ライフサイエンスコーパス: antiangiogenesis

1 combining antigen-specific immunotherapy and antiangiogenesis.

2 ation, antiproliferation, antimigration, and antiangiogenesis.

3 l of dominant-negative CCN2/CTGF mutants for antiangiogenesis.

4 marrow vascularization, suggesting a role in antiangiogenesis.

5 ased drug retention is a general response to antiangiogenesis.

6 FR-1 expression in tumor cells, but not with antiangiogenesis.

7 ding induction of apoptosis, cytostasis, and antiangiogenesis.

8 mechanisms suggested for this inhibition is antiangiogenesis.

9 as serum binding proteins on taxane-mediated antiangiogenesis.

10 iated antiproliferation, antimetastasis, and antiangiogenesis activities.

11 Attempts to identify surrogate markers of antiangiogenesis activity are currently ongoing, and may

12 reover, the thiazole analogues showed strong antiangiogenesis activity, blocking new blood vessel for

13 pical vehicle exhibited slight antitumor and antiangiogenesis activity.

14 el therapeutic target for dual antitumor and antiangiogenesis activity.

15 A phase I trial of the antiangiogenesis agent cilengitide (EMD 121974), an alph

16 tified to predict outcome with the use of an antiangiogenesis agent for cancer.

17 Bevacizumab was the first antiangiogenesis agent to gain approval by the Food and

18 cal data to identify the optimal dose for an antiangiogenesis agent, anti-EGFL7.

19 rived VEGF from an angiogenic factor into an antiangiogenesis agent.

20 briefly review data regarding anti-EGFR and antiangiogenesis agents before discussing the potential

21 The suppression of tumor blood perfusion by antiangiogenesis agents can be turned to therapeutic adv

22 This study confirms the activity of antiangiogenesis agents in advanced and recurrent cervic

23 Antiangiogenesis agents such as bevacizumab, a humanized

24 ally in tumor tissue they might be effective antiangiogenesis agents suitable for cancer therapy.

25 Patients with multiple myeloma receiving antiangiogenesis agents with chemotherapy and/or dexamet

26 Patients with multiple myeloma receiving antiangiogenesis agents with chemotherapy and/or dexamet

27 stone deacetylase and proteosome inhibitors, antiangiogenesis agents, Fms-like tyrosine kinase 3 (FLT

28 ents with promise include 90 Y microspheres, antiangiogenesis agents, inhibitors of growth factors an

29 d thus validate VE-cad as a novel target for antiangiogenesis agents.

30 There are also ongoing trials of antiangiogenesis agents.

31 re development of this and similar agents as antiangiogenesis and anticancer drugs.

32 enesis and may be a viable drug candidate in antiangiogenesis and anticancer therapies.

33 Antiangiogenesis and antitumor efficacy were associated

34 angiogenin could have a combined benefit of antiangiogenesis and chemotherapy in treating prostate c

35 was essential for Nutlin-3-mediated retinal antiangiogenesis and disruption of the p53 transcription

36 Therefore, combined antiangiogenesis and immune suppression will be more eff

37 the effective abrogation of scIL-12-mediated antiangiogenesis and T cell chemotaxis in mice receiving

38 F-kappaB) DNA binding, which is critical for antiangiogenesis, and that blocking the NF-kappaB pathwa

39 The use of VEGF antagonists as an antiangiogenesis approach offers a potential treatment f

40 s work may offer solutions for personalizing antiangiogenesis approaches and improving the outcome of

41 pathway may offer important new targets for antiangiogenesis approaches.

42 n is important for tumor growth and proposed antiangiogenesis as a novel approach to cancer therapy.

43 (SC-276) was advanced through antitumor and antiangiogenesis assays and was selected for development

44 (D)(LPR), a derivative molecule with strong antiangiogenesis attributes.

45 Antiangiogenesis-based cancer therapies, specifically th

46 s plays an important role in GBM growth, and antiangiogenesis-based therapies have shown clinical eff

47 g gene-based therapies, immunotherapies, and antiangiogenesis-based therapy.

48 t is suggested that the activity is based on antiangiogenesis, because in vitro tube formation is inh

49 tion, rapamycin (RAPA), which is used as the antiangiogenesis chemotherapeutic drug, can cutdown the

50 Using these methods, antiangiogenesis compounds that inhibit Flk-1 tyrosine k

51 US Food and Drug Administration approved the antiangiogenesis drug bevacizumab for women with advance

52 r [Co(II)Co(II)(EcMetAP)] incubated with the antiangiogenesis drug fumagillin are also presented.

53 in skin angiogenesis and can serve for rapid antiangiogenesis drug screening.

54 eratrol (1), phenstatin (2c), and the cancer antiangiogenesis drug sodium combretastatin A-4 phosphat

55 Recent approvals of antiangiogenesis drugs for clinical use in cancer and ma

56 hat MSMP inhibition combined with the use of antiangiogenesis drugs may be a new strategy to overcome

57 combination chemotherapies that incorporate antiangiogenesis drugs targeting VEGF receptor.

58 predict efficacy at the molecular level for antiangiogenesis drugs which are anticipated to result i

59 is orally bioavailable inhibitor exhibits an antiangiogenesis effect and a broad anticancer activity

60 s treated with combined drugs, suggesting an antiangiogenesis effect of this combination.

