ライフサイエンスコーパス: anti-angiogenic therapy

1 refractoriness found in cancers resistant to anti-angiogenic therapy.

2 ory strategies could improve the efficacy of anti-angiogenic therapy.

3 ogression and could be potential targets for anti-angiogenic therapy.

4 nts that mediate refractoriness of tumors to anti-angiogenic therapy.

5 rently being explored in clinical trials for anti-angiogenic therapy.

6 e efficacy of new therapeutic strategies and anti-angiogenic therapies.

7 (NPs) holds promise in molecular imaging and anti-angiogenic therapies.

8 naling that could serve as a basis for novel anti-angiogenic therapies.

9 rapeutic for use in combination with current anti-angiogenic therapies.

10 ibition and to suggest molecular targets for anti-angiogenic therapies.

11 esis regulation is needed to improve current anti-angiogenic therapies.

12 anti-vascular endothelial growth factor and anti-angiogenic therapies.

13 ucial to the further development of pro- and anti-angiogenic therapies.

14 ould provide a novel approach for developing anti-angiogenic therapies.

15 may represent a new opportunity for pro- and anti-angiogenic therapies.

16 ce of endothelial cells for cellular pro- or anti-angiogenic therapies.

17 nificant implications for the development of anti-angiogenic therapies.

18 rstanding of the mechanisms of resistance to anti-angiogenic therapies and better selection of patien

19 s they are critical sites for drug delivery, anti-angiogenic therapies and immunotherapy.

20 inically relevant mechanism of resistance to anti-angiogenic therapy and combined inhibition of angio

21 WHERE NEXT?: Although anti-angiogenic therapies are promising, the duration of

22 is and support the potential clinical use of anti-angiogenic therapy as a novel treatment modality fo

23 macular surgery, photodynamic therapies, and anti-angiogenic therapies, as well as small pilot studie

24 and angiogenesis in vivo, suggesting a novel anti-angiogenic therapy based on inducible p27 overexpre

25 As an example, we demonstrate using VAI that anti-angiogenic therapy can improve microcirculation and

26 ch likely contribute to this remodeling, but anti-angiogenic therapies do not improve AML patient out

27 Anti-angiogenic therapies for cancer such as VEGF neutra

28 al of low molecular weight heparin (LMWH) in anti-angiogenic therapy has been tempered by poor in viv

29 metastases, a setting in which results with anti-angiogenic therapy have been disappointing.

30 tional models can be used to predict optimal anti-angiogenic therapies in combination with other ther

31 nts lacking stromal Cav-1 might benefit from anti-angiogenic therapy in addition to standard regimens

32 hese results have important implications for anti-angiogenic therapy in breast cancer patients.

33 odel to investigate molecular mechanisms and anti-angiogenic therapy in CNV.

34 -8, CXCR2 blockade may be a novel target for anti-angiogenic therapy in colorectal adenocarcinoma.

35 r the use of SRPK1 inhibition as a potential anti-angiogenic therapy in PCa.

36 t transport in the external tissue (e.g., by anti-angiogenic therapy) increased tumor fragmentation m

37 Combined neuroprotective and anti-angiogenic therapies may be required to treat Mulle

38 n angiogenesis is inhibited, suggesting that anti-angiogenic therapies may not be sufficient to elimi

39 Anti-angiogenic therapy might also lead to mobilisation

40 Resistance to anti-angiogenic therapy might implicate alternative pro-

41 A/FGF18 pathway may be a rational target for anti-angiogenic therapy of HCC.

42 is for individualized treatment decisions in anti-angiogenic therapy of neovascular AMD and perhaps o

43 Moreover, anti-angiogenic therapies synergize with the first-line

44 gs provide strong implications for designing anti-angiogenic therapies that may differentially target

45 Anti-angiogenic therapies that target VEGF and the VEGF

46 inhibition provides a novel opportunity for anti-angiogenic therapy to complement VEGF or VEGFR2 blo

47 d leaky tumour vasculature might also enable anti-angiogenic therapy to increase the efficacy of radi

48 atified by germline BRCA status and previous anti-angiogenic therapy, to receive olaparib capsules 40

49 their involvement in adaptive resistance to anti-angiogenic therapy via enhanced metastasis.

50 Anti-angiogenic therapies--which 'normalize' the abnorma

51 are no effective treatments for patients on anti-angiogenic therapies whose tumours progress.

52 ed, it is likely that acquired resistance to anti-angiogenic therapy will involve alterations of the