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 rently being explored in clinical trials for anti-angiogenic therapy.
2 refractoriness found in cancers resistant to anti-angiogenic therapy.
3 ory strategies could improve the efficacy of anti-angiogenic therapy.
4 ogression and could be potential targets for anti-angiogenic therapy.
5 nts that mediate refractoriness of tumors to anti-angiogenic therapy.
6 on and growth, alone and in combination with anti-angiogenic therapy.
7 cheduling of anti-cancer drugs combined with anti-angiogenic therapy.
8 esis regulation is needed to improve current anti-angiogenic therapies.
9 e efficacy of new therapeutic strategies and anti-angiogenic therapies.
10 (NPs) holds promise in molecular imaging and anti-angiogenic therapies.
11 naling that could serve as a basis for novel anti-angiogenic therapies.
12 rapeutic for use in combination with current anti-angiogenic therapies.
13 ibition and to suggest molecular targets for anti-angiogenic therapies.
14  anti-vascular endothelial growth factor and anti-angiogenic therapies.
15 ucial to the further development of pro- and anti-angiogenic therapies.
16 ould provide a novel approach for developing anti-angiogenic therapies.
17 may represent a new opportunity for pro- and anti-angiogenic therapies.
18 ce of endothelial cells for cellular pro- or anti-angiogenic therapies.
19 nificant implications for the development of anti-angiogenic therapies.
20 er an alternative for the development of new anti-angiogenic therapies.
21 een shown to improve overall survival versus anti-angiogenic therapy alone in advanced solid tumours,
22 rstanding of the mechanisms of resistance to anti-angiogenic therapies and better selection of patien
23 s treated with systemic therapies, including anti-angiogenic therapies and immune checkpoint inhibito
24 s they are critical sites for drug delivery, anti-angiogenic therapies and immunotherapy.
25 inically relevant mechanism of resistance to anti-angiogenic therapy and combined inhibition of angio
26 ls implies the potential promising effect of anti-angiogenic therapy and immunotherapy in BC with lun
27 ing tissue stiffness improves the outcome of anti-angiogenic therapy and prolongs patient survival.
28                        WHERE NEXT?: Although anti-angiogenic therapies are promising, the duration of
29 is and support the potential clinical use of anti-angiogenic therapy as a novel treatment modality fo
30 macular surgery, photodynamic therapies, and anti-angiogenic therapies, as well as small pilot studie
31 and angiogenesis in vivo, suggesting a novel anti-angiogenic therapy based on inducible p27 overexpre
32 reviously treated with immune checkpoint and anti-angiogenic therapy based on results of the phase 3
33 As an example, we demonstrate using VAI that anti-angiogenic therapy can improve microcirculation and
34 ch likely contribute to this remodeling, but anti-angiogenic therapies do not improve AML patient out
35                                              Anti-angiogenic therapies for cancer such as VEGF neutra
36                                      Current anti-angiogenic therapy for cancer is based mainly on in
37 3 hFab as a next-generation disease-targeted anti-angiogenic therapy for CNV.
38 al of low molecular weight heparin (LMWH) in anti-angiogenic therapy has been tempered by poor in viv
39                                              Anti-angiogenic therapies have generated significant int
40 rded as essential to this purpose, thus far, anti-angiogenic therapies have shown only modest efficac
41  metastases, a setting in which results with anti-angiogenic therapy have been disappointing.
42 tromal cells has been an emerging concept in anti-angiogenic therapies, here, by using VM/AST patient
43 tional models can be used to predict optimal anti-angiogenic therapies in combination with other ther
44 nts lacking stromal Cav-1 might benefit from anti-angiogenic therapy in addition to standard regimens
45 hese results have important implications for anti-angiogenic therapy in breast cancer patients.
46 odel to investigate molecular mechanisms and anti-angiogenic therapy in CNV.
47 -8, CXCR2 blockade may be a novel target for anti-angiogenic therapy in colorectal adenocarcinoma.
48  for further investigation and modulation of anti-angiogenic therapy in GBM.
49 r the use of SRPK1 inhibition as a potential anti-angiogenic therapy in PCa.
50 t transport in the external tissue (e.g., by anti-angiogenic therapy) increased tumor fragmentation m
51 reated with gene aberration-related therapy, anti-angiogenic therapy led to significantly longer OS a
52                 Combined neuroprotective and anti-angiogenic therapies may be required to treat Mulle
53 n angiogenesis is inhibited, suggesting that anti-angiogenic therapies may not be sufficient to elimi
54                                              Anti-angiogenic therapy might also lead to mobilisation
55                                Resistance to anti-angiogenic therapy might implicate alternative pro-
56 A/FGF18 pathway may be a rational target for anti-angiogenic therapy of HCC.
57 is for individualized treatment decisions in anti-angiogenic therapy of neovascular AMD and perhaps o
58 ying synergy between checkpoint blockade and anti-angiogenic therapy remain elusive.
59 provide significantly improved evaluation of anti-angiogenic therapy response as compared with conven
60                                    Moreover, anti-angiogenic therapies synergize with the first-line
61 gs provide strong implications for designing anti-angiogenic therapies that may differentially target
62                                              Anti-angiogenic therapies that target VEGF and the VEGF
63  Randomisation was stratified by by previous anti-angiogenic therapy, time from initial diagnosis of
64  inhibition provides a novel opportunity for anti-angiogenic therapy to complement VEGF or VEGFR2 blo
65 d leaky tumour vasculature might also enable anti-angiogenic therapy to increase the efficacy of radi
66 atified by germline BRCA status and previous anti-angiogenic therapy, to receive olaparib capsules 40
67  their involvement in adaptive resistance to anti-angiogenic therapy via enhanced metastasis.
68                                              Anti-angiogenic therapies--which 'normalize' the abnorma
69  are no effective treatments for patients on anti-angiogenic therapies whose tumours progress.
70 ed, it is likely that acquired resistance to anti-angiogenic therapy will involve alterations of the