ライフサイエンスコーパス: antiangiogenic

1 sts and endothelial cells is profibrotic and antiangiogenic.

2 al status, and the use of corticosteroids or antiangiogenics.

3 recent data suggesting that the efficacy of antiangiogenic (AA) therapies is limited in some circums

4 neration ITZ analogues for their anti-Hh and antiangiogenic activities to probe more fully the struct

5 CSF) level in the EDM-TTF-1(+) conferred the antiangiogenic activities.

6 nase (FAK) have been recently shown to exert antiangiogenic activity against HUVEC cells and anticanc

7 G2) with a submicromolar IC(50) and also has antiangiogenic activity in vitro and in vivo.

8 on of endothelial cell migration ex vivo and antiangiogenic activity in vivo.

9 validation and mechanistic definition of the antiangiogenic activity of a novel mycotoxin, with poten

10 gth forms could also counter balance the pro/antiangiogenic activity of each other in in vitro angiog

11 Furthermore, the antiangiogenic activity of HT C6 was confirmed in vivo i

12 reover, our data reveal that the established antiangiogenic activity of protamine would rely on APJ a

13 dues on the affinity, anti-inflammatory, and antiangiogenic activity of these azapeptides have now be

14 designed, synthesized, and tested for their antiangiogenic activity using in vitro assays with human

15 rgets and their effects on metformin-induced antiangiogenic activity were assessed using luciferase a

16 ylase inhibitor) via an ester bond, exhibits antiangiogenic activity, being able to reduce human reti

17 Remarkably, VEGF-Ax exhibits potent antiangiogenic activity, both in vitro and in vivo, thus

18 ing loss of neuropilin-1 binding and gain of antiangiogenic activity.

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

20 Pazopanib is an oral antiangiogenic agent targeting VEGF receptors 1, 2, and

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

22 effective way of monitoring the efficacy of antiangiogenic agents and as a proxy measure of perfusio

23 However, antiangiogenic agents and HIF-2 inhibitors have limited

24 ay be a unique target in situations in which antiangiogenic agents are withdrawn, and dual targeting

25 Antiangiogenic agents combined with chemotherapy have ef

26 pport the combination of AXL inhibitors with antiangiogenic agents for advanced ccRCC.

27 pport the combination of AXL inhibitors with antiangiogenic agents for the treatment of RCC.

28 Antiangiogenic agents have established efficacy in the t

29 However, antiangiogenic agents have limited efficacy in cancer th

30 low proliferative tumor while lower doses of antiangiogenic agents improve drug penetration in a poor

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

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

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

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

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

36 ntaining bisphosphonates, a RANKL inhibitor, antiangiogenic agents, or mTOR inhibitors.

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

38 ast cancer treated with chemotherapeutic and antiangiogenic agents.

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

40 o those of continuous treatment with various antiangiogenic agents.

41 ck of tumor-homing capability of the current antiangiogenic agents.

42 nts for thyroid cancers, acting primarily as antiangiogenic agents.

43 oting effective subsequent therapy including antiangiogenic agents.

44 omatoid tumors to checkpoint blockade versus antiangiogenics alone, and develop personalized therapie

45 Both vascular aspects respond to antiangiogenic and antihyperglycemic pharmacological int

46 Antiangiogenic and antilymphangiogenic activities of the

47 Sunitinib maintained its antiangiogenic and antimetastatic activity but lost its

48 of a lead candidate (6z) that combined both antiangiogenic and antitumoral effects.

49 itargeted tyrosine kinase inhibitor that has antiangiogenic and antitumorigenic properties with poten

50 ng of endothelial FABP4 by siRNA in vivo has antiangiogenic and antitumour effects with minimal toxic

51 lial Stat3 ablation led to a shift toward an antiangiogenic and axon growth-inhibiting micromilieu af

52 We evaluated the effects of combined antiangiogenic and chemotherapy treatments on advanced s

53 Antiangiogenic and cytotoxic effects are considered the

54 resent data revealed that the conjugation of antiangiogenic and DNA-damaging agents can generate pote

55 ined with CD40 agonistic antibodies promoted antiangiogenic and immunostimulatory reprogramming of Pr

56 antiangiogenic protein, can activate latent antiangiogenic and proangiogenic sites, respectively.

57 that BMP7v treatment may represent a useful antiangiogenic and prodifferentiation agent, which rende

58 y, heightened proliferation, and potentiated antiangiogenic and profibrotic properties.

