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1  recent data suggesting that the efficacy of antiangiogenic (AA) therapies is limited in some circums
2 for the anti-inflammatory, antiscarring, and antiangiogenic actions of the AM.
3 neration ITZ analogues for their anti-Hh and antiangiogenic activities to probe more fully the struct
4 oteinase inhibitor (SERPIN) superfamily with antiangiogenic activities, were elevated in type 2 diabe
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 lampsia (PE), which have proinflammatory and antiangiogenic activity and are implicated in PE pathoph
8                          However, its potent antiangiogenic activity and the molecular targets of alp
9 from Aspergillus fumigatus, is known for its antiangiogenic activity due to binding to human methioni
10                 Remarkably, VEGF-Ax exhibits antiangiogenic activity in contrast to the proangiogenic
11 lead compound was then evaluated in vivo for antiangiogenic activity in the CAM model and in a xenogr
12  this step were then screened to isolate the antiangiogenic activity in vitro.
13 validation and mechanistic definition of the antiangiogenic activity of a novel mycotoxin, with poten
14                                          The antiangiogenic activity of alpha1(IV)NC1 is mediated, in
15 gth forms could also counter balance the pro/antiangiogenic activity of each other in in vitro angiog
16 reover, our data reveal that the established antiangiogenic activity of protamine would rely on APJ a
17 dues on the affinity, anti-inflammatory, and antiangiogenic activity of these azapeptides have now be
18  designed, synthesized, and tested for their antiangiogenic activity using in vitro assays with human
19 rgets and their effects on metformin-induced antiangiogenic activity were assessed using luciferase a
20 ylase inhibitor) via an ester bond, exhibits antiangiogenic activity, being able to reduce human reti
21          Remarkably, VEGF-Ax exhibits potent antiangiogenic activity, both in vitro and in vivo, thus
22 ta-D-glucopyranose) is a CMG2 inhibitor with antiangiogenic activity.
23 mination of the response to therapy with the antiangiogenic agent axitinib, a multiple receptor tyros
24  a standard clinical treatment course of the antiangiogenic agent sunitinib.
25 proval of an anti-VEGF antibody as the first antiangiogenic agent, many patients with cancer and ocul
26 C single-arm studies that did not include an antiangiogenic agent.
27 iled to show an overall survival benefit for antiangiogenic agents alone or in combination with chemo
28 ay be a unique target in situations in which antiangiogenic agents are withdrawn, and dual targeting
29 understanding of the mechanisms of action of antiangiogenic agents has hindered optimization and broa
30                                              Antiangiogenic agents have established efficacy in the t
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 es that the most efficacious applications of antiangiogenic agents rely upon a combination with cytot
34 r current antiangiogenic therapies, as these antiangiogenic agents target normal vasculature as well
35    The potential to heighten the efficacy of antiangiogenic agents was explored in this study based o
36 motherapy and radiotherapy), targeted drugs, antiangiogenic agents, and immunotherapy, including chec
37                  Further research with novel antiangiogenic agents, particularly in the maintenance s
38 ing in single-arm phase 2 studies evaluating antiangiogenic agents, this risk for all events (OR 4.34
39 oting effective subsequent therapy including antiangiogenic agents.
40 st experience of maintenance therapy is with antiangiogenic agents.
41 stoma has been the therapeutic evaluation of antiangiogenic agents.
42  using lower "vascular normalizing" doses of antiangiogenic agents.
43 hemorrhage in patients with HCC treated with antiangiogenic agents.
44 s well as a factor in guiding treatment with antiangiogenic agents.
45 o those of continuous treatment with various antiangiogenic agents.
46                     Sunitinib maintained its antiangiogenic and antimetastatic activity but lost its
47 s between M1-type polarized macrophages with antiangiogenic and antitumor activity and M2-type polari
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 protein, can activate latent antiangiogenic and proangiogenic sites, respectively.
54  CD36 and exhibited respectively significant antiangiogenic and slight angiogenic activities in a mic
55 rom 1997 to 2006; 12 of those studies tested antiangiogenic and/or anti-epidermal growth factor recep
56 ich suggests no positive interaction between antiangiogenics and tyrosine kinase inhibitors in the tr
57 xin from a novel source that exhibits potent antiangiogenic antitumor activity.
