and antiangiogenic agents.
16 nal therapies are enhanced or compromised by antiangiogenic agents.
17 at bind to tumor blood vessels normalized by antiangiogenic agents.
18  the intrinsic capacity to generate pro- and antiangiogenic agents.
19 ed in any therapeutic strategy incorporating antiangiogenic agents.
20 s well as a factor in guiding treatment with antiangiogenic agents.
21 bination with other antiproliferative and/or antiangiogenic agents.
22 e therapeutic efficacy of iron chelators and antiangiogenic agents.
23 o those of continuous treatment with various antiangiogenic agents.
24 erapeutic applications as antimetastatic and antiangiogenic agents.
25 evaluation of novel thalidomide analogues as antiangiogenic agents.
26 with the emerging class of drugs that act as antiangiogenic agents.
27 ctory" to produce high circulating levels of antiangiogenic agents.
28 ncer prevention and treatment programs or as antiangiogenic agents.
29 nant lesions in check, a role well-suited to antiangiogenic agents.
30  to develop optimum treatment strategies for antiangiogenic agents.
31 ionale for improved liver preservation using antiangiogenic agents.
32 an be used to evaluate efficacy of candidate antiangiogenic agents.
33  evaluated except when assessing response to antiangiogenic agents.
34 oting effective subsequent therapy including antiangiogenic agents.
35 st experience of maintenance therapy is with antiangiogenic agents.
36 stoma has been the therapeutic evaluation of antiangiogenic agents.
37  using lower "vascular normalizing" doses of antiangiogenic agents.
38 hemorrhage in patients with HCC treated with antiangiogenic agents.
39 -1 and HS6ST-2 as potential targets of novel antiangiogenic agents.
40 received no therapy or chemoradiation but no antiangiogenic agents.
41 asis after withdrawal of treatment with some antiangiogenic agents.
42 harmacodynamic and predictive biomarkers for antiangiogenic agents.
43 sed therapies, circulating tumor markers and antiangiogenic agents.
44 s been observed using extended-dose TMZ with antiangiogenic agents.
45 ealing the potential for Bcl-2 inhibitors as antiangiogenic agents.
46 angiogenic drive as well as the mechanism of antiangiogenic agents.
47 D, such as antioxidants, iron chelators, and antiangiogenic agents.
48 Similarly, combination of docetaxel with the antiangiogenic agent 2-methoxyestradiol also overcomes t
49                              Combinations of antiangiogenic agents (AAs) with cytotoxic agents have s
50 we show that they are remarkably synergistic antiangiogenic agents able to inhibit both the growth an
51 ing preclinical models further suggests that antiangiogenic agents actually increase invasive and met
52    We studied the effect of adding the novel antiangiogenic agent aflibercept (also known as ziv-afli
53 iled to show an overall survival benefit for antiangiogenic agents alone or in combination with chemo
54 dothelial Akt signaling, making rapamycin an antiangiogenic agent and endothelial Akt pathway inhibit
55            However, TSRI265 acts as a potent antiangiogenic agent and thereby blocks tumor growth in
56  effective way of monitoring the efficacy of antiangiogenic agents and as a proxy measure of perfusio
57                                     However, antiangiogenic agents and HIF-2 inhibitors have limited
58 tant efficacy information for VEGF-dependent antiangiogenic agents and the role of VEGF in cancer bio
59 ities, including matrix-targeting therapies, antiangiogenic agents, and immune-stimulatory drugs.
60 motherapy and radiotherapy), targeted drugs, antiangiogenic agents, and immunotherapy, including chec
61 cell stimulation limits the effectiveness of antiangiogenic agents, and suggest that to improve patie
62                                          The antiangiogenic agent apatinib has been shown to clinical
63 ic target of rapamycin (mTOR) inhibitors and antiangiogenic agents appear promising and are being pur
64                    It is possible that other antiangiogenic agents are also amenable to topical appli
65 strating synergistic antitumor activity when antiangiogenic agents are combined with cytotoxic agents
66 al in colorectal cancer) and a range of such antiangiogenic agents are currently in development.
