scholarly journals Angiogenesis inhibitors overcome tumor induced endothelial cell anergy

1999 ◽  
Vol 80 (2) ◽  
pp. 315-319 ◽  
Author(s):  
Arjan W. Griffioen ◽  
Cora A. Damen ◽  
Kevin H. Mayo ◽  
Annemarie F. Barendsz-Janson ◽  
Stefano Martinotti ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Angiogenesis Inhibitors ◽  
Cell Anergy

scholarly journals Endostatin: A Promising Drug for Antiangiogenic Therapy

1999 ◽  
Vol 14 (4) ◽  
pp. 263-267 ◽  
Author(s):  
L. Cirri ◽  
S. Donnini ◽  
L. Morbidelli ◽  
P. Chiarugi ◽  
M. Ziche ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Antiangiogenic Therapy ◽  
Specific Inhibitor ◽  
Angiogenesis Inhibitors ◽  
Endothelial Cell Proliferation ◽  
Platelet Factor ◽  
Collagen Xviii ◽  
And Migration

Angiogenesis, the formation of new blood vessels from existing capillaries, is critical for tumors to grow beyond a few in size. Tumor cells produce one or more angiogenic factors including fibroblast growth factor and vascular endothelial growth factor. Surprisingly, antiangiogenic factors or angiogenesis inhibitors have been isolated from tumors. Some angiogenesis inhibitors, such as angiostatin, are associated with tumors while others, such as platelet-factor 4 and interferon-alpha are not. Endostatin, a C-terminal product of collagen XVIII, is a specific inhibitor of endothelial cell proliferation, migration and angiogenesis. The mechanism by which endostatin inhibits endothelial cell proliferation and migration is unknown. Endostatin was originally expressed in a prokaryotic system and, late, in a yeast system, thanks to which it is possible to obtain a sufficient quantity of the protein in a soluble and refolded form to be used in preclincial and clinical trials.

scholarly journals Tumor-Endothelium Cross Talk Blocks Recruitment of Neutrophils to Endothelial Cells: A Novel Mechanism of Endothelial Cell Anergy

Neoplasia ◽  
2009 ◽  
Vol 11 (10) ◽  
pp. 1054-1063 ◽  
Author(s):  
Roman A. Blaheta ◽  
Maciej Powerski ◽  
Lukasz Hudak ◽  
Eva Juengel ◽  
Dietger Jonas ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cross Talk ◽  
Tumor Endothelium ◽  
Cell Anergy

Epigenetic Regulation of Tumor Endothelial Cell Anergy: Silencing of Intercellular Adhesion Molecule-1 by Histone Modifications

2006 ◽  
Vol 66 (22) ◽  
pp. 10770-10777 ◽  
Author(s):  
Debby M.E.I. Hellebrekers ◽  
Karolien Castermans ◽  
Emmanuelle Viré ◽  
Ruud P.M. Dings ◽  
Nicole T.H. Hoebers ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Histone Modifications ◽  
Adhesion Molecule ◽  
Epigenetic Regulation ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Tumor Endothelial Cell ◽  
Cell Anergy

Influence of angiogenesis inhibitors on endothelial cell morphology in vitro

Apmis ◽  
2006 ◽  
Vol 114 (3) ◽  
pp. 211-224 ◽  
Author(s):  
TINA FRIIS ◽  
ALASTAIR B. HANSEN ◽  
GUNNAR HOUEN ◽  
ANNE-MARIE ENGEL
Keyword(s):  
Endothelial Cell ◽  
Cell Morphology ◽  
Angiogenesis Inhibitors

Calreticulin and Calreticulin Fragments Are Endothelial Cell Inhibitors That Suppress Tumor Growth

Blood ◽  
1999 ◽  
Vol 94 (7) ◽  
pp. 2461-2468 ◽  
Author(s):  
Sandra E. Pike ◽  
Lei Yao ◽  
Joyce Setsuda ◽  
Karen D. Jones ◽  
Barry Cherney ◽  
...  
Keyword(s):  
Amino Acids ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
Tumor Growth ◽  
Angiogenesis Inhibitors ◽  
Full Length ◽  
Endothelial Cell Proliferation ◽  
Proliferation In Vitro