59 ibition of thrombospondin-1 (THBS1/TSP1), an antiangiogenic and proinflammatory cytokine that promote

60 CD36 and exhibited respectively significant antiangiogenic and slight angiogenic activities in a mic

61 rom 1997 to 2006; 12 of those studies tested antiangiogenic and/or anti-epidermal growth factor recep

62 ences cutaneous wound healing because of its antiangiogenic, anti-inflammatory, and antioxidant prope

63 that combination of agonistic anti-CD40 with antiangiogenic antibodies targeting 2 proangiogenic fact

64 2B)AR blockade results in antiproliferative, antiangiogenic, antimetastatic, and immunostimulatory ef

65 xin from a novel source that exhibits potent antiangiogenic antitumor activity.

66 Antiangiogenic approaches that have shown benefit in oth

67 Our data demonstrate that miR-155 exerts an antiangiogenic but proarteriogenic function in the regul

68 scular networks following treatment with the antiangiogenic cancer agent DC101.

69 verexpression of ETS1 reversed the abrogated antiangiogenic capacity of miR-145.

70 In this work, we describe a new antiangiogenic compound (22) that inhibits proangiogenic

71 n five analogues of a clinically established antiangiogenic compound (sunitinib), from which a lead c

72 ytyrosol synthetic derivative HT C6 as a new antiangiogenic compound and as a good candidate for an a

73 ovide a rationale for the development of new antiangiogenic compounds that could eventually lead to n

74 cells, turning them into dual cytotoxic and antiangiogenic compounds.

75 In summary, Q8 is a more effective antiangiogenic drug compared with quininib.

76 bit low penetrance angiogenesis deficits and antiangiogenic drug hypersensitivity.

77 enic compound and as a good candidate for an antiangiogenic drug in the treatment of angiogenesis-dep

78 nvasive imaging biomarker of response to the antiangiogenic drug sunitinib.

79 adiopaque embolization beads loaded with the antiangiogenic drug vandetanib may provide improved anti

80 In addition, sorafenib is described as an antiangiogenic drug, but it also acts on immunological c

81 ort for the concept that ENOX1 represents an antiangiogenic druggable target.

82 We proposed that normalization of TME using antiangiogenic drugs and/or mechanotherapeutics can over

83 ervascular tumor of neural origin, for which antiangiogenic drugs are currently being evaluated; howe

84 Bevacizumab is one of the most widely used antiangiogenic drugs in oncology, but the overall benefi

85 oma metastasis occurs at the early stage and antiangiogenic drugs such as Vegf morpholino and sunitin

86 suggest the use of PP2A-inhibitors as potent antiangiogenic drugs targeting specifically nascent bloo

87 However, the ability of antiangiogenic drugs to delay tumor progression and exte

88 ab, highlighting the need for more effective antiangiogenic drugs with novel mechanisms of action.

89 However, antiangiogenic drugs, peptide receptor radionuclide ther

90 VEGF pathway-targeting antiangiogenic drugs, such as bevacizumab, when combined

91 ogical examination, and anti-inflammatory or antiangiogenic drugs.

92 tumor infiltration and confer resistance to antiangiogenic drugs.

93 ictive biomarkers of the clinical benefit of antiangiogenic drugs.

94 CR-CSC-based mouse avatars, BMP7v exerts an antiangiogenic effect and sensitizes tumor cells to stan

95 giogenesis during therapy, despite a greater antiangiogenic effect of bevacizumab, such that a revers

96 hile p56/Lck short hairpin RNA inhibited the antiangiogenic effect of HKa.

97 The antiangiogenic effect of PRP was analysed by matrigel-ba

98 erved owing to the enhanced photothermal and antiangiogenic effect of RDLPNPs.

99 This sharp switch from proangiogenic to antiangiogenic effect of TNF observed with an escalating

100 autophagy, an antitumor immune response, an antiangiogenic effect, and a significant "bystander" ant

101 VEGF-A signaling, whereas IFNgamma shows an antiangiogenic effect.

102 mpair periodontal tissue repair, despite its antiangiogenic effect.

103 Q8 elicits antiangiogenic effects in a VEGF-independent in vitro mo

104 oxides 17,18-EEQ-EA and 19,20-EDP-EA exerted antiangiogenic effects in human microvascular endothelia

105 This suggests that local CsA has negligible antiangiogenic effects in the human cornea, at least in

106 receptor kinase inhibitor SU5416, increased antiangiogenic effects in vitro and in a zebrafish angio

107 We found that ANGPTL7 itself has strong antiangiogenic effects in vitro.

108 of VEGF by bevacizumab explain the additive antiangiogenic effects observed in combination with Q8.

109 he angiogenic process and in propagating the antiangiogenic effects of IMiDs in vitro.