67                            A large number of antiangiogenic agents are in development, however, new w
68 ay be a unique target in situations in which antiangiogenic agents are withdrawn, and dual targeting
69 of renal cell carcinoma, the expanded use of antiangiogenic agents as well as interest in other inhib
70 mination of the response to therapy with the antiangiogenic agent axitinib, a multiple receptor tyros
71 hemotherapy regimens and the addition of the antiangiogenic agent bevacizumab (B).
72                                          The antiangiogenic agent bevacizumab has been approved for t
73 isk of venous thromboembolism with the novel antiangiogenic agent bevacizumab, a recombinant humanize
74                                              Antiangiogenic agents block the effects of tumor-derived
75 human tumor xenografts were treated with the antiangiogenic agent brivanib alaninate, which is curren
76 rting an alternative hypothesis-that certain antiangiogenic agents can also transiently "normalize" t
77                                        Thus, antiangiogenic agents can be used to increase tumor drug
78 Preclinical and clinical evidence shows that antiangiogenic agents can decrease tumor vessel permeabi
79  disrupting agent ZD6126 (200 mg/kg), or the antiangiogenic agent cediranib (6 mg/kg, daily).
80 uch strategies involve the use of endogenous antiangiogenic agents, chemotherapy, gene therapy, antia
81 st that definitive clinical trials combining antiangiogenic agent combinations with docetaxel are war
82                                              Antiangiogenic agents combined with chemotherapy have ef
83  Identification of predictive biomarkers for antiangiogenic agents continues to be elusive and remain
84  targeting agent, combretastatin A4P, or the antiangiogenic agent, contortrostatin, promotes transcri
85                    Our findings suggest that antiangiogenic agents could be effective in the treatmen
86 g material for the synthesis of LY317615, an antiangiogenic agent currently under development at Eli
87  addition, a subset of patients treated with antiangiogenic agents develop tumor recurrence character
88 icroarray analysis, the effects of two known antiangiogenic agents (endostatin and fumagillin) on the
89 ine kinase inhibitor sunitinib is used as an antiangiogenic agent for the treatment of several types
90 pport the combination of AXL inhibitors with antiangiogenic agents for advanced ccRCC.
91 pport the development of SPHK1 inhibitors as antiangiogenic agents for cancer therapy.
92 (5) integrin have entered clinical trials as antiangiogenic agents for cancer treatment but generally
93 design of tight-binding inhibitors of Ang as antiangiogenic agents for human therapy.
94 ific aspects of NV in the retina and to test antiangiogenic agents for inhibition of intraretinal and
95 pport the combination of AXL inhibitors with antiangiogenic agents for the treatment of RCC.
96 t targeting this pathway may yield effective antiangiogenic agents for treatment of cancer and other
97                                          The antiangiogenic agent fumagillin (Fg) and its analog TNP-
98 intermediate for side-chain analogues of the antiangiogenic agent fumagillin.
99                                 In addition, antiangiogenic agents, gene therapy, molecular targeting
100                 The use of thalidomide as an antiangiogenic agent has met with only limited success i
101                 Vascular normalization using antiangiogenic agents has been proposed as a means to im
102 understanding of the mechanisms of action of antiangiogenic agents has hindered optimization and broa
103 ination of immune checkpoint inhibitors with antiangiogenic agents has revolutionized the treatment l
104 ieved over the past few years, and the first antiangiogenic agents have been recently approved for us
105                                              Antiangiogenic agents have established efficacy in the t
106                                     However, antiangiogenic agents have limited efficacy in cancer th
107                         Clinical trials with antiangiogenic agents have not been able to validate pla
108 ars of preclinical and clinical development, antiangiogenic agents have recently entered the clinic a
109                                              Antiangiogenic agents have the potential to modulate the
110 ammalian target of rapamycin inhibitors, and antiangiogenic agents, have shown significant efficacy i
111 low proliferative tumor while lower doses of antiangiogenic agents improve drug penetration in a poor
112                               Combination of antiangiogenic agents improves gemcitabine response, wit
113 e results show that VEGF-A(165)b is a potent antiangiogenic agent in a mouse model of age-related mac
