ライフサイエンスコーパス: antiangiogenic agent

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 s well as a factor in guiding treatment with antiangiogenic agents.

14 at bind to tumor blood vessels normalized by antiangiogenic agents.

15 the intrinsic capacity to generate pro- and antiangiogenic agents.

16 ed in any therapeutic strategy incorporating antiangiogenic agents.

17 bination with other antiproliferative and/or antiangiogenic agents.

18 e therapeutic efficacy of iron chelators and antiangiogenic agents.

19 erapeutic applications as antimetastatic and antiangiogenic agents.

20 evaluation of novel thalidomide analogues as antiangiogenic agents.

21 st experience of maintenance therapy is with antiangiogenic agents.

22 stoma has been the therapeutic evaluation of antiangiogenic agents.

23 with the emerging class of drugs that act as antiangiogenic agents.

24 ctory" to produce high circulating levels of antiangiogenic agents.

25 using lower "vascular normalizing" doses of antiangiogenic agents.

26 ncer prevention and treatment programs or as antiangiogenic agents.

27 nant lesions in check, a role well-suited to antiangiogenic agents.

28 to develop optimum treatment strategies for antiangiogenic agents.

29 ionale for improved liver preservation using antiangiogenic agents.

30 an be used to evaluate efficacy of candidate antiangiogenic agents.

31 o those of continuous treatment with various antiangiogenic agents.

32 hemorrhage in patients with HCC treated with antiangiogenic agents.

33 -1 and HS6ST-2 as potential targets of novel antiangiogenic agents.

34 received no therapy or chemoradiation but no antiangiogenic agents.

35 asis after withdrawal of treatment with some antiangiogenic agents.

36 harmacodynamic and predictive biomarkers for antiangiogenic agents.

37 sed therapies, circulating tumor markers and antiangiogenic agents.

38 s been observed using extended-dose TMZ with antiangiogenic agents.

39 ealing the potential for Bcl-2 inhibitors as antiangiogenic agents.

40 angiogenic drive as well as the mechanism of antiangiogenic agents.

41 D, such as antioxidants, iron chelators, and antiangiogenic agents.

42 oting effective subsequent therapy including antiangiogenic agents.

43 nal therapies are enhanced or compromised by antiangiogenic agents.

44 Similarly, combination of docetaxel with the antiangiogenic agent 2-methoxyestradiol also overcomes t

45 Combinations of antiangiogenic agents (AAs) with cytotoxic agents have s

46 we show that they are remarkably synergistic antiangiogenic agents able to inhibit both the growth an

47 ing preclinical models further suggests that antiangiogenic agents actually increase invasive and met

48 We studied the effect of adding the novel antiangiogenic agent aflibercept (also known as ziv-afli

49 iled to show an overall survival benefit for antiangiogenic agents alone or in combination with chemo

50 dothelial Akt signaling, making rapamycin an antiangiogenic agent and endothelial Akt pathway inhibit

51 However, TSRI265 acts as a potent antiangiogenic agent and thereby blocks tumor growth in

52 tant efficacy information for VEGF-dependent antiangiogenic agents and the role of VEGF in cancer bio

53 motherapy and radiotherapy), targeted drugs, antiangiogenic agents, and immunotherapy, including chec

54 cell stimulation limits the effectiveness of antiangiogenic agents, and suggest that to improve patie

55 ic target of rapamycin (mTOR) inhibitors and antiangiogenic agents appear promising and are being pur

56 It is possible that other antiangiogenic agents are also amenable to topical appli

57 strating synergistic antitumor activity when antiangiogenic agents are combined with cytotoxic agents

58 al in colorectal cancer) and a range of such antiangiogenic agents are currently in development.

59 A large number of antiangiogenic agents are in development, however, new w

60 ay be a unique target in situations in which antiangiogenic agents are withdrawn, and dual targeting

61 of renal cell carcinoma, the expanded use of antiangiogenic agents as well as interest in other inhib

62 mination of the response to therapy with the antiangiogenic agent axitinib, a multiple receptor tyros

63 The antiangiogenic agent bevacizumab has been approved for t

64 isk of venous thromboembolism with the novel antiangiogenic agent bevacizumab, a recombinant humanize

65 Antiangiogenic agents block the effects of tumor-derived

66 human tumor xenografts were treated with the antiangiogenic agent brivanib alaninate, which is curren

67 rting an alternative hypothesis-that certain antiangiogenic agents can also transiently "normalize" t

68 Thus, antiangiogenic agents can be used to increase tumor drug

69 Preclinical and clinical evidence shows that antiangiogenic agents can decrease tumor vessel permeabi

70 disrupting agent ZD6126 (200 mg/kg), or the antiangiogenic agent cediranib (6 mg/kg, daily).

