ライフサイエンスコーパス: neoangiogenesis

1 Ps may be clinically effective in augmenting neoangiogenesis.

2 how bone marrow derived cells contribute to neoangiogenesis.

3 entify PML as a novel suppressor of mTOR and neoangiogenesis.

4 ciated with an osteoblast bone formation and neoangiogenesis.

5 ith the expression of osteoblast markers and neoangiogenesis.

6 earch to identify factors that support tumor neoangiogenesis.

7 activity constitutes a barrier to effective neoangiogenesis.

8 endowed with protumoral activities, such as neoangiogenesis.

9 cancer progression, presumably by preventing neoangiogenesis.

10 d inflammation was associated with increased neoangiogenesis.

11 Tumor growth requires neoangiogenesis.

12 tions in the hosts, including stimulation of neoangiogenesis.

13 ng of AMCs into areas of MM tumor growth and neoangiogenesis.

14 proliferation and invasiveness coupled with neoangiogenesis.

15 stromal endothelial cells that mediate tumor neoangiogenesis.

16 g to the degree of vascular inflammation and neoangiogenesis.

17 solid tumors one had to target the inherent neoangiogenesis.

18 sites of ischemic injury where they promote neoangiogenesis.

19 ritical role in vascular tone regulation and neoangiogenesis.

20 nic liver diseases associated with increased neoangiogenesis.

21 emained mostly intact and showed very little neoangiogenesis.

22 on of Angiopoietin-1 in pericytes to enhance neoangiogenesis.

23 n, result in vision loss because of aberrant neoangiogenesis.

24 ne tumor (pNET) model commonly used to study neoangiogenesis.

25 ial progenitor cells in the process of tumor neoangiogenesis.

26 ecreased beta8 expression leads to defective neoangiogenesis.

27 scular endothelial growth factor protein and neoangiogenesis.

28 raft growth in mice while markedly impairing neoangiogenesis.

29 l components of the earliest phases of tumor neoangiogenesis.

30 al neoplasia, stimulating cell migration and neoangiogenesis.

31 ment of VEGF in MDSC transplantation-induced neoangiogenesis.

32 its and extravasated red blood cells, making neoangiogenesis a key component of the tumor.

33 RII) are the predominant regulators of tumor neoangiogenesis, a key element for tumor growth and prog

34 Artery tertiary lymphoid organs show marked neoangiogenesis, aberrant lymphangiogenesis, and extensi

35 thelial growth factor (VEGF) expression, and neoangiogenesis after retinal hypoxia.

36 on, exhibit a decrease in glioma volumes and neoangiogenesis and an increase in antitumorigenic GAM i

37 oster disease development by promoting tumor neoangiogenesis and by enhancing cancer metastasis.

38 alysis of brain tumors including the rate of neoangiogenesis and cellularity.

39 tion of Cxcl9 led to a strong attenuation of neoangiogenesis and experimental liver fibrosis in vivo.

40 ner, thus favoring tumor growth by promoting neoangiogenesis and immunosuppression.

41 c-Cbl deletion was associated with enhanced neoangiogenesis and increased expression of vascular end

42 (KSHV) and is characterized by uncontrolled neoangiogenesis and inflammation.

43 oproteinase (MMP)-2 has been associated with neoangiogenesis and it has been proposed that the levels

44 tumor microenvironment severely compromised neoangiogenesis and lymphangiogenesis during pancreatic

45 the in vivo effects of the matrix protein on neoangiogenesis and lymphoid organization.

46 onstitute a favorable environment to support neoangiogenesis and may explain why vascular insults syn

47 rmalities in the pancreas included fibrosis, neoangiogenesis and mild macrophage infiltration, and th

48 ees of cellularity, mitoses, hypoxia-induced neoangiogenesis and necrosis, features that characterize

49 factors did not have any benefit in terms of neoangiogenesis and perfusion and had minimal effect on

50 tch receptor signaling is required for tumor neoangiogenesis and provides a new target for tumor ther

51 dent remodeling of the myofibers may promote neoangiogenesis and restoration of blood perfusion in sk

52 ransmural inflammation induces microvascular neoangiogenesis and results in lumen-occlusive intimal h

53 Neoangiogenesis and STAT3 hyperactivation are known to b

54 of COUP-TFII in adults severely compromised neoangiogenesis and suppressed tumor growth in xenograft

55 uggest that JNK1 plays a key role in retinal neoangiogenesis and that it represents a new pharmacolog

56 iseased mouse and human arteries in areas of neoangiogenesis and that these cells constitute a main c

57 UM resolved typical features of neoangiogenesis and tumor cell invasion with a spatial r

58 Neoangiogenesis and vascular injury are observed in IBD

59 r3(-/-) mice was strongly linked to enhanced neoangiogenesis and VEGF/VEGFR2 expression compared with

60 an important protumorigenic role by favoring neoangiogenesis and/or by suppressing antitumor immune r

61 ltered production of inflammatory cytokines, neoangiogenesis, and autoreactive T lymphocytes have all

62 A/histone epigenetic complex, antiapoptosis, neoangiogenesis, and immune modulation.

63 ression through induction of tumor invasion, neoangiogenesis, and immunosuppression.

