ライフサイエンスコーパス: antiangiogenic therapy

1 redict which mRCC patients will benefit from antiangiogenic therapy.

2 ng for improvements in blood perfusion after antiangiogenic therapy.

3 vasculature, similar to that occurring with antiangiogenic therapy.

4 biomarkers exist to image tumor responses to antiangiogenic therapy.

5 sessing the response of vascularized PEDs to antiangiogenic therapy.

6 GBM) to characterize the response of rGBM to antiangiogenic therapy.

7 patient care and monitoring the response to antiangiogenic therapy.

8 and 28 days after combined chemotherapy and antiangiogenic therapy.

9 ggesting COUP-TFII as a candidate target for antiangiogenic therapy.

10 n after 28 days of combined chemotherapy and antiangiogenic therapy.

11 in pancreatic tumors can predict response to antiangiogenic therapy.

12 -catenin, this may provide a good target for antiangiogenic therapy.

13 ontribute in inherent/acquired resistance to antiangiogenic therapy.

14 s not been considered an important target in antiangiogenic therapy.

15 could be an effective approach for enhancing antiangiogenic therapy.

16 se-2 (MetAP2) represents a novel approach to antiangiogenic therapy.

17 tification of potential rational targets for antiangiogenic therapy.

18 o have a reduced growth response to targeted antiangiogenic therapy.

19 tors or markers for tumor vessel response to antiangiogenic therapy.

20 ing and monitoring tumor vessel responses to antiangiogenic therapy.

21 cusses promising avenues of investigation in antiangiogenic therapy.

22 cancer, suggesting possible new targets for antiangiogenic therapy.

23 ls and interstitium that are associated with antiangiogenic therapy.

24 ting both DLL4 and VEGF pathways may improve antiangiogenic therapy.

25 ibitors and that ATRs are useful targets for antiangiogenic therapy.

26 ring the tumor vasculature more resistant to antiangiogenic therapy.

27 se for monitoring tumor vascular response to antiangiogenic therapy.

28 tions for their development as biomarkers of antiangiogenic therapy.

29 rrently evaluated as potential biomarkers of antiangiogenic therapy.

30 rins on tumor blood vessels before and after antiangiogenic therapy.

31 etriotic growth and the efficacy of systemic antiangiogenic therapy.

32 flow in mouse tumors engineered to simulate antiangiogenic therapy.

33 ls but not changes in microvessel density in antiangiogenic therapy.

34 umor types that shows a clinical response to antiangiogenic therapy.

35 human tumors may represent a potential novel antiangiogenic therapy.

36 ctor and modulator of endostatin efficacy in antiangiogenic therapy.

37 uggest its usefulness in angioprevention and antiangiogenic therapy.

38 g responses to anticancer therapy, including antiangiogenic therapy.

39 with implications for the rational design of antiangiogenic therapy.

40 target to endothelial cells for efficacious antiangiogenic therapy.

41 wide have received some form of experimental antiangiogenic therapy.

42 xamined potential surrogates for response to antiangiogenic therapy.

43 gnaling could serve as a marker of effective antiangiogenic therapy.

44 herapies, especially for tumors treated with antiangiogenic therapy.

45 ly neovascularized and so may be amenable to antiangiogenic therapy.

46 o dynamic balance, which can be modulated by antiangiogenic therapy.

47 presents a promising strategy for delivering antiangiogenic therapy.

48 d could be helpful in selecting patients for antiangiogenic therapy.

49 umor progression can be restricted solely by antiangiogenic therapy.

50 ted negative effects following withdrawal of antiangiogenic therapy.

51 th treatment-naive BCVA and BCVA outcomes in antiangiogenic therapy.

52 with clear-cell mRCC previously treated with antiangiogenic therapy.

53 inhibited tumor rebound after withdrawal of antiangiogenic therapy.

54 nal measurement of ovarian tumor response to antiangiogenic therapy.

55 t to Nck as an emergent target for effective antiangiogenic therapy.

56 ve outcomes of patients with GBM who receive antiangiogenic therapy.

57 assessment of early treatment response after antiangiogenic therapy.

58 with Angpt/Tie2 has the potential to improve antiangiogenic therapy.

59 e an antitumor agent and open a new field of antiangiogenic therapy.

60 es is not necessarily decreased by effective antiangiogenic therapy.

61 2 followed tumor volume in studies featuring antiangiogenic therapy.

62 ectively block tumor progression and improve antiangiogenic therapy.

63 orafenib might be a ceiling for single-agent antiangiogenic therapy.