114             Epothilone B may be an effective antiangiogenic agent in a variety of tumor types.
115 ized and nonrandomized studies evaluating an antiangiogenic agent in HCC showed that whereas the use
116 s led to the evaluation of thalidomide as an antiangiogenic agent in the treatment of several cancers
117 tients, our study suggests a strategy to use antiangiogenic agents in breast cancer more effectively
118                                        Novel antiangiogenic agents in cancer treatment such as bevaci
119 this article, we review the recent data with antiangiogenic agents in NSCLC and their implications fo
120  in clinical investigation and practice with antiangiogenic agents in patients with ovarian cancer, w
121 wever, little is known about the efficacy of antiangiogenic agents in pediatric malignancies.
122  trials reveal only limited effectiveness of antiangiogenic agents in prolonging patient survival.
123 oxygenase 2 (COX-2) inhibitors are promising antiangiogenic agents in several preclinical models.
124  these enzymes are currently being tested as antiangiogenic agents in various malignancies.
125       Strategies to safely incorporate novel antiangiogenic agents into combined-modality therapy in
126     Additionally, the combination of several antiangiogenic agents is also being explored.
127                       One biomarker-PEDF, an antiangiogenic agent-is a novel, predictive biomarker of
128 proval of an anti-VEGF antibody as the first antiangiogenic agent, many patients with cancer and ocul
129  and suggest that a combination therapy with antiangiogenic agents may be a particularly promising ap
130                    The clinical potential of antiangiogenic agents may be increased by combining them
131                  These results indicate that antiangiogenic agents may not be beneficial in unselecte
132       Ligand-targeted nanotherapy to deliver antiangiogenic agents may represent an effective way to
133 d from rats pretreated with three well-known antiangiogenic agents (minocycline, interferon alfa-2b,
134 ts, toxicities, and resistance mechanisms to antiangiogenic agents must be considered as these therap
135 e tumor regression and to maintain dormancy, antiangiogenic agents need to be chronically administere
136                        Parstatin is a potent antiangiogenic agent of ocular neovascularization and ma
137 nvestigated combinations of gemcitabine with antiangiogenic agents of various mechanisms for PDAC, in
138                                        Since antiangiogenic agents often exert an indirect, cytostati
139 n to the clinician on the effect of specific antiangiogenic agents on individual tumors.
140                               The effects of antiangiogenic agents on molecules and processes that al
141  be used to screen for safer antiprogestins, antiangiogenic agents, or for compounds that reactivate
142 ntaining bisphosphonates, a RANKL inhibitor, antiangiogenic agents, or mTOR inhibitors.
143 ndeed, we demonstrated that judicious use of antiangiogenic agents--originally designed to starve tum
144                  Further research with novel antiangiogenic agents, particularly in the maintenance s
145 ombined therapy with a FAK inhibitor and the antiangiogenic agents pazopanib and bevacizumab reduced
146                                              Antiangiogenic agents prevent the formation of new tumou
147                                              Antiangiogenic agents produce high radiographic response
148 sociated with increased thrombospondin-1 (an antiangiogenic agent) production and small vessel occlus
149 , cellular therapies, other immunotherapies, antiangiogenic agents, radiotherapy, cryotherapy and som
150 es that the most efficacious applications of antiangiogenic agents rely upon a combination with cytot
151 itargeted approach involving selective local antiangiogenic agents should contribute to prevention of
152       Treatment of RCC in nude mice with the antiangiogenic agent sorafenib resulted in markedly decr
153 nt glioblastoma (GBM) are often treated with antiangiogenic agents, such as bevacizumab (BEV).
154  the possibility of effective treatment with antiangiogenic agents, such as endostatin.