Several angiogenesis inhibitors are fragments of larger proteins that are themselves not active as angiogenesis inhibitors. Vasostatin, the N-terminal domain of calreticulin inclusive of amino acids 1-180, is an angiogenesis inhibitor that exerts antitumor effects in vivo. In the present study, we examined whether the full-length calreticulin molecule shares the antiangiogenic and antitumor activities of vasostatin. Similar to vasostatin, calreticulin selectively inhibited endothelial cell proliferation in vitro, but not cells of other lineages, and suppressed angiogenesis in vivo. When inoculated into athymic mice, calreticulin inhibited Burkitt tumor growth comparably with vasostatin. Calreticulin lacking the N-terminal 1-120 amino acids inhibited endothelial cell proliferation in vitro and Burkitt tumor growth in vivo comparably with vasostatin. An internal calreticulin fragment encompassing amino acids 120-180 also inhibited endothelial cell proliferation in vitro and angiogenesis in vivo comparably with calreticulin and vasostatin. These results suggest that the antiangiogenic activities of vasostatin reside in a domain that is accessible from the full-length calreticulin molecule and localize to calreticulin N-terminal amino acids 120-180. Thus, calreticulin and calreticulin fragments are inhibitors of angiogenesis that directly target endothelial cells, inhibit angiogenesis, and suppress tumor growth. This information may be critical in designing targeted inhibitors of pathological angiogenesis that underlies cancer and other diseases.

Endothelial Cell Anergy is Mediated by bFGF through the Sustained Activation of p38-MAPK and NF-κB Inhibition

2006 ◽  
Vol 19 (4) ◽  
pp. 761-773 ◽  
Author(s):  
V. Flati ◽  
L.I. Pastore ◽  
A.W. Griffioen ◽  
S. Satijn ◽  
E. Tomato ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
P38 Mapk ◽  
Cell Anergy ◽  
Sustained Activation

scholarly journals The Angiostatic 16K Human Prolactin Overcomes Endothelial Cell Anergy and Promotes Leukocyte Infiltration via Nuclear Factor-κB Activation

2007 ◽  
Vol 21 (6) ◽  
pp. 1422-1429 ◽  
Author(s):  
Sébastien P. Tabruyn ◽  
Céline Sabatel ◽  
Ngoc-Quynh-Nhu Nguyen ◽  
Catherine Verhaeghe ◽  
Karolien Castermans ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Leukocyte Infiltration ◽  
Human Prolactin ◽  
Cell Anergy

Angiogenesis at the Interface between Basic and Clinical Research

1999 ◽  
Vol 14 (4) ◽  
pp. 202-206 ◽  
Author(s):  
A. Albini ◽  
D. Noonan ◽  
L. Santi
Keyword(s):  
Endothelial Cell ◽  
Rapid Evolution ◽  
Chronic Administration ◽  
Angiogenesis Inhibitors ◽  
Selective Inhibition ◽  
Chemotherapeutic Agents ◽  
Angiogenic Factor ◽  
Cell Functions ◽  
High Doses ◽  
New Compounds

The field of antiangiogenesis has shown a remarkably rapid evolution from the discovery at the bench to translation into the clinic. Currently a wide variety of compounds are in clinical trial as inhibitors of angiogenesis, and new compounds are being frequently added. The target cell of most angiogenesis inhibitors is the endothelial cell, with inhibitors that selectively affect a number of endothelial cell functions acquired during angiogenesis, including activation, proliferation, migration, invasion and survival. The endothelial cell may also be targeted by chemotherapeutic agents currently in use. The high doses and intermittent treatment schedules used to fight resistant tumor cells may be altered towards lower doses and chronic administration to obtain selective inhibition of angiogenic factor-stimulated endothelial cells as adjuvant therapy. Finally, gene therapy is a promising route for the delivery of novel protein inhibitors of angiogenesis, and is actively being investigated.

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