64 rtance, VEGF has been at the center stage of antiangiogenic therapy.

65 may mediate a mesenchymal-type resistance to antiangiogenic therapy.

66 sent in GSC and are resistant to traditional antiangiogenic therapies.

67 implications for the design of both pro- and antiangiogenic therapies.

68 sensitive reporter of the hypoxic effects of antiangiogenic therapies.

69 s of patients with cancer who are undergoing antiangiogenic therapies.

70 one of the most potent cytokines targeted in antiangiogenic therapies.

71 intrinsic hormone resistance may respond to antiangiogenic therapies.

72 on is critically involved in the response to antiangiogenic therapies.

73 of both IL-8 and VEGF signaling may improve antiangiogenic therapies.

74 suggests indications for clinical trials of antiangiogenic therapies.

75 sis-related diseases and provide a guide for antiangiogenic therapies.

76 nificant implications for the development of antiangiogenic therapies.

77 s, and the potential activity of alternative antiangiogenic therapies.

78 cells is critical for developing appropriate antiangiogenic therapies.

79 genic factors has important implications for antiangiogenic therapies.

80 creatic islets, and demonstrated efficacy of antiangiogenic therapies.

81 es attractive targets for the development of antiangiogenic therapies.

82 allow for an improved response assessment to antiangiogenic therapies.

83 , age, tumor type and involvement, and prior antiangiogenic therapies.

84 s that affect vascular permeability, such as antiangiogenic therapies.

85 oit this seminal pathway and improve current antiangiogenic therapies.

86 oma has lent support to the increased use of antiangiogenic therapies.

87 Antiangiogenic therapy (AAT) is a treatment option that

88 her CXCL5 or CXCR2 may be a critical adjunct antiangiogenic therapy against pancreatic cancer.

89 dentify novel targets for the development of antiangiogenic therapies aimed at the treatment of Kapos

90 e oncologists unknowingly been administering antiangiogenic therapy all these years?

91 to the application of immunotherapy alone or antiangiogenic therapy alone, which delayed the tumor gr

92 Antiangiogenic therapy also selects for aggressive pheno

93 Antiangiogenic therapy, although effective in shrinking

94 uation of the effectiveness of commonly used antiangiogenic therapies and determination of their opti

95 erlying mechanisms of resistance specific to antiangiogenic therapy and develop strategies to overcom

96 nism by which neuroblastoma can partly evade antiangiogenic therapy and may explain why experimental

97 gs challenge both the original rationale for antiangiogenic therapy and our understanding of the phys

98 mor hypoxia is associated with resistance to antiangiogenic therapy and poor prognosis.

99 a suggest mitochondria as a novel target for antiangiogenic therapy and provide mechanistic insights

100 -Met pathway in development of resistance to antiangiogenic therapy and suggests a potential strategy

101 dy tested the hypothesis that combination of antiangiogenic therapy and tumor immunotherapy of cancer

102 onse and nonenhancing tumor progression from antiangiogenic therapies, and pseudoprogression from rad

103 discuss successes and challenges of current antiangiogenic therapy, and highlight emerging antiangio

104 modalities including systemic chemotherapy, antiangiogenic therapy, and hospitalization.

105 infiltration into tumors after withdrawal of antiangiogenic therapy, and lowering platelet counts mar

106 CC as an important candidate target gene for antiangiogenic therapy, and PDGF-CC inhibition may be of

107 on factors were selected chemotherapy, prior antiangiogenic therapy, and platinum-free interval.

108 ikely reflects an onset of hypoxia caused by antiangiogenic therapy, and that beta1 inhibition is wel

109 However, not all patients benefit from antiangiogenic therapy, and those tumors that initially

110 umors were implanted, mice were treated with antiangiogenic therapy (anti-VEGFR-2 mAb, 1.4 mg/30 g bo

111 Antiangiogenic therapies are being pursued as a means of

112 Antiangiogenic therapies are starting to give promising

113 ly improved vascular function as a result of antiangiogenic therapy are explored, as are the implicat

114 nexpected finding is that repeated cycles of antiangiogenic therapy are followed by prolonged tumour

115 Interestingly, early-stage antiangiogenic therapy arrested the progression of moder

116 naling remains a major challenge for current antiangiogenic therapies, as these antiangiogenic agents

117 ivo appears to be crucial for the success of antiangiogenic therapy based on integrin antagonism.