155 PET after longitudinal administration of the antiangiogenic agent sunitinib (a 2-wk dosing regimen).
156 er administration of the clinically relevant antiangiogenic agent sunitinib revealed a reduction in t
157  a standard clinical treatment course of the antiangiogenic agent sunitinib.
158 lioblastoma xenografts to treatment with the antiangiogenic agent sunitinib.
159 poxia in human breast cancer xenografts, the antiangiogenic agents sunitinib and bevacizumab increase
160  tyrosine kinase inhibitor), bevacizumab (an antiangiogenic agent), tanespimycin (a heat shock protei
161 r current antiangiogenic therapies, as these antiangiogenic agents target normal vasculature as well
162  of gene therapy for systemic delivery of an antiangiogenic agent targeting an endothelium-specific r
163                         Pazopanib is an oral antiangiogenic agent targeting VEGF receptors 1, 2, and
164 e with most of the standard chemotherapeutic antiangiogenic agents tested: cortisone acetate, vincris
165                    Linomide is a p.o. active antiangiogenic agent that has been demonstrated to be ef
166                          Apatinib is a novel antiangiogenic agent that targets vascular endothelial g
167 angiogenic agents with chemotherapy, or with antiangiogenic agents that also directly target the canc
168 present study shows the potential utility of antiangiogenic agents that target the endothelium-specif
169 ing in single-arm phase 2 studies evaluating antiangiogenic agents, this risk for all events (OR 4.34
170 ablish angiostatin as an antitumorigenic and antiangiogenic agent through a mechanism implicating tum
171       Preclinical studies suggested that the antiangiogenic agent TNP-470 was synergistic with cytoto
172         PDT followed by administration of an antiangiogenic agent, TNP-470, abolished this increase a
173                     The addition of specific antiangiogenic agents to differentiation therapy or chem
174  concert, from basic mechanisms of action of antiangiogenic agents to new combination approaches to c
175                                      Current antiangiogenic agents used to treat cancer only partiall
176 therapy-mediated approach to the delivery of antiangiogenic agents using adeno-associated virus (AAV)
177 nution of dysplastic microvasculature by the antiangiogenic agent, vascular endothelial growth factor
178 to the preovulatory stage in the presence of antiangiogenic agent, VEGFR-2-neutralizing Ab's.
179    The mechanism of action of these drugs as antiangiogenic agents was 2-fold.
180 patients treated with extended-dose TMZ with antiangiogenic agents was caused by TMZ alone.
181    The potential to heighten the efficacy of antiangiogenic agents was explored in this study based o
182                           Seeking PEDF-based antiangiogenic agents we generated and tested peptides r
183 imilar pattern of expression for both of the antiangiogenic agents we tested.
184 s a physiological target for the Fg class of antiangiogenic agents, we have generated a conditional M
185 her than rectal resection, immunotherapy, or antiangiogenic agents were excluded.
186    We hypothesized that thalidomide, an oral antiangiogenic agent, when combined with chemotherapy, a
187 e to therapy, particularly in the setting of antiangiogenic agents, which confound the interpretation
188                   The VTAs are distinct from antiangiogenic agents, which prevent new blood vessel fo
189                                              Antiangiogenic agents, which target normal, proliferatin
190 valuate the strategy of combining a putative antiangiogenic agent with a cytotoxic agent in patients
191                         Thus, orlistat is an antiangiogenic agent with a novel mechanism of action.
192                              Sorafenib is an antiangiogenic agent with activity in renal cancer.
193                Combinations of more than one antiangiogenic agent with gemcitabine were generally mor
194 a rationale for the exploration of combining antiangiogenic agents with ACT for the treatment of pati
195 me primarily with the use of combinations of antiangiogenic agents with chemotherapy, or with antiang
196 ofiling of tumors, and new ways of combining antiangiogenic agents with cytotoxic agents may lead to
197 tion with cell cycle-dependent chemotherapy, antiangiogenic agents with hypoxia-inducible factor-1 in
198                                    Combining antiangiogenic agents with multiple mechanisms of action
199 g and DCE CT can depict vascular response to antiangiogenic agents with response evident at day 7.

 
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