110 unction in angiogenesis and in mediating the antiangiogenic effects of IMiDs remains unclear.

111 an endothelial tube assay and attenuated the antiangiogenic effects of sFlt1.

112 Mechanistically, the antiangiogenic effects of sorafenib led to increased bon

113 c-pharmacodynamic models mainly focus on the antiangiogenic effects on tumor growth but do not provid

114 actor (TNF), can have both proangiogenic and antiangiogenic effects, depending on the dose and the pr

115 tion of specific antimitotic and nonspecific antiangiogenic effects.

116 fic and as a result can yield either pro- or antiangiogenic effects.

117 nt pathways, through which IMiDs exert their antiangiogenic effects.

118 expression, alveolar cell apoptosis, and the antiangiogenic factor GAX, and decreased expression of H

119 nd the role of placental factors such as the antiangiogenic factor, sFLT1 (soluble fms-like tyrosine

120 artery remodeling and abnormal secretion of antiangiogenic factors are thought to be important in th

121 The unbalanced production of pro- and antiangiogenic factors in tumors can lead to aberrant va

122 A high expression of antiangiogenic factors leads to the loss of neovasculari

123 which, in turn, may induce transcription of antiangiogenic factors, soluble fms-like tyrosine kinase

124 d to p53 thereby preventing the induction of antiangiogenic factors.

125 s-related functions and up expression of the antiangiogenic factors.

126 lated by a delicate balance between pro- and antiangiogenic factors.

127 We show that the ratio of pro/antiangiogenic forms of CgA is altered in multiple myelo

128 ogenous CXCL4L1, which is independent of its antiangiogenic function.

129 hemokine that has been suggested to exert an antiangiogenic function.

130 p53 is a key factor for inducing antiangiogenic genes and RCC are highly vascularized, wh

131 l of SH-11037, a synthetic derivative of the antiangiogenic homoisoflavonoid cremastranone, in models

132 l, underscoring the therapeutic potential of antiangiogenic immunotherapy in cancer.

133 etic (c(AmpRGD)) and the clinically approved antiangiogenic kinase inhibitor sunitinib, three novel d

134 Blockade of C5a receptor 1 synergized with antiangiogenic Listeria monocytogenes-based vaccines to

135 F(165)b expression in macrophages induces an antiangiogenic M1-like phenotype that directly impairs a

136 rmal placentation with subsequent release of antiangiogenic markers, mediated primarily by soluble fm

137 g e-miRNAs in refractory ICAD, suggesting an antiangiogenic mechanism underlying IMM failure.

138 potential adjuvant treatments to LT, such as antiangiogenic medications, when recurrent disease appea

139 -135a-3p is rapidly induced and serves as an antiangiogenic microRNA (miRNA) by targeting endothelial

140 methylation leading to induced expression of antiangiogenic miR-221 by GATA2-dependent demethylation

141 t the combination of PTX-loaded NPs with the antiangiogenic molecular inhibitor BIBF 1120 (BIBF) prom

142 ental evidence that K5-N,OS(H) represents an antiangiogenic multitarget molecule with potential impli

143 ere scanned before and 24 hours after either antiangiogenic (n = 9) or saline-only (n = 8) treatment.

144 ell (HUVECs) proliferation, indicating their antiangiogenic nature.

145 ninib analogues and identified a more potent antiangiogenic novel chemical entity (IUPAC name (E)-2-(

146 This study showed that antiangiogenic or corticosteroid intravitreal treatment

147 njugation of SAN1 did not disrupt any of its antiangiogenic or cytotoxic properties in GnRH-R-express

148 Novel combinations of these drugs with other antiangiogenics or other classes of drugs are being deve

149 the discovery and characterization of novel antiangiogenic pathways have been particularly impactful

150 nd metastasis by catalyzing the formation of antiangiogenic peptides.

151 and underlie escape mechanisms from current antiangiogenic pharmacotherapies.

152 ith increased endothelial cell apoptosis, an antiangiogenic plasma profile, and elevated levels of ci

153 x, recasting GIPCs as negative modulators of antiangiogenic PLXND1 signaling and suggest that PLXND1

154 orts the idea that Akt can be either pro- or antiangiogenic, possibly due to compensation by multiple

155 In this study, we explored the antiangiogenic potential of six synthetic hydroxytyrosyl

156 embryo angiogenesis assay again confirms the antiangiogenic properties of 1 and 4.

157 Thus, recombinant TcCalr has important antiangiogenic properties, detected in vitro, ex vivo, a

158 dies have shown that Abeta peptides can have antiangiogenic properties, which may contribute to vascu

159 ate for oxylipins with anti-inflammatory and antiangiogenic properties.