58                                              Antiangiogenic approaches that have shown benefit in oth
59  Our data demonstrate that miR-155 exerts an antiangiogenic but proarteriogenic function in the regul
60 genesis, and have conceptual implication for antiangiogenic cancer therapy.
61 e drugs that might also bypass the so-called antiangiogenic ceiling and have led to selective treatme
62 ations for the redox-mediated release of the antiangiogenic cleavage product from HRG.
63                         Further, we analyzed antiangiogenic components in RAC exosomes using an angio
64  effects, with exosomes from RACs containing antiangiogenic components that might protect the eye fro
65              In this work, we describe a new antiangiogenic compound (22) that inhibits proangiogenic
66 n five analogues of a clinically established antiangiogenic compound (sunitinib), from which a lead c
67 and erlotinib emerge as attractive candidate antiangiogenic compounds for prevention and treatment of
68 ovide a rationale for the development of new antiangiogenic compounds that could eventually lead to n
69  cells, turning them into dual cytotoxic and antiangiogenic compounds.
70 essing the presence of tumor vasculature and antiangiogenic drug activity.
71           In summary, Q8 is a more effective antiangiogenic drug compared with quininib.
72 nvasive imaging biomarker of response to the antiangiogenic drug sunitinib.
73              Tasquinimod is an orally active antiangiogenic drug that is currently in phase III clini
74    In addition, sorafenib is described as an antiangiogenic drug, but it also acts on immunological c
75 ort for the concept that ENOX1 represents an antiangiogenic druggable target.
76  toxins exert increased toxicity compared to antiangiogenic drugs and may therefore overcome these li
77   Bevacizumab is one of the most widely used antiangiogenic drugs in oncology, but the overall benefi
78                  Targeted treatments such as antiangiogenic drugs or poly (ADP-ribose) polymerase inh
79 oma metastasis occurs at the early stage and antiangiogenic drugs such as Vegf morpholino and sunitin
80                                          Ten antiangiogenic drugs targeting VEGF or its receptors are
81                      However, the ability of antiangiogenic drugs to delay tumor progression and exte
82 ab, highlighting the need for more effective antiangiogenic drugs with novel mechanisms of action.
83                                     However, antiangiogenic drugs, peptide receptor radionuclide ther
84                       VEGF pathway-targeting antiangiogenic drugs, such as bevacizumab, when combined
85 well tolerated in children, with evidence of antiangiogenic effect and potential clinical benefit in
86 giogenesis during therapy, despite a greater antiangiogenic effect of bevacizumab, such that a revers
87 hile p56/Lck short hairpin RNA inhibited the antiangiogenic effect of HKa.
88                                          The antiangiogenic effect of PRP was analysed by matrigel-ba
89 erved owing to the enhanced photothermal and antiangiogenic effect of RDLPNPs.
90  autophagy, an antitumor immune response, an antiangiogenic effect, and a significant "bystander" ant
91 mpair periodontal tissue repair, despite its antiangiogenic effect.
92 doses of type I IFNs occurs through a direct antiangiogenic effect.
93  VEGF-A signaling, whereas IFNgamma shows an antiangiogenic effect.
94                                   Q8 elicits antiangiogenic effects in a VEGF-independent in vitro mo
95  that miR-146a is a critical mediator of the antiangiogenic effects in endothelial cells.
96 oxides 17,18-EEQ-EA and 19,20-EDP-EA exerted antiangiogenic effects in human microvascular endothelia
97  This suggests that local CsA has negligible antiangiogenic effects in the human cornea, at least in
98  receptor kinase inhibitor SU5416, increased antiangiogenic effects in vitro and in a zebrafish angio
99      We found that ANGPTL7 itself has strong antiangiogenic effects in vitro.
100  of VEGF by bevacizumab explain the additive antiangiogenic effects observed in combination with Q8.
101 an endothelial tube assay and attenuated the antiangiogenic effects of sFlt1.
102                         Mechanistically, the antiangiogenic effects of sorafenib led to increased bon
103 epleting intracerebral copper, also exhibits antiangiogenic effects on brain tumor growth in mice.
104          The results showed that miR-499 had antiangiogenic effects on the HUVECs and suppressed the
105 imizing efficacy of chemotherapeutic agents, antiangiogenic effects, and altering antitumor immunity.
106 f thalidomide, an immunomodulatory drug with antiangiogenic effects, is limited by its toxicity.