64 tegrin beta3 is critical for tumor invasion, neoangiogenesis, and inflammation, making it a promising

65 e alternative activation, immunosuppression, neoangiogenesis, and melanoma tumor outgrowth.

66 several effects including reducing fibrosis, neoangiogenesis, and neomyogenesis.

67 rrow stromal alterations marked by fibrosis, neoangiogenesis, and osteomyelosclerosis.

68 ion and the functional role of EPCs in tumor neoangiogenesis are controversial.

69 l mechanism by which neurofibromin regulates neoangiogenesis are not known.

70 (+) effector T cells developed microvascular neoangiogenesis as well as hyperplasia of the intimal la

71 This vascular pattern is not suggestive for neoangiogenesis, as arteriovenous shunts from malignant

72 The ability to undergo neoangiogenesis, as measured in a window-chamber model,

73 proliferation at early stages and promoting neoangiogenesis at late stages of progression.

74 etastasis, concomitant with a suppression of neoangiogenesis at secondary sites, while leaving primar

75 nhibitors p130 and p27 show defects in tumor neoangiogenesis, both in xenografts and spontaneously ar

76 ssels, suggesting that VEGF is essential for neoangiogenesis but not survival of mature vessels in th

77 is ameliorative effect is linked to enhanced neoangiogenesis (CD31 staining and microfil perfusion) b

78 Both inflammation and neoangiogenesis contribute to abdominal aortic aneurysm

79 ating that VEGF is essential for endometrial neoangiogenesis during postmenstrual/postpartum repair.

80 h as macrophages, have been shown to promote neoangiogenesis during tumor growth and wound healing.

81 ation of these systems may minimise both the neoangiogenesis essential for tumour growth and associat

82 ed to the ability of breast tumors to induce neoangiogenesis, even in the face of cytotoxic chemother

83 l, we determined that heart regeneration and neoangiogenesis following MI depends on neonatal macroph

84 rived growth factors and cytokines stimulate neoangiogenesis from surrounding capillaries to support

85 Tumor-associated neoangiogenesis has recently become a suitable target fo

86 b, an inhibitor of key molecules involved in neoangiogenesis, has an established role in the treatmen

87 Increased vascularity and neoangiogenesis have been implicated in the progression

88 ritis patients with and without up-regulated neoangiogenesis identified interferon-gamma and vascular

89 induce impressive reversal of skin fibrosis, neoangiogenesis, improved functionality and quality of l

90 plays critical roles in tumor metastasis and neoangiogenesis in a variety of cancers.

91 Histology demonstrated increased neoangiogenesis in both treatment groups.

92 ted at the KDR, one of the key regulators of neoangiogenesis in cancer.

93 We therefore investigated neoangiogenesis in carbon tetrachloride (CCl(4))-induced

94 ibited the sprouts of mouse aortic rings and neoangiogenesis in chick embryo chorioallantoic membrane

95 To study the regulation of neoangiogenesis in giant cell arteritis, temporal arteri

96 netic resonance and optical toolkit to study neoangiogenesis in glioma models.

97 sporadic renal carcinomas, and it stimulates neoangiogenesis in growing solid tumors.

98 mediated endothelial cell proliferation and neoangiogenesis in human Matrigel and placental angiogen

99 from hypoxia-treated tumor cells results in neoangiogenesis in human umbilical vein endothelial cell

100 Sustained VEGF delivery alone led to neoangiogenesis in ischemic limbs, with complete return

101 in parameters, EPC numbers and function, and neoangiogenesis in lupus-prone mice, independent of dise

102 P-DKO mice were more effective in supporting neoangiogenesis in Matrigel plugs.

103 s studies of APN-null mice revealed impaired neoangiogenesis in model systems without cancer cells an

104 ings show that the A2 system enables retinal neoangiogenesis in OIR by enhancing perivascular activat

105 sponse, and to accelerate tissue healing and neoangiogenesis in the face of noxious stimuli.