160 the intake of virgin olive oil, having shown antiangiogenic properties.

161 le Fms-like tyrosine kinase-1 (sFlt-1) is an antiangiogenic protein believed to mediate the signs and

162 s analyses in endothelial cells returned the antiangiogenic protein thrombospondin-1 as a common targ

163 g chromogranin A (CgA, CHGA), classically an antiangiogenic protein, can activate latent antiangiogen

164 ike tyrosine kinase 1 (sFLT1), a circulating antiangiogenic protein, precede clinical signs and sympt

165 pigment epithelium-derived factor (PEDF), an antiangiogenic protein, to regulate retinal pigment epit

166 is Review, we discuss the pathogenic role of antiangiogenic proteins released by the placenta in the

167 a (ccRCC), AXL expression is associated with antiangiogenic resistance and poor survival.

168 Our results unravel specific features of antiangiogenic resistance, with potential therapeutic im

169 l-targeted H(2)S donor, AP39, suppressed the antiangiogenic response and restored the mitochondrial b

170 dase activity, reversed oxidative stress and antiangiogenic response in hypoxic trophoblasts.

171 dependent activity coupled with the additive antiangiogenic response observed in combination with bev

172 conclusion, SC-MRI enabled monitoring of the antiangiogenic response of 786-0 RCC xenografts to sunit

173 model of angiogenesis and exerts an additive antiangiogenic response with the anti-VEGF biologic beva

174 ner, while most other semaphorins, including antiangiogenic semaphorins such as sema3A do not.

175 roangiogenic KDR and negatively, in part, of antiangiogenic SFRP4 Twist1 reprogramming enhanced the e

176 dothelial cells and to induce either pro- or antiangiogenic signaling.

177 Previous studies discovered quininib, an antiangiogenic small molecule antagonist of cysteinyl le

178 the mechanism of resistance to sunitinib, an antiangiogenic small molecule, and to exploit this mecha

179 ased assay that responds to complex pro- and antiangiogenic soluble factors with an in vitro readout

180 In tumors, antiangiogenic, specifically anti-VEGF, treatments can "

181 ated by GATA2 transcriptionally and targeted antiangiogenic SPRED1 and FOXO3a contributing to GATA2-m

182 rogram lung cancer secreted proteome into an antiangiogenic state, offering a novel basis to account

183 se findings might pave the way toward novel, antiangiogenic strategies in disorders that are characte

184 Currently, antiangiogenic strategies in metastatic breast cancer ha

185 options for treating these diseases include antiangiogenic strategies that can lead to the undesirab

186 their growth, has never been explored as an antiangiogenic target in cancer therapy.

187 otential target for the development of novel antiangiogenic therapeutics, and blockade of its product

188 cular tumors are not a known complication of antiangiogenic therapeutics.

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

190 The limited efficacy of current antiangiogenic therapies calls for a better understandin

191 Antiangiogenic therapies have failed to confer survival

192 ntal mechanisms that explain the efficacy of antiangiogenic therapies in retinal vascular disease.

193 e with suppression of tumor growth, and that antiangiogenic therapies may be ineffective for melanoma

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

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

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

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

198 enal cell carcinoma (ccRCC) after failure of antiangiogenic therapies, but its activity on brain meta

199 Antiangiogenic therapies, such as sunitinib, have revolu

200 ugh many ccRCC patients initially respond to antiangiogenic therapies, virtually all develop progress

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

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

203 allow for an improved response assessment to antiangiogenic therapies.

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

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

206 condition associated with antiresorptive and antiangiogenic therapies.

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

208 which may represent a target for innovative antiangiogenic therapies.

209 hronic kidney disease and patients receiving antiangiogenic therapies.

210 Antiangiogenic therapy (AAT) is a treatment option that

211 nd its cognate ligand apelin in VEGFA/VEGFR2 antiangiogenic therapy against distinct subtypes of GBM.

212 Antiangiogenic therapy also selects for aggressive pheno

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

214 an be uniquely exploited in combination with antiangiogenic therapy as a promising new biologic appro

215 Tumors escape antiangiogenic therapy by activation of proangiogenic si

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

217 Even if antiangiogenic therapy can block such secondary angiogen

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

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

220 Antiangiogenic therapy effects were detected earlier and

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

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

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

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

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

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

227 Antiangiogenic therapy is efficacious in metastatic rena

228 Intravitreal antiangiogenic therapy is the major therapeutic breakthr

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

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

231 Prudent antiangiogenic therapy might transiently normalize blood

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

233 Antiangiogenic therapy of glioblastoma (GBM) with bevaci

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

235 Antiangiogenic therapy resistance occurs frequently in p

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

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

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

239 Antiangiogenic therapy with antibodies against VEGF (bev

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

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

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

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

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

245 num-free interval, residual tumour, previous antiangiogenic therapy, and study group language, and we

246 and whether IRE1alpha inhibition can enhance antiangiogenic therapy-previously found to be ineffectiv

247 act as a surrogate marker of the benefit of antiangiogenic therapy.