107 tion of specific antimitotic and nonspecific antiangiogenic effects.
108 expression, alveolar cell apoptosis, and the antiangiogenic factor GAX, and decreased expression of H
109 ng in the tumor microenvironment through the antiangiogenic factor IGFBP5.
110  factor-binding protein 5 (IGFBP5), a potent antiangiogenic factor implicated in tumor suppression.
111  factor and later as the most potent natural antiangiogenic factor, a stem cell niche factor, and an
112  (MMP)-14 at the cell surface to release the antiangiogenic factor, soluble endoglin (sEng).
113 is associated with overexpression of a novel antiangiogenic factor, VEGF-A165b, that may play a patho
114                We show that the ratio of pro/antiangiogenic forms of CgA is altered in multiple myelo
115 ogenous CXCL4L1, which is independent of its antiangiogenic function.
116 hemokine that has been suggested to exert an antiangiogenic function.
117 l of SH-11037, a synthetic derivative of the antiangiogenic homoisoflavonoid cremastranone, in models
118                                Our trials of antiangiogenics in patients with newly diagnosed and rec
119  this study, we examined the role of a novel antiangiogenic isoform of vascular endothelial growth fa
120 etic (c(AmpRGD)) and the clinically approved antiangiogenic kinase inhibitor sunitinib, three novel d
121    These results indicate that miR-223 is an antiangiogenic microRNA that prevents endothelial cell p
122 methylation leading to induced expression of antiangiogenic miR-221 by GATA2-dependent demethylation
123 t the combination of PTX-loaded NPs with the antiangiogenic molecular inhibitor BIBF 1120 (BIBF) prom
124 ental evidence that K5-N,OS(H) represents an antiangiogenic multitarget molecule with potential impli
125 ere scanned before and 24 hours after either antiangiogenic (n = 9) or saline-only (n = 8) treatment.
126 ell (HUVECs) proliferation, indicating their antiangiogenic nature.
127 ninib analogues and identified a more potent antiangiogenic novel chemical entity (IUPAC name (E)-2-(
128                       This study showed that antiangiogenic or corticosteroid intravitreal treatment
129 njugation of SAN1 did not disrupt any of its antiangiogenic or cytotoxic properties in GnRH-R-express
130 cificity, and has no detectable teratogenic, antiangiogenic or neurotoxic effects at potent anti-infl
131             Tumor growth was inhibited after antiangiogenic or radiation therapy.
132 ial of these tracers to monitor responses of antiangiogenic or radiation therapy.
133 Novel combinations of these drugs with other antiangiogenics or other classes of drugs are being deve
134 tiangiogenic therapy, and highlight emerging antiangiogenic paradigms.
135        These studies reveal a SHP-1-mediated antiangiogenic pathway induced by CD36-TSP-1 interaction
136 nd metastasis by catalyzing the formation of antiangiogenic peptides.
137  and underlie escape mechanisms from current antiangiogenic pharmacotherapies.
138  is a novel tumor suppressor that induces an antiangiogenic phenotype and suppresses tumor growth, in
139 ith increased endothelial cell apoptosis, an antiangiogenic plasma profile, and elevated levels of ci
140 orts the idea that Akt can be either pro- or antiangiogenic, possibly due to compensation by multiple
141 embryo angiogenesis assay again confirms the antiangiogenic properties of 1 and 4.
142 , a proteasome inhibitor with anticancer and antiangiogenic properties used in the clinic for treatme
143 st because of their unique antimigration and antiangiogenic properties.
144 n of the protease activated receptor-1, with antiangiogenic properties.
145 ate for oxylipins with anti-inflammatory and antiangiogenic properties.
146 le Fms-like tyrosine kinase-1 (sFlt-1) is an antiangiogenic protein believed to mediate the signs and
147 s analyses in endothelial cells returned the antiangiogenic protein thrombospondin-1 as a common targ
148 g chromogranin A (CgA, CHGA), classically an antiangiogenic protein, can activate latent antiangiogen
149 ike tyrosine kinase 1 (sFlt1), a circulating antiangiogenic protein, is elevated in kidney diseases a
150 ike tyrosine kinase 1 (sFLT1), a circulating antiangiogenic protein, precede clinical signs and sympt
151 pigment epithelium-derived factor (PEDF), an antiangiogenic protein, to regulate retinal pigment epit
152     Our results unravel specific features of antiangiogenic resistance, with potential therapeutic im
153 dependent activity coupled with the additive antiangiogenic response observed in combination with bev
154 conclusion, SC-MRI enabled monitoring of the antiangiogenic response of 786-0 RCC xenografts to sunit
155 model of angiogenesis and exerts an additive antiangiogenic response with the anti-VEGF biologic beva
156     Given that VEGF can elicit both pro- and antiangiogenic responses depending upon the balance of s
157 ner, while most other semaphorins, including antiangiogenic semaphorins such as sema3A do not.