118 RC-52 xenografts after treatment with either antiangiogenic therapy (bevacizumab or sorafenib) or tum

119 ools with which to easily evaluate potential antiangiogenic therapies beyond eye research.

120 Tumors escape antiangiogenic therapy by activation of proangiogenic si

121 e effect and to potentiate responsiveness to antiangiogenic therapy by concomitantly targeting ECM-mo

122 Improvements in antiangiogenic therapy can be engendered by metronomic d

123 lioblastoma tumors, and the effectiveness of antiangiogenic therapy can be enhanced when combined wit

124 m between two angiostatic molecules and that antiangiogenic therapy can be used to inhibit ovarian ca

125 nd IFV profiles in tumors, we show here that antiangiogenic therapy can decrease IFP by decreasing th

126 Antiangiogenic therapy can enhance radiation-induced tum

127 Antiangiogenic therapy can produce transient tumor regre

128 ndings offer strong evidence that short-term antiangiogenic therapy can promote a transient vessel no

129 g laser photocoagulation, vitrectomy, and/or antiangiogenic therapy confirmed by an external adjudica

130 Most antiangiogenic therapies currently being evaluated in cl

131 as the potential to be manipulated in future antiangiogenic therapy design.

132 asiveness, paradoxically induced by the very antiangiogenic therapy designed to destroy the tumor.

133 Despite clear antitumor efficacy, antiangiogenic therapy did not alter tumor uptake of (11

134 Therefore, antiangiogenic therapy directed against a tumour's endot

135 om clinical trials of both proangiogenic and antiangiogenic therapies does not suggest that inhibitio

136 fied PDGF-DD as an important target gene for antiangiogenic therapy due to its pleiotropic effects on

137 Antiangiogenic therapy effects were detected earlier and

138 ides consistent assessment of tumor rCBV and antiangiogenic therapy efficacy.

139 In this context, antiangiogenic therapy emerged as a promising treatment

140 r SK-RC-52 xenografts was not affected after antiangiogenic therapy, except in head and neck squamous

141 r reviews the evidence supporting the use of antiangiogenic therapies for adult soft tissue sarcomas.

142 This indicates that antiangiogenic therapies for tumors that express high le

143 a useful animal model for testing potential antiangiogenic therapies for VHL disease treatment.

144 tion would have a dose-sparing effect on rK5 antiangiogenic therapy for brain tumors and further sugg

145 response are desperately needed to customize antiangiogenic therapy for cancer patients.

146 Phase I clinical trials of endostatin as an antiangiogenic therapy for cancer, the protein was admin

147 ctions of RAC exosomes, we might improve the antiangiogenic therapy for CNV in age-related macular de

148 As we are interested in antiangiogenic therapy for glioblastoma tumors, and the

149 plications of alteration of Sp1 signaling in antiangiogenic therapy for pancreatic cancer and other c

150 ew challenge for uninterrupted and sustained antiangiogenic therapy for treatment of human cancers.

151 Sunitinib is an antiangiogenic therapy given as a first-line treatment f

152 rker synaptophysin expression indicated that antiangiogenic therapy given at an early-stage disease r

153 Antiangiogenic therapy has been thought to hold signific

154 Antiangiogenic therapy has raised the hopes both of canc

155 Antiangiogenic therapy has shown clear activity and impr

156 Antiangiogenic therapies have a number of potential adva

157 There is increasing evidence that antiangiogenic therapies have activity in high-grade gli

158 Successful antiangiogenic therapies have been developed for the tre

159 Antiangiogenic therapies have failed to confer survival

160 istic of metastatic disease, and clinically, antiangiogenic therapies have shown value in the setting

161 Tumor-bearing mice treated with combined antiangiogenic therapy (IM862 or EMAP-II) and PDT had im

162 One day after initiation of antiangiogenic therapy, imaging signal was significantly

163 ma is a highly vascularized brain tumor, and antiangiogenic therapy improves its progression-free sur

164 Antiangiogenic therapy improves survival in patients wit

165 Diffuse FVT permit studies of antiangiogenic therapies in areas distant from laser pho

166 r knowledge, this is the first evaluation of antiangiogenic therapy in a spontaneous autochthonous tu

167 jor role for Gal-1 as a tractable target for antiangiogenic therapy in advanced stages of the disease

168 ssels may serve as biomarkers or targets for antiangiogenic therapy in cancer.

169 er clinical development of caplostatin as an antiangiogenic therapy in childhood neuroblastoma.

170 Resistance to antiangiogenic therapy in glioblastoma (GBM) patients ma

171 The role of antiangiogenic therapy in mCRPC remains investigational.

172 nificantly contribute to the response toward antiangiogenic therapy in melanoma.

