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1 combining antigen-specific immunotherapy and antiangiogenesis.
2 ereby eliciting notable tumor inhibition and antiangiogenesis.
3 ation, antiproliferation, antimigration, and antiangiogenesis.
4 ple receptor tyrosine kinases, exerts potent antiangiogenesis.
5 l of dominant-negative CCN2/CTGF mutants for antiangiogenesis.
6 marrow vascularization, suggesting a role in antiangiogenesis.
7 ased drug retention is a general response to antiangiogenesis.
8 FR-1 expression in tumor cells, but not with antiangiogenesis.
9 ding induction of apoptosis, cytostasis, and antiangiogenesis.
10  mechanisms suggested for this inhibition is antiangiogenesis.
11 as serum binding proteins on taxane-mediated antiangiogenesis.
12 iated antiproliferation, antimetastasis, and antiangiogenesis activities.
13    Attempts to identify surrogate markers of antiangiogenesis activity are currently ongoing, and may
14 reover, the thiazole analogues showed strong antiangiogenesis activity, blocking new blood vessel for
15 pical vehicle exhibited slight antitumor and antiangiogenesis activity.
16 el therapeutic target for dual antitumor and antiangiogenesis activity.
17                       A phase I trial of the antiangiogenesis agent cilengitide (EMD 121974), an alph
18 tified to predict outcome with the use of an antiangiogenesis agent for cancer.
19                    Bevacizumab was the first antiangiogenesis agent to gain approval by the Food and
20 cal data to identify the optimal dose for an antiangiogenesis agent, anti-EGFL7.
21 rived VEGF from an angiogenic factor into an antiangiogenesis agent.
22  briefly review data regarding anti-EGFR and antiangiogenesis agents before discussing the potential
23  The suppression of tumor blood perfusion by antiangiogenesis agents can be turned to therapeutic adv
24          This study confirms the activity of antiangiogenesis agents in advanced and recurrent cervic
25                                              Antiangiogenesis agents such as bevacizumab, a humanized
26 ally in tumor tissue they might be effective antiangiogenesis agents suitable for cancer therapy.
27     Patients with multiple myeloma receiving antiangiogenesis agents with chemotherapy and/or dexamet
28 stone deacetylase and proteosome inhibitors, antiangiogenesis agents, Fms-like tyrosine kinase 3 (FLT
29 ents with promise include 90 Y microspheres, antiangiogenesis agents, inhibitors of growth factors an
30             There are also ongoing trials of antiangiogenesis agents.
31 d thus validate VE-cad as a novel target for antiangiogenesis agents.
32 re development of this and similar agents as antiangiogenesis and anticancer drugs.
33 enesis and may be a viable drug candidate in antiangiogenesis and anticancer therapies.
34                                              Antiangiogenesis and antitumor efficacy were associated
35  angiogenin could have a combined benefit of antiangiogenesis and chemotherapy in treating prostate c
36  was essential for Nutlin-3-mediated retinal antiangiogenesis and disruption of the p53 transcription
37                          Therefore, combined antiangiogenesis and immune suppression will be more eff
38 ted to a synergistic mechanism that combines antiangiogenesis and photoinduced cancer immunotherapy.
39 the effective abrogation of scIL-12-mediated antiangiogenesis and T cell chemotaxis in mice receiving
40 F-kappaB) DNA binding, which is critical for antiangiogenesis, and that blocking the NF-kappaB pathwa
41            The use of VEGF antagonists as an antiangiogenesis approach offers a potential treatment f
42 s work may offer solutions for personalizing antiangiogenesis approaches and improving the outcome of
43  pathway may offer important new targets for antiangiogenesis approaches.
44 n is important for tumor growth and proposed antiangiogenesis as a novel approach to cancer therapy.
45  (SC-276) was advanced through antitumor and antiangiogenesis assays and was selected for development
46  (D)(LPR), a derivative molecule with strong antiangiogenesis attributes.
47                                              Antiangiogenesis-based cancer therapies, specifically th
48 s plays an important role in GBM growth, and antiangiogenesis-based therapies have shown clinical eff
49 g gene-based therapies, immunotherapies, and antiangiogenesis-based therapy.
50 t is suggested that the activity is based on antiangiogenesis, because in vitro tube formation is inh
51 tion, rapamycin (RAPA), which is used as the antiangiogenesis chemotherapeutic drug, can cutdown the
52                         Using these methods, antiangiogenesis compounds that inhibit Flk-1 tyrosine k
53 US Food and Drug Administration approved the antiangiogenesis drug bevacizumab for women with advance
54 r [Co(II)Co(II)(EcMetAP)] incubated with the antiangiogenesis drug fumagillin are also presented.
55 in skin angiogenesis and can serve for rapid antiangiogenesis drug screening.
56 eratrol (1), phenstatin (2c), and the cancer antiangiogenesis drug sodium combretastatin A-4 phosphat
57                          Recent approvals of antiangiogenesis drugs for clinical use in cancer and ma
58 hat MSMP inhibition combined with the use of antiangiogenesis drugs may be a new strategy to overcome
59  combination chemotherapies that incorporate antiangiogenesis drugs targeting VEGF receptor.
60  predict efficacy at the molecular level for antiangiogenesis drugs which are anticipated to result i
61 is orally bioavailable inhibitor exhibits an antiangiogenesis effect and a broad anticancer activity
62 s treated with combined drugs, suggesting an antiangiogenesis effect of this combination.
