ライフサイエンスコーパス: angiogenic therapy

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

2 trategies could improve the efficacy of anti-angiogenic therapy.

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

4 hat mediate refractoriness of tumors to anti-angiogenic therapy.

5 eneration" forms of FGF-1 for application in angiogenic therapy.

6 f a gender difference in response to cardiac angiogenic therapy.

7 y being explored in clinical trials for anti-angiogenic therapy.

8 icacy of new therapeutic strategies and anti-angiogenic therapies.

9 may also lend itself for a better design of angiogenic therapies.

10 holds promise in molecular imaging and anti-angiogenic therapies.

11 g that could serve as a basis for novel anti-angiogenic therapies.

12 rtantly, the PPCM is entirely rescued by pro-angiogenic therapies.

13 tic for use in combination with current anti-angiogenic therapies.

14 on and to suggest molecular targets for anti-angiogenic therapies.

15 regulation is needed to improve current anti-angiogenic therapies.

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

17 hat VE-PTP may be a new potential target for angiogenic therapies.

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

19 cs of angiogenesis and assessing efficacy of angiogenic therapies.

20 provide a novel approach for developing anti-angiogenic therapies.

21 epresent a new opportunity for pro- and anti-angiogenic therapies.

22 endothelial cells for cellular pro- or anti-angiogenic therapies.

23 ant implications for the development of anti-angiogenic therapies.

24 ding of the mechanisms of resistance to anti-angiogenic therapies and better selection of patients wi

25 y are critical sites for drug delivery, anti-angiogenic therapies and immunotherapy.

26 lly relevant mechanism of resistance to anti-angiogenic therapy and combined inhibition of angiogenes

27 opment of new techniques to treat CS include angiogenic therapy, antifibrosis treatments, and stem ce

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

29 d support the potential clinical use of anti-angiogenic therapy as a novel treatment modality for thi

30 ar surgery, photodynamic therapies, and anti-angiogenic therapies, as well as small pilot studies exp

31 ngiogenesis in vivo, suggesting a novel anti-angiogenic therapy based on inducible p27 overexpression

32 example, we demonstrate using VAI that anti-angiogenic therapy can improve microcirculation and oxyg

33 kely contribute to this remodeling, but anti-angiogenic therapies do not improve AML patient outcomes

34 Anti-angiogenic therapies for cancer such as VEGF neutralizin

35 Cell-mediated angiogenic therapy for ischemic heart disease has had di

36 low molecular weight heparin (LMWH) in anti-angiogenic therapy has been tempered by poor in vivo del

37 Angiogenic therapies have been used to stimulate blood v

38 stases, a setting in which results with anti-angiogenic therapy have been disappointing.

39 l models can be used to predict optimal anti-angiogenic therapies in combination with other therapeut

40 acking stromal Cav-1 might benefit from anti-angiogenic therapy in addition to standard regimens.

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

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

43 XCR2 blockade may be a novel target for anti-angiogenic therapy in colorectal adenocarcinoma.

44 ression could provide a new target for rapid angiogenic therapy in ischemic disease states.

45 use of SRPK1 inhibition as a potential anti-angiogenic therapy in PCa.

46 nsport in the external tissue (e.g., by anti-angiogenic therapy) increased tumor fragmentation may re

47 Combined neuroprotective and anti-angiogenic therapies may be required to treat Muller cel

48 iogenesis is inhibited, suggesting that anti-angiogenic therapies may not be sufficient to eliminate

49 Anti-angiogenic therapy might also lead to mobilisation of ci

50 Resistance to anti-angiogenic therapy might implicate alternative pro-angio

51 18 pathway may be a rational target for anti-angiogenic therapy of HCC.

52 r individualized treatment decisions in anti-angiogenic therapy of neovascular AMD and perhaps other

53 e of endothelial progenitor cells (EPCs) for angiogenic therapies or as biomarkers to assess cardiova

54 We hypothesized that angiogenic therapies powerfully self-regulate by dynamic

55 findings may allow for development of novel angiogenic therapies relying on secreted growth factors

56 ilities of immune-modifying, antibiotic, and angiogenic therapies remain to be proven.

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

58 ovide strong implications for designing anti-angiogenic therapies that may differentially target endo

59 enesis, which has important implications for angiogenic therapies that target NO.

60 Anti-angiogenic therapies that target VEGF and the VEGF recep

61 bition provides a novel opportunity for anti-angiogenic therapy to complement VEGF or VEGFR2 blockade

62 ky tumour vasculature might also enable anti-angiogenic therapy to increase the efficacy of radiation

63 ed by germline BRCA status and previous anti-angiogenic therapy, to receive olaparib capsules 400 mg

64 r involvement in adaptive resistance to anti-angiogenic therapy via enhanced metastasis.

65 Anti-angiogenic therapies--which 'normalize' the abnormal blo

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

67 t is likely that acquired resistance to anti-angiogenic therapy will involve alterations of the tumor