173 The efficacy of antiangiogenic therapy in neovascular AMD is strongly de

174 iogenic factors may be potential targets for antiangiogenic therapy in ovarian cancer.

175 c (CT) images, and predict tumor response to antiangiogenic therapy in patients with metastatic renal

176 s comparable to post-surgical treatment with antiangiogenic therapy in patients with mRCC, but it may

177 elucidate a novel mechanism of resistance to antiangiogenic therapy in which hypoxia-mediated autopha

178 to which their net extraction is improved by antiangiogenic therapy, in turn, depends on the extent t

179 e accurate monitoring of patient response to antiangiogenic therapies (including treatment suspension

180 However, current antiangiogenic therapy induces serious adverse effects i

181 plored the hypothesis that hypoxia caused by antiangiogenic therapy induces tumor cell autophagy as a

182 and predict which patients may benefit from antiangiogenic therapies is of great importance.

183 Antiangiogenic therapy is a promising alternative for pr

184 Antiangiogenic therapy is efficacious in metastatic rena

185 ing it important to determine which contexts antiangiogenic therapy is most appropriate.

186 tion of continuous low-dose chemotherapy and antiangiogenic therapy is predicted to have the most sig

187 Recent evidence suggests that antiangiogenic therapy is sensitive to p53 status in tum

188 Intravitreal antiangiogenic therapy is the major therapeutic breakthr

189 teration of Sp1 signaling on the efficacy of antiangiogenic therapy is unclear, yet understanding the

190 inflammatory agents, or other non-VEGF-based antiangiogenic therapies, is actively investigated.

191 rapy in certain hormone-dependent tumors and antiangiogenic therapy lead to vessel regression and hav

192 in the tumor microenvironment in response to antiangiogenic therapy, leading to drug resistance.

193 Antiangiogenic therapy leads to devascularization that l

194 Antiangiogenic therapies like bevacizumab offer promise

195 detected changes in tumor uptake after acute antiangiogenic therapy markedly earlier than any signifi

196 gimens, targeted molecular agents, and other antiangiogenic therapies may have activity in recurrent

197 ing strategies of combinations of immune and antiangiogenic therapies may lead to further advancement

198 bitors from a single tumor and suggests that antiangiogenic therapies may provide an avenue for futur

199 tumor vessel numbers and function following antiangiogenic therapy may also affect intratumoral deli

200 tic that complements and improves concurrent antiangiogenic therapy may be a promising treatment stra

201 In conclusion, tumor perfusion changes after antiangiogenic therapy may distinguish responders vs. no

202 Judicious application of antiangiogenic therapy may normalize the structure and f

203 Antiangiogenic therapy may prove to be effective in the

204 Tumor blood vessels normalized by antiangiogenic therapy may provide improved delivery of

205 s, whereas current treatment, and especially antiangiogenic therapy, may trigger spatial heterogeneit

206 -switch" model to explain how the targets of antiangiogenic therapy might change as a function of tum

207 Prudent antiangiogenic therapy might transiently normalize blood

208 eflects the viability of tumor tissue during antiangiogenic therapy more reliably than contrast-enhan

209 Therefore, successful antiangiogenic therapies must be able to block all of th

210 s of their growth and dissemination, optimal antiangiogenic therapy necessitates inhibition of multip

211 molecular aspects of tumor angiogenesis and antiangiogenic therapy of cancer in combination with con

212 y survey critical scientific advances in the antiangiogenic therapy of cancer.

213 e as an "unconventional" MMP-9 inhibitor for antiangiogenic therapy of cervical cancer and potentiall

214 ation of the blood-brain barrier (BBB) after antiangiogenic therapy of gliomas with bevacizumab may r

215 Antiangiogenic therapy of the chimeras bearing establish

216 Recent advances in antiangiogenic therapies offer possible primary or adjun

217 However, the effect of antiangiogenic therapy on cycling tumor hypoxia remains

218 The impact of antiangiogenic therapy on the Sp1/vascular endothelial g

219 In particular, the impact of antiangiogenic therapy on tumor blood flow and oxygenati

220 The effects of antiangiogenic therapy on tumors relapsing after irradia

221 decade and propose strategies for improving antiangiogenic therapy outcomes for malignant and nonmal

222 Bevacizumab is the first antiangiogenic therapy proven to slow metastatic disease

223 munotherapy in simultaneous combination with antiangiogenic therapy provides a more efficient strateg