63                                  The in vivo antiangiogenesis effects mediated by chNKG2D-bearing T c
64 drug that is activated intratumorally, where antiangiogenesis-enhanced retention of the therapeutic m
65 ctor (pigment epithelium-derived factor), an antiangiogenesis factor (cornea-derived transcript 6), a
66 ondin-2 (TSP-2), has been shown to act as an antiangiogenesis factor in a carcinogen-induced model of
67 ted by a balance between proangiogenesis and antiangiogenesis factors and that this balance varies in
68                                         Host antiangiogenesis factors defend against tumor growth.
69 combine gene aberration-related therapy with antiangiogenesis for the treatment of advanced malignanc
70 ur study thus demonstrates that AAV-mediated antiangiogenesis gene therapy offers efficient and susta
71    Antigen-specific cancer immunotherapy and antiangiogenesis have emerged as two attractive strategi
72 hange could be used as an early predictor of antiangiogenesis in ectopic and orthotopic colon carcino
73 ectly with synergistic antiproliferation and antiangiogenesis in vitro.
74  assay and also in a mouse Matrigel model of antiangiogenesis in which 49 and 55 show significant inh
75 his barrier can sometimes be circumvented by antiangiogenesis-induced normalization of tumor vasculat
76 dicate that we have identified a more potent antiangiogenesis inhibitor peptide that may be used as a
77 compounds currently under evaluation include antiangiogenesis inhibitors and retinoids.
78 ial body of evidence supports the utility of antiangiogenesis inhibitors as a strategy to block or at
79                                              Antiangiogenesis is a promising approach to cancer thera
80                                              Antiangiogenesis is emerging as efficient strategy for t
81 pared with wild-type E7 DNA, suggesting that antiangiogenesis may have contributed to the antitumor e
82                         We hypothesized that antiangiogenesis mediated by TSR-containing proteins cou
83 stant tumors, indicating that an escape from antiangiogenesis occurred.
84 ng cell-cycle arrest, cell death, repair, or antiangiogenesis processes.
85             Compounds 1-3 showed interesting antiangiogenesis properties in an in vitro tubulogenic a
86 , and translational (anti-) angiogenesis and antiangiogenesis research.
87 therapy resistance to current strategies for antiangiogenesis.See related commentary by Amoozgar et a
88 olytically cleaved to release Endostatin, an antiangiogenesis signaling factor.
89 ent study provides a molecular framework for antiangiogenesis signaling, thus impinging on a myriad o
90                                              Antiangiogenesis strategies in particular appear promisi
91  the existing VEGF-A/VEGFR-2 signaling-based antiangiogenesis strategies.
92 retinoic acid (CRA) as a differentiation and antiangiogenesis strategy for prostate cancer.
93 r than VEGF alone, will be a novel efficient antiangiogenesis strategy to treat cancer.
94 us vector carrying TMD1 could be a promising antiangiogenesis strategy.
95 ronomic chemotherapy is attributed widely to antiangiogenesis, the significance of this mechanism rem
96  vascular endothelial growth factor-centered antiangiogenesis therapies, which mainly lead to vascula
97 e advantages over existing cytokine-targeted antiangiogenesis therapies.
98  may assist in the selection of patients for antiangiogenesis therapy and the development of this cla
99 arkers may explain why certain patients fail antiangiogenesis therapy and they may support the use of
100  EGFR kinase inhibitors may be effective for antiangiogenesis therapy by specifically targeting the t
101 s preexisting blood vessels of the tumor and antiangiogenesis therapy capitalize on the requirement o
102 t BH4 synthesis may be a rational target for antiangiogenesis therapy for tumors.
103                                              Antiangiogenesis therapy has become a vital part of the
104 -concept of the efficacy and tolerability of antiangiogenesis therapy in advanced cervical cancer.
105     Its highly vascular nature suggests that antiangiogenesis therapy might be useful.
106      Our studies imply that antivascular and antiangiogenesis therapy that results in severe glucose
107 PI3Kbeta inhibition may be a useful adjuvant antiangiogenesis therapy with sunitinib.
108  identifying patients who would benefit from antiangiogenesis therapy, and separating treatment respo
109 ctors underlying the resistance of cancer to antiangiogenesis therapy, we conducted genomic analyses
110 ity to improve conventional chemotherapy and antiangiogenesis therapy.
111 e that may enable more precise deployment of antiangiogenesis therapy.
112 eir early differential perfusion response to antiangiogenesis therapy.
113 ttractive strategy to overcome resistance to antiangiogenesis therapy.
114 f PLCgamma1 would be a compelling target for antiangiogenesis therapy.
115  and is potentially an attractive target for antiangiogenesis therapy.
116  be a new strategy to overcome resistance to antiangiogenesis therapy.
117 nto an apoptotic factor, a novel approach to antiangiogenesis therapy.
118 nes CD148 as a valuable molecular target for antiangiogenesis therapy.
119 bility might compromise the effectiveness of antiangiogenesis therapy.
120 ors represent critical molecular targets for antiangiogenesis therapy.
121 th may be accelerated following cessation of antiangiogenesis therapy; however, the underlying mechan
122                                        Using antiangiogenesis treatment to prevent corneal neovascula
123 These data support the concept that targeted antiangiogenesis, using virally mediated gene transfer,
124 roangiogenesis (Vegfr2, Ccr3, and Pdgfb) and antiangiogenesis (Vegfr1 and Unc5b) as targets of Notch
125 tin-like domain of TM-TM domain 1 (rTMD1)-in antiangiogenesis were investigated.

 
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