158 servations suggest that elevated circulating antiangiogenic serpins in diabetic patients may contribu
159 dothelial cells and to induce either pro- or antiangiogenic signaling.
160          We reported earlier the delivery of antiangiogenic single chain antibodies by using oncolyti
161     Previous studies discovered quininib, an antiangiogenic small molecule antagonist of cysteinyl le
162 the mechanism of resistance to sunitinib, an antiangiogenic small molecule, and to exploit this mecha
163 ased assay that responds to complex pro- and antiangiogenic soluble factors with an in vitro readout
164                                   In tumors, antiangiogenic, specifically anti-VEGF, treatments can "
165 egrowth in PAD to increased expression of an antiangiogenic splice variant of VEGF-A.
166 ated by GATA2 transcriptionally and targeted antiangiogenic SPRED1 and FOXO3a contributing to GATA2-m
167 rogram lung cancer secreted proteome into an antiangiogenic state, offering a novel basis to account
168 se findings might pave the way toward novel, antiangiogenic strategies in disorders that are characte
169                                   Currently, antiangiogenic strategies in metastatic breast cancer ha
170 tomised treatment, which should increase the antiangiogenic survival ceiling.
171 cytes may represent a novel, nonendothelial, antiangiogenic target for lymphoma therapy.
172 Inhibition of p110alpha may thus offer a new antiangiogenic therapeutic opportunity in cancer.
173 otential target for the development of novel antiangiogenic therapeutics, and blockade of its product
174 cular tumors are not a known complication of antiangiogenic therapeutics.
175 ools with which to easily evaluate potential antiangiogenic therapies beyond eye research.
176                                   Successful antiangiogenic therapies have been developed for the tre
177                                              Antiangiogenic therapies have failed to confer survival
178                                              Antiangiogenic therapies like bevacizumab offer promise
179 ing strategies of combinations of immune and antiangiogenic therapies may lead to further advancement
180 eted therapy (radiation/chemo) together with antiangiogenic therapies reduced GBM tumor size but incr
181                                              Antiangiogenic therapies show some therapeutic potential
182 onse and nonenhancing tumor progression from antiangiogenic therapies, and pseudoprogression from rad
183 naling remains a major challenge for current antiangiogenic therapies, as these antiangiogenic agents
184    However, rapid emergence of resistance to antiangiogenic therapies, such as bevacizumab, greatly l
185                                              Antiangiogenic therapies, such as sunitinib, have revolu
186 ve of this study was to evaluate alternative antiangiogenic therapies, which target multiple VEGF fam
187 , age, tumor type and involvement, and prior antiangiogenic therapies.
188 allow for an improved response assessment to antiangiogenic therapies.
189 oit this seminal pathway and improve current antiangiogenic therapies.
190 s that affect vascular permeability, such as antiangiogenic therapies.
191 sent in GSC and are resistant to traditional antiangiogenic therapies.
192 s, and the potential activity of alternative antiangiogenic therapies.
193                                              Antiangiogenic therapy (AAT) is a treatment option that
194 RC-52 xenografts after treatment with either antiangiogenic therapy (bevacizumab or sorafenib) or tum
195                                              Antiangiogenic therapy also selects for aggressive pheno
196 erlying mechanisms of resistance specific to antiangiogenic therapy and develop strategies to overcom
197 gs challenge both the original rationale for antiangiogenic therapy and our understanding of the phys
198                                Tumors escape antiangiogenic therapy by activation of proangiogenic si
199 e effect and to potentiate responsiveness to antiangiogenic therapy by concomitantly targeting ECM-mo
200 ndings offer strong evidence that short-term antiangiogenic therapy can promote a transient vessel no
201 g laser photocoagulation, vitrectomy, and/or antiangiogenic therapy confirmed by an external adjudica
202 as the potential to be manipulated in future antiangiogenic therapy design.