71 uch strategies involve the use of endogenous antiangiogenic agents, chemotherapy, gene therapy, antia

72 st that definitive clinical trials combining antiangiogenic agent combinations with docetaxel are war

73 Identification of predictive biomarkers for antiangiogenic agents continues to be elusive and remain

74 targeting agent, combretastatin A4P, or the antiangiogenic agent, contortrostatin, promotes transcri

75 Our findings suggest that antiangiogenic agents could be effective in the treatmen

76 g material for the synthesis of LY317615, an antiangiogenic agent currently under development at Eli

77 addition, a subset of patients treated with antiangiogenic agents develop tumor recurrence character

78 icroarray analysis, the effects of two known antiangiogenic agents (endostatin and fumagillin) on the

79 ine kinase inhibitor sunitinib is used as an antiangiogenic agent for the treatment of several types

80 pport the development of SPHK1 inhibitors as antiangiogenic agents for cancer therapy.

81 (5) integrin have entered clinical trials as antiangiogenic agents for cancer treatment but generally

82 design of tight-binding inhibitors of Ang as antiangiogenic agents for human therapy.

83 ific aspects of NV in the retina and to test antiangiogenic agents for inhibition of intraretinal and

84 t targeting this pathway may yield effective antiangiogenic agents for treatment of cancer and other

85 The antiangiogenic agent fumagillin (Fg) and its analog TNP-

86 intermediate for side-chain analogues of the antiangiogenic agent fumagillin.

87 In addition, antiangiogenic agents, gene therapy, molecular targeting

88 The use of thalidomide as an antiangiogenic agent has met with only limited success i

89 Vascular normalization using antiangiogenic agents has been proposed as a means to im

90 understanding of the mechanisms of action of antiangiogenic agents has hindered optimization and broa

91 ieved over the past few years, and the first antiangiogenic agents have been recently approved for us

92 Antiangiogenic agents have established efficacy in the t

93 Clinical trials with antiangiogenic agents have not been able to validate pla

94 ars of preclinical and clinical development, antiangiogenic agents have recently entered the clinic a

95 Antiangiogenic agents have the potential to modulate the

96 Combination of antiangiogenic agents improves gemcitabine response, wit

97 e results show that VEGF-A(165)b is a potent antiangiogenic agent in a mouse model of age-related mac

98 Epothilone B may be an effective antiangiogenic agent in a variety of tumor types.

99 ized and nonrandomized studies evaluating an antiangiogenic agent in HCC showed that whereas the use

100 s led to the evaluation of thalidomide as an antiangiogenic agent in the treatment of several cancers

101 tients, our study suggests a strategy to use antiangiogenic agents in breast cancer more effectively

102 Novel antiangiogenic agents in cancer treatment such as bevaci

103 this article, we review the recent data with antiangiogenic agents in NSCLC and their implications fo

104 in clinical investigation and practice with antiangiogenic agents in patients with ovarian cancer, w

105 wever, little is known about the efficacy of antiangiogenic agents in pediatric malignancies.

106 trials reveal only limited effectiveness of antiangiogenic agents in prolonging patient survival.

107 oxygenase 2 (COX-2) inhibitors are promising antiangiogenic agents in several preclinical models.

108 these enzymes are currently being tested as antiangiogenic agents in various malignancies.

109 Strategies to safely incorporate novel antiangiogenic agents into combined-modality therapy in

110 Additionally, the combination of several antiangiogenic agents is also being explored.

111 proval of an anti-VEGF antibody as the first antiangiogenic agent, many patients with cancer and ocul

112 and suggest that a combination therapy with antiangiogenic agents may be a particularly promising ap

113 The clinical potential of antiangiogenic agents may be increased by combining them

114 These results indicate that antiangiogenic agents may not be beneficial in unselecte

115 Ligand-targeted nanotherapy to deliver antiangiogenic agents may represent an effective way to

116 d from rats pretreated with three well-known antiangiogenic agents (minocycline, interferon alfa-2b,

117 ts, toxicities, and resistance mechanisms to antiangiogenic agents must be considered as these therap

118 e tumor regression and to maintain dormancy, antiangiogenic agents need to be chronically administere

119 Parstatin is a potent antiangiogenic agent of ocular neovascularization and ma

120 nvestigated combinations of gemcitabine with antiangiogenic agents of various mechanisms for PDAC, in

121 Since antiangiogenic agents often exert an indirect, cytostati

122 n to the clinician on the effect of specific antiangiogenic agents on individual tumors.

