ライフサイエンスコーパス: tumor endothelial cell

1 ve and selective thrombogen when targeted to tumor endothelial cells.

2 arly, in the extracellular matrix and in the tumor endothelial cells.

3 that target P-selectin, which is enriched in tumor endothelial cells.

4 wn to suppress the proliferation of isolated tumor endothelial cells.

5 ity requires CMG2 expression on host-derived tumor endothelial cells.

6 gargin prodrug (G202) that selectively kills tumor endothelial cells.

7 vein endothelial cells (HUVECs) as model of tumor endothelial cells.

8 onal factor, Kruppel-like factor-2 (KLF2) in tumor endothelial cells.

9 n vivo these nanoparticles bind primarily to tumor endothelial cells.

10 nt and functional consequences of binding to tumor endothelial cells.

11 hey only show cytotoxic activity against the tumor endothelial cells.

12 d normalized microtubule organization in the tumor endothelial cells.

13 target of rapamycin inhibition compared with tumor endothelial cells.

14 produced when VEGF binds to its receptors on tumor endothelial cells.

15 induced EGFR activation and proliferation of tumor endothelial cells.

16 or-derived chromosomal material in the mouse tumor endothelial cells.

17 ells may not be most representative of human tumor endothelial cells.

18 c localization of 99Tcm-labeled CD105 mab in tumor endothelial cells.

19 up-regulation of VEGF receptor expression on tumor endothelial cells.

20 1 is involved in pathological disorders like tumor endothelial cell adhesion and migration and theref

21 cells is involved in promoting angiogenesis, tumor-endothelial cell adhesion, and metastasis of prost

22 We demonstrate the expression of HEYL in tumor endothelial cells and additionally establish the a

23 n the tumor environment, leading to abnormal tumor endothelial cells and blood vessels.

24 be vascular damage with initial apoptosis in tumor endothelial cells and delayed tumor cell apoptosis

25 These were expressed by immunopurified tumor endothelial cells and localized to tumor vasculatu

26 Combination treatment kills tumor endothelial cells and synergistically promotes wid

27 delivers its payload to the mitochondria of tumor endothelial cells and tumor cells, (ii) conjugatio

28 a of the head and neck, induces apoptosis of tumor endothelial cells and tumor cells, and is well tol

29 n i.v. injection, appearing in the nuclei of tumor endothelial cells and tumor cells.

30 mbrane glycoprotein that is overexpressed in tumor endothelial cells, and it promotes sprouting angio

31 erplay between the proliferation kinetics of tumor endothelial cells (angiogenesis) and tumor cells h

32 ortant concept in tumor angiogenesis is that tumor endothelial cells are assumed to be genetically no

33 Recent findings suggest that tumor endothelial cells are permanently modified compare

34 reted immunostimulatory cytokines and killed tumor endothelial cells as well as TEM8-positive TNBC ce

35 ion effect and CD44-mediated transcytosis in tumor endothelial cells as well as tumor cells.

36 referentially target discrete populations of tumor endothelial cells associated with the smaller peri

37 Surprisingly, tumor endothelial cells begin to undergo apoptosis befor

38 ndicate that Ang2 plays a protective role in tumor endothelial cells by activating Tie2, thereby limi

39 We conclude that tumor endothelial cells can acquire cytogenetic abnormal

40 lation of integrin alphavbeta3 expression on tumor endothelial cells can be quantitatively visualized

41 cell antitumor immunity and demonstrate that tumor endothelial cells can be targeted for immunotherap

42 cells (CRCs), including CTCs and circulating tumor endothelial cells (CECs).

43 asion; reduced endothelial cell migration in tumor/endothelial cell cocultures; and suppressed mitoch

44 angiogenesis, was also significantly more in tumor endothelial cells collected from the dopamine-depl

45 and loss of NRG-induced growth inhibition in tumor endothelial cells constitutes a switch that promot

46 , freshly isolated CD11b(+) cells stimulated tumor endothelial cell cord formation by 10-fold in an i

47 at high doses of radiation (>=10 Gy) trigger tumor endothelial cell death, resulting in indirect kill

48 partly due to an incomplete understanding of tumor endothelial cell (EC) biology.