203            Despite clear antitumor efficacy, antiangiogenic therapy did not alter tumor uptake of (11
204                                              Antiangiogenic therapy effects were detected earlier and
205                             In this context, antiangiogenic therapy emerged as a promising treatment
206 ctions of RAC exosomes, we might improve the antiangiogenic therapy for CNV in age-related macular de
207 ew challenge for uninterrupted and sustained antiangiogenic therapy for treatment of human cancers.
208                              Sunitinib is an antiangiogenic therapy given as a first-line treatment f
209                                              Antiangiogenic therapy has shown clear activity and impr
210 ma is a highly vascularized brain tumor, and antiangiogenic therapy improves its progression-free sur
211 jor role for Gal-1 as a tractable target for antiangiogenic therapy in advanced stages of the disease
212                                Resistance to antiangiogenic therapy in glioblastoma (GBM) patients ma
213                                  The role of antiangiogenic therapy in mCRPC remains investigational.
214                              The efficacy of antiangiogenic therapy in neovascular AMD is strongly de
215 c (CT) images, and predict tumor response to antiangiogenic therapy in patients with metastatic renal
216                             However, current antiangiogenic therapy induces serious adverse effects i
217                                              Antiangiogenic therapy is efficacious in metastatic rena
218                                 Intravitreal antiangiogenic therapy is the major therapeutic breakthr
219  tumor vessel numbers and function following antiangiogenic therapy may also affect intratumoral deli
220 tic that complements and improves concurrent antiangiogenic therapy may be a promising treatment stra
221 In conclusion, tumor perfusion changes after antiangiogenic therapy may distinguish responders vs. no
222                                      Prudent antiangiogenic therapy might transiently normalize blood
223 eflects the viability of tumor tissue during antiangiogenic therapy more reliably than contrast-enhan
224 ation of the blood-brain barrier (BBB) after antiangiogenic therapy of gliomas with bevacizumab may r
225                 In particular, the impact of antiangiogenic therapy on tumor blood flow and oxygenati
226  decade and propose strategies for improving antiangiogenic therapy outcomes for malignant and nonmal
227                     Bevacizumab is the first antiangiogenic therapy proven to slow metastatic disease
228              The mechanisms of resistance to antiangiogenic therapy remain incompletely understood.
229                                              Antiangiogenic therapy resistance occurs frequently in p
230 junctive CXCR4 antagonists may help overcome antiangiogenic therapy resistance, benefiting GBM patien
231 etabolic traits of tumors can be selected by antiangiogenic therapy suggests insights into the evolut
232  Thus, beta1 integrins promote resistance to antiangiogenic therapy through potentiation of multiple
233 sion of this molecule is an ideal target for antiangiogenic therapy to treat cancer.
234                                              Antiangiogenic therapy with antibodies against VEGF (bev
235 nitor response of colon cancer xenografts to antiangiogenic therapy with functional and molecular US
236 f disease manifestations and is a target for antiangiogenic therapy with the monoclonal antibody beva
237 tient management and monitor the response to antiangiogenic therapy with the optimum noninvasive imag
238 rgeting pBMDC influx along with radiation or antiangiogenic therapy would be critical to prevent vasc
239  discuss successes and challenges of current antiangiogenic therapy, and highlight emerging antiangio
240 infiltration into tumors after withdrawal of antiangiogenic therapy, and lowering platelet counts mar
241 on factors were selected chemotherapy, prior antiangiogenic therapy, and platinum-free interval.
242 ikely reflects an onset of hypoxia caused by antiangiogenic therapy, and that beta1 inhibition is wel
243 r SK-RC-52 xenografts was not affected after antiangiogenic therapy, except in head and neck squamous
244 ncer that responds to checkpoint blockade or antiangiogenic therapy, uncovering a protective role by
245                                These include antiangiogenic therapy, vasodilatory agents, antilymphog
246 e absence of VEGF, following radiotherapy or antiangiogenic therapy, we documented an increase in Ang
247 redict which mRCC patients will benefit from antiangiogenic therapy.
248 ted negative effects following withdrawal of antiangiogenic therapy.
249 th treatment-naive BCVA and BCVA outcomes in antiangiogenic therapy.
250 with clear-cell mRCC previously treated with antiangiogenic therapy.