123 The effects of antiangiogenic agents on molecules and processes that al

124 be used to screen for safer antiprogestins, antiangiogenic agents, or for compounds that reactivate

125 ndeed, we demonstrated that judicious use of antiangiogenic agents--originally designed to starve tum

126 Further research with novel antiangiogenic agents, particularly in the maintenance s

127 ombined therapy with a FAK inhibitor and the antiangiogenic agents pazopanib and bevacizumab reduced

128 Antiangiogenic agents prevent the formation of new tumou

129 Antiangiogenic agents produce high radiographic response

130 sociated with increased thrombospondin-1 (an antiangiogenic agent) production and small vessel occlus

131 , cellular therapies, other immunotherapies, antiangiogenic agents, radiotherapy, cryotherapy and som

132 es that the most efficacious applications of antiangiogenic agents rely upon a combination with cytot

133 itargeted approach involving selective local antiangiogenic agents should contribute to prevention of

134 Treatment of RCC in nude mice with the antiangiogenic agent sorafenib resulted in markedly decr

135 the possibility of effective treatment with antiangiogenic agents, such as endostatin.

136 PET after longitudinal administration of the antiangiogenic agent sunitinib (a 2-wk dosing regimen).

137 er administration of the clinically relevant antiangiogenic agent sunitinib revealed a reduction in t

138 a standard clinical treatment course of the antiangiogenic agent sunitinib.

139 lioblastoma xenografts to treatment with the antiangiogenic agent sunitinib.

140 poxia in human breast cancer xenografts, the antiangiogenic agents sunitinib and bevacizumab increase

141 tyrosine kinase inhibitor), bevacizumab (an antiangiogenic agent), tanespimycin (a heat shock protei

142 r current antiangiogenic therapies, as these antiangiogenic agents target normal vasculature as well

143 of gene therapy for systemic delivery of an antiangiogenic agent targeting an endothelium-specific r

144 e with most of the standard chemotherapeutic antiangiogenic agents tested: cortisone acetate, vincris

145 Linomide is a p.o. active antiangiogenic agent that has been demonstrated to be ef

146 angiogenic agents with chemotherapy, or with antiangiogenic agents that also directly target the canc

147 present study shows the potential utility of antiangiogenic agents that target the endothelium-specif

148 ing in single-arm phase 2 studies evaluating antiangiogenic agents, this risk for all events (OR 4.34

149 ablish angiostatin as an antitumorigenic and antiangiogenic agent through a mechanism implicating tum

150 Preclinical studies suggested that the antiangiogenic agent TNP-470 was synergistic with cytoto

151 PDT followed by administration of an antiangiogenic agent, TNP-470, abolished this increase a

152 The addition of specific antiangiogenic agents to differentiation therapy or chem

153 concert, from basic mechanisms of action of antiangiogenic agents to new combination approaches to c

154 Current antiangiogenic agents used to treat cancer only partiall

155 therapy-mediated approach to the delivery of antiangiogenic agents using adeno-associated virus (AAV)

156 nution of dysplastic microvasculature by the antiangiogenic agent, vascular endothelial growth factor

157 to the preovulatory stage in the presence of antiangiogenic agent, VEGFR-2-neutralizing Ab's.

158 The mechanism of action of these drugs as antiangiogenic agents was 2-fold.

159 patients treated with extended-dose TMZ with antiangiogenic agents was caused by TMZ alone.

160 The potential to heighten the efficacy of antiangiogenic agents was explored in this study based o

161 Seeking PEDF-based antiangiogenic agents we generated and tested peptides r

162 imilar pattern of expression for both of the antiangiogenic agents we tested.

163 s a physiological target for the Fg class of antiangiogenic agents, we have generated a conditional M

164 We hypothesized that thalidomide, an oral antiangiogenic agent, when combined with chemotherapy, a

165 e to therapy, particularly in the setting of antiangiogenic agents, which confound the interpretation

166 The VTAs are distinct from antiangiogenic agents, which prevent new blood vessel fo

167 Antiangiogenic agents, which target normal, proliferatin

168 valuate the strategy of combining a putative antiangiogenic agent with a cytotoxic agent in patients

169 Thus, orlistat is an antiangiogenic agent with a novel mechanism of action.

170 Sorafenib is an antiangiogenic agent with activity in renal cancer.

171 Combinations of more than one antiangiogenic agent with gemcitabine were generally mor

172 a rationale for the exploration of combining antiangiogenic agents with ACT for the treatment of pati

173 me primarily with the use of combinations of antiangiogenic agents with chemotherapy, or with antiang

174 ofiling of tumors, and new ways of combining antiangiogenic agents with cytotoxic agents may lead to

175 tion with cell cycle-dependent chemotherapy, antiangiogenic agents with hypoxia-inducible factor-1 in

176 Combining antiangiogenic agents with multiple mechanisms of action

177 g and DCE CT can depict vascular response to antiangiogenic agents with response evident at day 7.