61 The in vivo antiangiogenesis effects mediated by chNKG2D-bearing T c

62 drug that is activated intratumorally, where antiangiogenesis-enhanced retention of the therapeutic m

63 ctor (pigment epithelium-derived factor), an antiangiogenesis factor (cornea-derived transcript 6), a

64 ondin-2 (TSP-2), has been shown to act as an antiangiogenesis factor in a carcinogen-induced model of

65 ted by a balance between proangiogenesis and antiangiogenesis factors and that this balance varies in

66 Host antiangiogenesis factors defend against tumor growth.

67 ur study thus demonstrates that AAV-mediated antiangiogenesis gene therapy offers efficient and susta

68 Antigen-specific cancer immunotherapy and antiangiogenesis have emerged as two attractive strategi

69 hange could be used as an early predictor of antiangiogenesis in ectopic and orthotopic colon carcino

70 ectly with synergistic antiproliferation and antiangiogenesis in vitro.

71 assay and also in a mouse Matrigel model of antiangiogenesis in which 49 and 55 show significant inh

72 his barrier can sometimes be circumvented by antiangiogenesis-induced normalization of tumor vasculat

73 dicate that we have identified a more potent antiangiogenesis inhibitor peptide that may be used as a

74 compounds currently under evaluation include antiangiogenesis inhibitors and retinoids.

75 ial body of evidence supports the utility of antiangiogenesis inhibitors as a strategy to block or at

76 Antiangiogenesis is emerging as efficient strategy for t

77 pared with wild-type E7 DNA, suggesting that antiangiogenesis may have contributed to the antitumor e

78 We hypothesized that antiangiogenesis mediated by TSR-containing proteins cou

79 stant tumors, indicating that an escape from antiangiogenesis occurred.

80 ng cell-cycle arrest, cell death, repair, or antiangiogenesis processes.

81 Compounds 1-3 showed interesting antiangiogenesis properties in an in vitro tubulogenic a

82 , and translational (anti-) angiogenesis and antiangiogenesis research.

83 olytically cleaved to release Endostatin, an antiangiogenesis signaling factor.

84 ent study provides a molecular framework for antiangiogenesis signaling, thus impinging on a myriad o

85 Antiangiogenesis strategies in particular appear promisi

86 the existing VEGF-A/VEGFR-2 signaling-based antiangiogenesis strategies.

87 retinoic acid (CRA) as a differentiation and antiangiogenesis strategy for prostate cancer.

88 r than VEGF alone, will be a novel efficient antiangiogenesis strategy to treat cancer.

89 us vector carrying TMD1 could be a promising antiangiogenesis strategy.

90 ronomic chemotherapy is attributed widely to antiangiogenesis, the significance of this mechanism rem

91 vascular endothelial growth factor-centered antiangiogenesis therapies, which mainly lead to vascula

92 e advantages over existing cytokine-targeted antiangiogenesis therapies.

93 may assist in the selection of patients for antiangiogenesis therapy and the development of this cla

94 arkers may explain why certain patients fail antiangiogenesis therapy and they may support the use of

95 EGFR kinase inhibitors may be effective for antiangiogenesis therapy by specifically targeting the t

96 s preexisting blood vessels of the tumor and antiangiogenesis therapy capitalize on the requirement o

97 t BH4 synthesis may be a rational target for antiangiogenesis therapy for tumors.

98 Antiangiogenesis therapy has become a vital part of the

99 -concept of the efficacy and tolerability of antiangiogenesis therapy in advanced cervical cancer.

100 Its highly vascular nature suggests that antiangiogenesis therapy might be useful.

101 Our studies imply that antivascular and antiangiogenesis therapy that results in severe glucose

102 identifying patients who would benefit from antiangiogenesis therapy, and separating treatment respo

103 ctors underlying the resistance of cancer to antiangiogenesis therapy, we conducted genomic analyses

104 eir early differential perfusion response to antiangiogenesis therapy.

105 be a new strategy to overcome resistance to antiangiogenesis therapy.

106 ttractive strategy to overcome resistance to antiangiogenesis therapy.

107 f PLCgamma1 would be a compelling target for antiangiogenesis therapy.

108 and is potentially an attractive target for antiangiogenesis therapy.

109 nto an apoptotic factor, a novel approach to antiangiogenesis therapy.

110 nes CD148 as a valuable molecular target for antiangiogenesis therapy.

111 bility might compromise the effectiveness of antiangiogenesis therapy.

112 ors represent critical molecular targets for antiangiogenesis therapy.

113 ity to improve conventional chemotherapy and antiangiogenesis therapy.

114 th may be accelerated following cessation of antiangiogenesis therapy; however, the underlying mechan

115 Using antiangiogenesis treatment to prevent corneal neovascula

116 These data support the concept that targeted antiangiogenesis, using virally mediated gene transfer,

117 roangiogenesis (Vegfr2, Ccr3, and Pdgfb) and antiangiogenesis (Vegfr1 and Unc5b) as targets of Notch

118 tin-like domain of TM-TM domain 1 (rTMD1)-in antiangiogenesis were investigated.