49 ion centers in cells, and often up to 30% of tumor endothelial cells (ECs) acquire excess (>2) centro

50 established mice with CMG2 only expressed in tumor endothelial cells (ECs) and determined the specifi

51 Here, we show that tumor endothelial cells (ECs) have a hyper-glycolytic me

52 Tumor endothelial cells (ECs) promote cancer progression

53 Here, we uncover a role for DR5 signaling in tumor endothelial cells (ECs).

54 Although deletion of Atm in proliferating tumor endothelial cells enhanced the response of sarcoma

55 Various cancer cells and actively dividing tumor-endothelial cells express the thyrointegrin alphav

56 In addition, tumor endothelial cells expressed molecular markers spec

57 Transcriptional profiling of microdissected tumor endothelial cells from human ovarian cancers revea

58 Akt3 exerted negative effects on tumor endothelial cell growth and migration by inhibitin

59 Tumor endothelial cells have excess centrosomes and are

60 o disrupt PDGFR-mediated pericyte support of tumor endothelial cells in concert with maximum-tolerate

61 vated protein localizes predominantly to the tumor endothelial cells in the highly vascularized gliom

62 tantly, we show that F3-Cis-Np bind to human tumor endothelial cells in vitro and to human tumor vess

63 ficity to both human ovarian tumor cells and tumor endothelial cells in vitro, they only show cytotox

64 agent that downregulates Id1 effectively in tumor endothelial cells in vivo.

65 e chain reaction (qRT-PCR) of immunopurified tumor endothelial cells, in situ hybridization, immunohi

66 xhibit increased tumor-initiating potential, tumor-endothelial cell interaction, and lung metastasis.

67 The T antigen-mediated, tumor-endothelial cell interactions could be efficiently

68 TFD100 blocks gal3-mediated angiogenesis, tumor-endothelial cell interactions, and metastasis of p

69 mining the dissemination of cancer cells via tumor-endothelial cell interactions, with possible impli

70 ation of signaling pathways, chemokines, and tumor-endothelial cell interactions.

71 tion of molecular signaling, chemokines, and tumor-endothelial cell interactions.

72 loid in long-term culture, the aneuploidy of tumor endothelial cells is exacerbated in culture sugges

73 Although the importance of Id1 in tumor endothelial cells is well established, the express

74 contrast, Ang2, which is highly expressed by tumor endothelial cells, is thought to inhibit Tie2 acti

75 igen (PA) protein binds to receptors, either tumor endothelial cell marker 8 (TEM8) or CMG2 (capillar

76 Permanently altered tumor endothelial cells may represent a significant popu

77 In an in vitro tumor endothelial cell model, tumor necrosis factor-alph

78 tly, expression of EGFL6 in cancer cells and tumor endothelial cells not only increased tumor angioge

79 er whose expression is distinctly induced in tumor endothelial cells of both brain and peripheral vas

80 that DLL4 is up-regulated in tumor cells and tumor endothelial cells of human glioblastoma.

81 m the three most prominent cell types in the tumor: endothelial cells, pericytes, and adipocytes.

82 ogression reversed the effect of Atm loss on tumor endothelial cell radiosensitivity.

83 As a consequence of their expressing EGFR, tumor endothelial cells responded to EGF and other EGF f

84 signal-regulated kinase (ERK) activation in tumor endothelial cells, revealed by immunostaining for

85 ion of mouse embryonic fibroblasts and human tumor endothelial cells significantly increases the numb

86 xins, coupled with the specific targeting of tumor endothelial cells, suggests that our strategy shou

87 dosialin) was recently identified as a novel tumor endothelial cell surface marker potentially involv

88 , these data suggest that SU6668 may prevent tumor endothelial cell survival directly (vascular endot

89 ng in the regulation of tumor vasculature or tumor endothelial cell (TEC) function is not known.

90 zed that a similar phenomenon holds true for tumor endothelial cells (TECs) as well.

91 The impact of TME-dependent heterogeneity of tumor endothelial cells (TECs) on tumorigenesis is uncle

92 We discovered that tumor endothelial cells (TECs), but not normal ECs, expr

93 EPC may be a better model of human tumor endothelial cells than HUVEC and HMVEC and, thus,

94 endothelial growth factor (VEGF) to protect tumor endothelial cells, the effect on tumor vasculature

95 found that the more efficient ability of the tumor endothelial cells to resensitize following dosing

96 urthermore, due to their expression of EGFR, tumor endothelial cells, unlike normal endothelial cells

97 2% of gold-labeled liposomes associated with tumor endothelial cells were adherent to the luminal sur

98 ysis showed that freshly isolated uncultured tumor endothelial cells were aneuploid and had abnormal

99 Unexpectedly, tumor endothelial cells were cytogenetically abnormal.

100 at the structural chromosomal aberrations in tumor endothelial cells were heterogeneous, indicating t

101 o simulate the angiogenic environment of the tumor, endothelial cells were isolated and propagated in

102 In contrast, tumor endothelial cells, which do not express ErbB3, wer

103 eferentially binds to and is internalized by tumor endothelial cells, which leads to VEGFR-2 down-reg

104 copy revealed rHDL-RGD to be associated with tumor endothelial cells, while rHDL and rHDL-RAD nanopar

105 Mechanistically, tumor endothelial cells with supernumerary centrosomes h

106 tor receptor-2 (VEGFR-2) immunoreactivity in tumor endothelial cells, with 95% loss over 6 hours.

107 ne surveillance, define an important role of tumor endothelial cells within this process, and suggest