106 to improve myocardial perfusion by enhancing neoangiogenesis in the failing heart.

107 be attributed, at least in part, to enhanced neoangiogenesis in the infarcted region via upregulation

108 integrin resulted in a dramatic increase in neoangiogenesis in the wound microenvironment.

109 es into endothelial cells that contribute to neoangiogenesis in tumors.

110 mature endothelial cells, and contribute to neoangiogenesis in vivo during tumor angiogenesis and wo

111 to fibronectin (Fn) during embryogenesis and neoangiogenesis, including many cancers.

112 cific and hypoxia-inducible VEGF expression, neoangiogenesis, infarct-size reduction, and cardiac fun

113 inantly of vascular endothelial cell origin, neoangiogenesis, inflammatory cell infiltration, and ede

114 Neoangiogenesis involves both bone marrow-derived myelom

115 Neoangiogenesis is a pivotal therapeutic target in gliob

116 Neoangiogenesis is an important pathophysiological featu

117 et for treatment of diseases where excessive neoangiogenesis is the underlying pathology.

118 uitously expressed TPCs include VEGF-induced neoangiogenesis, LDL-cholesterol trafficking and degrada

119 Inhibition of Tie2 resulted in impaired neoangiogenesis, leading to a delay in hematopoietic rec

120 Using in vivo models of functional neoangiogenesis, LY2228820 dimesylate treatment reduced

121 The growth and neoangiogenesis of P2X7-expressing tumors was blocked by

122 Neoangiogenesis or establishment of new blood supply is

123 lial progenitor cell (EPC) function, in vivo neoangiogenesis, plaque development, and occlusive throm

124 Induction of neoangiogenesis plays an important role in the pathogene

125 l progenitor cells (EPCs) may play a role in neoangiogenesis (postnatal vasculogenesis).

126 of HJD subjects, implicating hypoxia in the neoangiogenesis process.

127 Management of neoangiogenesis remains a high-value therapeutic goal.

128 HIF-1alpha pathway as a critical mediator of neoangiogenesis required for skeletal regeneration and s

129 The neoangiogenesis resulted in decreased apoptosis of hyper

130 ta also implicate DCs in regulation of tumor neoangiogenesis, suggesting a novel role of DCs in tumor

131 ERRgamma is a hypoxia-independent inducer of neoangiogenesis that can promote reparative revasculariz

132 antiangiogenic properties and the prominent neoangiogenesis that occurs in MMM.

133 owth by inducing newly formed blood vessels (neoangiogenesis) that sustain tumor cell viability and g

134 e we identify PML as a critical inhibitor of neoangiogenesis (the formation of new blood vessels) in

135 or and further production of VEGF to support neoangiogenesis, thereby favoring the development of the

136 F may provide a novel mechanism for inducing neoangiogenesis through both direct actions on local Trk

137 ic synergy correlates with the inhibition of neoangiogenesis through the downregulation of COX-2, iNO

138 vity to growth inhibitory signals, sustained neoangiogenesis, tissue invasiveness and migration capab

139 adation of extracellular matrix and promotes neoangiogenesis to facilitate tumor growth.

140 ting strategies that reduce inflammation and neoangiogenesis to reduce the incidence of restenosis.

141 cell proliferation, collagen deposition, and neoangiogenesis to the levels observed in control animal

142 In murine models of neoangiogenesis, UPI peptide increased VEGF-driven angio

143 cts that are preferentially expressed during neoangiogenesis: vascular endothelial growth factor rece

144 y stimulating podosome nucleation, motility, neoangiogenesis, vasculogenic mimicry, and osteoclastoge

145 ls play a key role in both tumorigenesis and neoangiogenesis via the production of matrix metalloprot

146 Neoangiogenesis was found in all valves with ossificatio

147 Neoangiogenesis was inhibited by SC-'236, which could ac

148 After AAV-VEGF inoculation, neoangiogenesis was observed in the ischemic heart model

149 n similar sized breast tumors, TAM and tumor neoangiogenesis was reduced.

150 In vivo, TIMs and neoangiogenesis were associated.

151 growth difference of tumor xenografts or in neoangiogenesis were found in beta3KOP mice, in contrast

152 erial inflammatory infiltrates and increased neoangiogenesis were observed in apoE(-/-) IFNAR(-/-) mi

153 non-ischemic ears or ischemic limbs induced neoangiogenesis, with a 2-fold increase in the capillary

154 cells of the newly formed capillaries during neoangiogenesis within malignant human brain tumors expr

155 Although neoangiogenesis within the infarcted tissue is an integr