224 n integrin expression on tumor vessels after antiangiogenic therapy raises the possibility that integ

225 eted therapy (radiation/chemo) together with antiangiogenic therapies reduced GBM tumor size but incr

226 The mechanisms of resistance to antiangiogenic therapy remain incompletely understood.

227 g force for tumor growth and metastasis, and antiangiogenic therapy represents one of the most promis

228 Current antiangiogenic therapies require frequent injections, an

229 Antiangiogenic therapy resistance occurs frequently in p

230 junctive CXCR4 antagonists may help overcome antiangiogenic therapy resistance, benefiting GBM patien

231 this time period of improved oxygenation by antiangiogenic therapy resulted in a synergistic delay i

232 city of the tumor vasculature in the face of antiangiogenic therapy (see the related article beginnin

233 The widely held view is that these antiangiogenic therapies should destroy the tumor vascul

234 Antiangiogenic therapies show some therapeutic potential

235 paid to the microvascular endothelium and to antiangiogenic therapies, specific studies on the lympha

236 However, rapid emergence of resistance to antiangiogenic therapies, such as bevacizumab, greatly l

237 Antiangiogenic therapies, such as sunitinib, have revolu

238 etabolic traits of tumors can be selected by antiangiogenic therapy suggests insights into the evolut

239 ailing hypotheses on how these tumors escape antiangiogenic therapy: switch to VEGF-independent angio

240 Antiangiogenic therapies targeting the vascular endothel

241 endometrium is a major limitation for use of antiangiogenic therapy targeting endometrial vessels.

242 herefore be a potential target for nontoxic, antiangiogenic therapy that could prevent tumor recurren

243 about unexpected complications arising from antiangiogenic therapy that may potentially involve TF.

244 owever, for long-term tumor-free survival by antiangiogenic therapy, the factors controlling tumor ne

245 reasing the growth rate of the tumor with an antiangiogenic therapy, the low-avidity repertoire of ne

246 Thus, beta1 integrins promote resistance to antiangiogenic therapy through potentiation of multiple

247 ective inhibition of antiapoptotic pathways, antiangiogenic therapy, tissue-selective therapy (includ

248 ications for the translation of experimental antiangiogenic therapies to the clinic.

249 Therefore, effective antiangiogenic therapies to treat VEGF-producing, VEGFR-

250 sion of this molecule is an ideal target for antiangiogenic therapy to treat cancer.

251 In tumors treated with antiangiogenic therapy, tumor MR estimate of sO(2) was d

252 ncer that responds to checkpoint blockade or antiangiogenic therapy, uncovering a protective role by

253 gy inhibitors may help prevent resistance to antiangiogenic therapy used in the clinic.

254 These include antiangiogenic therapy, vasodilatory agents, antilymphog

255 Antiangiogenic therapy was administered until a mean 1-m

256 Noninvasive monitoring of antiangiogenic therapy was performed by serial power Dop

257 To model effective antiangiogenic therapy, we disrupted the VEGF gene in th

258 e absence of VEGF, following radiotherapy or antiangiogenic therapy, we documented an increase in Ang

259 ve of this study was to evaluate alternative antiangiogenic therapies, which target multiple VEGF fam

260 ifferently to hypoxia and, as a consequence, antiangiogenic therapies will not be suitable for both s

261 dation of these biomarkers in the context of antiangiogenic therapy will be required.

262 yeloid cells contribute to refractoriness to antiangiogenic therapy with an anti-VEGF-A antibody.

263 Antiangiogenic therapy with antibodies against VEGF (bev

264 Antiangiogenic therapy with bevacizumab combined with ch

265 Antiangiogenic therapy with endostatin in animals requir

266 nitor response of colon cancer xenografts to antiangiogenic therapy with functional and molecular US

267 perimental animals have shown that combining antiangiogenic therapy with radiation can enhance tumor

268 Antiangiogenic therapy with the humanized VEGF antibody

269 f disease manifestations and is a target for antiangiogenic therapy with the monoclonal antibody beva

270 tient management and monitor the response to antiangiogenic therapy with the optimum noninvasive imag

271 sized that immunotherapy in combination with antiangiogenic therapy would be a more efficient strateg

272 rgeting pBMDC influx along with radiation or antiangiogenic therapy would be critical to prevent vasc

273 t phase of human cancer may be vulnerable to antiangiogenic therapy years before symptoms, or before

274 ently been implicated in tumor resistance to antiangiogenic therapy, yet their precise involvement in