戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 y being explored in clinical trials for anti-angiogenic therapy.
2 ctoriness found in cancers resistant to anti-angiogenic therapy.
3 trategies could improve the efficacy of anti-angiogenic therapy.
4 sion and could be potential targets for anti-angiogenic therapy.
5 hat mediate refractoriness of tumors to anti-angiogenic therapy.
6 eneration" forms of FGF-1 for application in angiogenic therapy.
7 f a gender difference in response to cardiac angiogenic therapy.
8 d growth, alone and in combination with anti-angiogenic therapy.
9 ling of anti-cancer drugs combined with anti-angiogenic therapy.
10 regulation is needed to improve current anti-angiogenic therapies.
11 icacy of new therapeutic strategies and anti-angiogenic therapies.
12  may also lend itself for a better design of angiogenic therapies.
13  holds promise in molecular imaging and anti-angiogenic therapies.
14 g that could serve as a basis for novel anti-angiogenic therapies.
15 rtantly, the PPCM is entirely rescued by pro-angiogenic therapies.
16 tic for use in combination with current anti-angiogenic therapies.
17 on and to suggest molecular targets for anti-angiogenic therapies.
18 -vascular endothelial growth factor and anti-angiogenic therapies.
19 hat VE-PTP may be a new potential target for angiogenic therapies.
20  to the further development of pro- and anti-angiogenic therapies.
21 cs of angiogenesis and assessing efficacy of angiogenic therapies.
22 provide a novel approach for developing anti-angiogenic therapies.
23 epresent a new opportunity for pro- and anti-angiogenic therapies.
24  endothelial cells for cellular pro- or anti-angiogenic therapies.
25 ant implications for the development of anti-angiogenic therapies.
26 ssue vascularization are primary targets for angiogenic therapies.
27  alternative for the development of new anti-angiogenic therapies.
28 hown to improve overall survival versus anti-angiogenic therapy alone in advanced solid tumours, but
29 ding of the mechanisms of resistance to anti-angiogenic therapies and better selection of patients wi
30 ated with systemic therapies, including anti-angiogenic therapies and immune checkpoint inhibitors.
31 y are critical sites for drug delivery, anti-angiogenic therapies and immunotherapy.
32     This model has therapeutic resistance to angiogenic therapies and maintains long term deficits in
33       Current therapeutic strategies such as angiogenic therapy and anti-inflammatory therapy for tre
34 lly relevant mechanism of resistance to anti-angiogenic therapy and combined inhibition of angiogenes
35 plies the potential promising effect of anti-angiogenic therapy and immunotherapy in BC with lung met
36 issue stiffness improves the outcome of anti-angiogenic therapy and prolongs patient survival.
37 opment of new techniques to treat CS include angiogenic therapy, antifibrosis treatments, and stem ce
38                                          Pro-angiogenic therapies are an important tool for improving
39                   WHERE NEXT?: Although anti-angiogenic therapies are promising, the duration of resp
40 d support the potential clinical use of anti-angiogenic therapy as a novel treatment modality for thi
41 ar surgery, photodynamic therapies, and anti-angiogenic therapies, as well as small pilot studies exp
42 ngiogenesis in vivo, suggesting a novel anti-angiogenic therapy based on inducible p27 overexpression
43 usly treated with immune checkpoint and anti-angiogenic therapy based on results of the phase 3 LITES
44  example, we demonstrate using VAI that anti-angiogenic therapy can improve microcirculation and oxyg
45 kely contribute to this remodeling, but anti-angiogenic therapies do not improve AML patient outcomes
46                                         Anti-angiogenic therapies for cancer such as VEGF neutralizin
47                                 Current anti-angiogenic therapy for cancer is based mainly on inhibit
48 b as a next-generation disease-targeted anti-angiogenic therapy for CNV.
49                                Cell-mediated angiogenic therapy for ischemic heart disease has had di
50  low molecular weight heparin (LMWH) in anti-angiogenic therapy has been tempered by poor in vivo del
51                                              Angiogenic therapies have been used to stimulate blood v
52                                         Anti-angiogenic therapies have generated significant interest
53 as essential to this purpose, thus far, anti-angiogenic therapies have shown only modest efficacy in
54 stases, a setting in which results with anti-angiogenic therapy have been disappointing.
55 l cells has been an emerging concept in anti-angiogenic therapies, here, by using VM/AST patient samp
56 l models can be used to predict optimal anti-angiogenic therapies in combination with other therapeut
57 acking stromal Cav-1 might benefit from anti-angiogenic therapy in addition to standard regimens.
58 results have important implications for anti-angiogenic therapy in breast cancer patients.
59 to investigate molecular mechanisms and anti-angiogenic therapy in CNV.
60 XCR2 blockade may be a novel target for anti-angiogenic therapy in colorectal adenocarcinoma.
61 further investigation and modulation of anti-angiogenic therapy in GBM.
62 ression could provide a new target for rapid angiogenic therapy in ischemic disease states.
63  use of SRPK1 inhibition as a potential anti-angiogenic therapy in PCa.
64 nsport in the external tissue (e.g., by anti-angiogenic therapy) increased tumor fragmentation may re
65 d with gene aberration-related therapy, anti-angiogenic therapy led to significantly longer OS after
66            Combined neuroprotective and anti-angiogenic therapies may be required to treat Muller cel
67 iogenesis is inhibited, suggesting that anti-angiogenic therapies may not be sufficient to eliminate
68                                         Anti-angiogenic therapy might also lead to mobilisation of ci
69                           Resistance to anti-angiogenic therapy might implicate alternative pro-angio
70 18 pathway may be a rational target for anti-angiogenic therapy of HCC.
71 r individualized treatment decisions in anti-angiogenic therapy of neovascular AMD and perhaps other
72 e of endothelial progenitor cells (EPCs) for angiogenic therapies or as biomarkers to assess cardiova
73                         We hypothesized that angiogenic therapies powerfully self-regulate by dynamic
74  findings may allow for development of novel angiogenic therapies relying on secreted growth factors
75 ilities of immune-modifying, antibiotic, and angiogenic therapies remain to be proven.
76 synergy between checkpoint blockade and anti-angiogenic therapy remain elusive.
77 de significantly improved evaluation of anti-angiogenic therapy response as compared with conventiona
78                               Moreover, anti-angiogenic therapies synergize with the first-line anti-
79 ovide strong implications for designing anti-angiogenic therapies that may differentially target endo
80 enesis, which has important implications for angiogenic therapies that target NO.
81                                         Anti-angiogenic therapies that target VEGF and the VEGF recep
82 omisation was stratified by by previous anti-angiogenic therapy, time from initial diagnosis of metas
83 bition provides a novel opportunity for anti-angiogenic therapy to complement VEGF or VEGFR2 blockade
84 ky tumour vasculature might also enable anti-angiogenic therapy to increase the efficacy of radiation
85 8K signaling axis, providing new targets for angiogenic therapy to promote tissue repair.
86 l trials that have evaluated the efficacy of angiogenic therapy to revascularize the infarcted heart
87 ed by germline BRCA status and previous anti-angiogenic therapy, to receive olaparib capsules 400 mg
88 r involvement in adaptive resistance to anti-angiogenic therapy via enhanced metastasis.
89 red in chitosan scaffolds as next generation angiogenic therapies which exert biological activity via
90                                         Anti-angiogenic therapies--which 'normalize' the abnormal blo
91 no effective treatments for patients on anti-angiogenic therapies whose tumours progress.
92 t is likely that acquired resistance to anti-angiogenic therapy will involve alterations of the tumor