248 redict which mRCC patients will benefit from antiangiogenic therapy.

249 g responses to anticancer therapy, including antiangiogenic therapy.

250 herapies, especially for tumors treated with antiangiogenic therapy.

251 ted negative effects following withdrawal of antiangiogenic therapy.

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

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

254 inhibited tumor rebound after withdrawal of antiangiogenic therapy.

255 nal measurement of ovarian tumor response to antiangiogenic therapy.

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

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

258 assessment of early treatment response after antiangiogenic therapy.

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

260 atic renal cell carcinoma (RCC) treated with antiangiogenic therapy.

261 vent resistance could fulfill the promise of antiangiogenic therapy.

262 essiveness and thus enhances the efficacy of antiangiogenic therapy.

263 out-or before-angiogenesis or in response to antiangiogenic therapy.

264 h factor]), and an increase in the levels of antiangiogenic (TNFalpha [tumor necrosis factor alpha],

265 Whereas adding antiangiogenics to chemotherapy has been a successful st

266 ere randomized to receive either single-dose antiangiogenic treatment (bevacizumab, n = 14) or contro

267 optimized vision outcomes by combination of antiangiogenic treatment and vaso-occlusive PDT.

268 followed tumor evolution during escape from antiangiogenic treatment as cancer cells coopted, and ap

269 icantly decreased (P </= .03) after a single antiangiogenic treatment compared with those in the cont

270 g nontargeted microbubbles for assessment of antiangiogenic treatment effects in a murine model of hu

271 nd functional in vivo imaging information on antiangiogenic treatment effects in human colon cancer x

272 Initiation of antiangiogenic treatment halted their growth.

273 We found that low doses of antiangiogenic treatment improve immunotherapy when the

274 T tracer, in mRCC patients before and during antiangiogenic treatment in a pilot study.

275 during tumor progression and in response to antiangiogenic treatment in gliomas and brain metastases

276 No validated predictive biomarkers for antiangiogenic treatment of metastatic renal cell carcin

277 also reveal molecular mechanisms underlying antiangiogenic treatment resistance, suggesting potentia

278 modeling reveals a more detailed response to antiangiogenic treatment than a single static image is a

279 Background Relevance of antiangiogenic treatment with bevacizumab in patients wi

280 indicate that not all patients benefit from antiangiogenic treatment, necessitating the development

281 sels (P = .03) significantly decreased after antiangiogenic treatment.

282 nducible factor-1alpha (HIF1alpha) caused by antiangiogenic treatment.

283 ization in eyes receiving recurrent periodic antiangiogenic treatment.

284 n and oxygenation in tumor tissue undergoing antiangiogenic treatment.

285 ment decisions and for assessing response to antiangiogenic treatment.

286 y and reduce the side effects of established antiangiogenic treatments for distinct GBM subtypes.

287 APLNR acts synergistically with established antiangiogenic treatments in glioblastoma and blunts the

288 s model highlight the risks of cytotoxic and antiangiogenic treatments in the context of tumor hetero

289 el to account for the cytostatic activity of antiangiogenic treatments.

290 Proinflammatory and antiangiogenic Tregs play an essential pathogenetic role

291 e way for the clinical approval of the first antiangiogenic tumor drug 15 years later.

292 h is involved in mechanisms of resistance to antiangiogenic tumour therapy.

293 e in a murine model of mBC resistance to the antiangiogenic tyrosine kinase inhibitor sunitinib.

294 Antiangiogenic tyrosine kinase inhibitors (TKI) that tar

295 w insights into the molecular mechanisms for antiangiogenic upregulation in a mitochondrial-driven en

296 Cediranib is an oral antiangiogenic vascular endothelial growth factor recept

297 In contrast, in the BS, melatonin releases antiangiogenic VEGF-Axxxb from the PT, inhibiting infund

298 65a, 165 for the 165 amino acid product) and antiangiogenic VEGFxxxb (VEGF165b) isoforms.

299 The antiangiogenic VEGFxxxb isoforms are thought to antagoni

300 d rBF significantly decreased (P </= .04) in antiangiogenic versus saline-treated tumors.