251  inhibited tumor rebound after withdrawal of antiangiogenic therapy.
252 nal measurement of ovarian tumor response to antiangiogenic therapy.
253 t to Nck as an emergent target for effective antiangiogenic therapy.
254 ve outcomes of patients with GBM who receive antiangiogenic therapy.
255 assessment of early treatment response after antiangiogenic therapy.
256 with Angpt/Tie2 has the potential to improve antiangiogenic therapy.
257 e an antitumor agent and open a new field of antiangiogenic therapy.
258 es is not necessarily decreased by effective antiangiogenic therapy.
259 2 followed tumor volume in studies featuring antiangiogenic therapy.
260 ectively block tumor progression and improve antiangiogenic therapy.
261 orafenib might be a ceiling for single-agent antiangiogenic therapy.
262 rtance, VEGF has been at the center stage of antiangiogenic therapy.
263 g responses to anticancer therapy, including antiangiogenic therapy.
264 herapies, especially for tumors treated with antiangiogenic therapy.
265 sociated with increased expression levels of antiangiogenic thrombospondin-1 and inhibited S1177 phos
266 h factor]), and an increase in the levels of antiangiogenic (TNFalpha [tumor necrosis factor alpha],
267 ere randomized to receive either single-dose antiangiogenic treatment (bevacizumab, n = 14) or contro
268  optimized vision outcomes by combination of antiangiogenic treatment and vaso-occlusive PDT.
269 doxycycline could be used to enhance current antiangiogenic treatment approaches in various condition
270 icantly decreased (P </= .03) after a single antiangiogenic treatment compared with those in the cont
271 g nontargeted microbubbles for assessment of antiangiogenic treatment effects in a murine model of hu
272 nd functional in vivo imaging information on antiangiogenic treatment effects in human colon cancer x
273  to diagnose tumor progression and to assess antiangiogenic treatment effects.
274 s needed regarding safety, dose, and type of antiangiogenic treatment for ROP.
275 d the effect of a preventive and therapeutic antiangiogenic treatment in a diet-induced mouse model f
276 T tracer, in mRCC patients before and during antiangiogenic treatment in a pilot study.
277       No validated predictive biomarkers for antiangiogenic treatment of metastatic renal cell carcin
278  also reveal molecular mechanisms underlying antiangiogenic treatment resistance, suggesting potentia
279 modeling reveals a more detailed response to antiangiogenic treatment than a single static image is a
280                         Individualization of antiangiogenic treatment using data from clinical trials
281 ious disciplines, most prominently including antiangiogenic treatment with bevacizumab.
282  indicate that not all patients benefit from antiangiogenic treatment, necessitating the development
283 ization in eyes receiving recurrent periodic antiangiogenic treatment.
284 ght serve as a tool to stratify patients for antiangiogenic treatment.
285 sels (P = .03) significantly decreased after antiangiogenic treatment.
286 nducible factor-1alpha (HIF1alpha) caused by antiangiogenic treatment.
287 s model highlight the risks of cytotoxic and antiangiogenic treatments in the context of tumor hetero
288 e way for the clinical approval of the first antiangiogenic tumor drug 15 years later.
289 h is involved in mechanisms of resistance to antiangiogenic tumour therapy.
290 e in a murine model of mBC resistance to the antiangiogenic tyrosine kinase inhibitor sunitinib.
291                                              Antiangiogenic tyrosine kinase inhibitors (TKI) that tar
292                         Cediranib is an oral antiangiogenic vascular endothelial growth factor recept
293 reduced expression of pro-angiogenic but not antiangiogenic VEGF isoforms.
294 e that inflammation-driven expression of the antiangiogenic VEGF-A isoform can contribute to impaired
295 PAD is associated with elevated levels of an antiangiogenic VEGF-A splice isoform (VEGF-A165b) and a
296   In contrast, in the BS, melatonin releases antiangiogenic VEGF-Axxxb from the PT, inhibiting infund
297 65a, 165 for the 165 amino acid product) and antiangiogenic VEGFxxxb (VEGF165b) isoforms.
298                                          The antiangiogenic VEGFxxxb isoforms are thought to antagoni
299 d rBF significantly decreased (P </= .04) in antiangiogenic versus saline-treated tumors.
300 the possible beneficial effects of combining antiangiogenic with tumor-specific immunotherapeutic app

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