Relevant bibliographies by topics / Angiostatine

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers
  5. Reports

Academic literature on the topic 'Angiostatine'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Angiostatine"

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Dudani, Anil K., Jelica Mehic, and Anthony Martyres. "Interaction of Plasminogen and Angiostatin with Heat Shock Proteins." Blood 108, no. 11 (November 16, 2006): 1622. http://dx.doi.org/10.1182/blood.v108.11.1622.1622.

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Abstract Previous studies from this laboratory have demonstrated that plasminogen and angiostatin bind to endothelial cell (EC) surface-associated actin via their kringles in a specific manner. Heat shock proteins (hsps) like hsp 27 are constitutively expressed by vascular ECs and regulate actin polymerization, cell growth and migration. Since many hsps have also been found to be highly abundant on cell surfaces and there is evidence that bacterial surface hsps may interact with human plasminogen, the purpose of this study was to determine whether human plasminogen and angiostatin would interact with human hsps. ELISAs were developed in our laboratory to assess these interactions. It was observed that plasminogen bound to hsps 27, 60 and 70. In all cases, binding was inhibited (85–90%) by excess (50 mM) lysine indicating kringle involvement. Angiostatin predominantly bound to hsp 27 and to hsp 70 in a concentration- and kringle-dependent manner. As observed previously for actin, there was dose-dependent inhibition of angiostatin’s interaction with hsp 27 by plasminogen. In addition, thirty-fold molar excess actin inhibited (up to 50%), the interaction of plasminogen with all hsps. However, thirty-fold molar excess actin could only inhibit the interaction of angiostatin with hsp 27 by 15–20%. FACS analyses indicated the presence of hsps 27, 60 and 70 on the surface of MCF-7 breast cancer cells but not on human umbilical vein ECs. Polyclonal antibodies to hsp 27 significantly inhibited the interaction of plasminogen and angiostatin with MCF-7 surface-associated hsp27 in a dose-dependent manner. Collectively, these data indicate that while plasminogen interacts specifically with hsp 27, 60 and 70, angiostatin interacts predominantly with hsp 27 and to some extent with hsp 70; plasminogen only partially displaces angiostatins binding to hsp 27; actin only partially displaces plasminogen/angiostatin binding to hsps and surface-associated hsp 27 can mediate the binding of both plasminogen and angiostatin to MCF-7 cells.
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BILOUS, V. L. "PRODUCTION AND APPLICATION OF ANGIOSTATINS FOR THE TREATMENT OF OCULAR NEOVASCULAR DISEASES." Biotechnologia Acta 14, no. 1 (February 2021): 5–24. http://dx.doi.org/10.15407/biotech14.01.005.

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Angiostatins comprise a group of kringle-containing proteolytically-derived fragments of plasminogen/plasmin, which act as potent inhibitory mediators of endothelial cells proliferation and migration. Angiostatins are involved in modulation of vessel growth in healthy tissues and various pathological conditions associated with aberrant neovascularization. The aim of the present paper was to summarize available information, including our own experimental data, on prospects of angiostatin application for treatment of ocular neovascular diseases (OND), focusing on retinal pathologies and corneal injury. In particular, literature data on prospective and retrospective studies, clinical trials and animal models relating to the pathophysiology, investigation and management of OND are described. Special emphasis was made on the laboratory approaches of production of different angiostatin isoforms, as well as comparison of antiangiogenic capacities of native and recombinant angiostatin polypeptides. Several studies reported that angiostatins may completely abolish pathologic angiogenesis in diabetic proliferative retinopathy without affecting normal retinal vessel development and without exhibiting adverse side effects. Angiostatins have been tested as a tool for corneal antiangiogenesis target therapy in order to manage diverse ocular surface pathological conditions induced by traumas, chemical burns, previous surgery, chronic contact lens wear, autoimmune diseases, keratitis and viral infections (herpes, COVID-19), corneal graft rejection, etc. Among all known angiostatin species, isolated K5 plasminogen fragment was shown to display the most potent inhibitory activity against proliferation of endothelial cells via triggering multiple signaling pathways, which lead to cell death and resulting angiogenesis suppression. Application of adenoviral genetic construct encoding angiostatin K5 as a promising tool for OND treatment illustrates a vivid example of upcoming revolution in local gene therapy. Further comprehensive studies are necessary to elucidate the clinical potential and optimal regimes of angiostatinbased intervention modalities for treating ocular neovascularization.
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Lee, Tong-Young, Stefan Muschal, Elke A. Pravda, Judah Folkman, Amir Abdollahi, and Kashi Javaherian. "Angiostatin regulates the expression of antiangiogenic and proapoptotic pathways via targeted inhibition of mitochondrial proteins." Blood 114, no. 9 (August 27, 2009): 1987–98. http://dx.doi.org/10.1182/blood-2008-12-197236.

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Angiostatin, a proteolytic fragment of plasminogen, is a potent endogenous antiangiogenic agent. The molecular mechanisms governing angiostatin's antiangiogenic and antitumor effects are not well understood. Here, we report the identification of mitochondrial compartment as the ultimate target of angiostatin. After internalization of angiostatin into the cell, at least 2 proteins within the mitochondria bind this molecule: malate dehydrogenase, a member of Krebs cycle, and adenosine triphosphate synthase. In vitro and in vivo studies revealed differential regulation of key prosurvival and angiogenesis-related proteins in angiostatin-treated tumors and tumor-endothelium. Angiostatin induced apoptosis via down-regulation of mitochondrial BCL-2. Angiostatin treatment led to down-regulation of c-Myc and elevated levels of another key antiangiogenic protein, thrombospondin-1, reinforcing its antitumor and antiangiogenic effects. Further evidence is provided for reduced recruitment and infiltration of bone marrow–derived macrophages in angiostatin-treated tumors. The observed effects of angiostatin were restricted to the tumor site and were not observed in other major organs of the mice, indicating unique tumor specific bioavailability. Together, our data suggest mitochondria as a novel target for antiangiogenic therapy and provide mechanistic insights to the antiangiogenic and antitumor effects of angiostatin.
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Levine, Howard A., Serdal Pamuk, Brian D. Sleeman, and Marit Nilsen-Hamilton. "Mathematical Modelling of Tumour Angiogenesis and the Action of Angiostatin as a Protease Inhibitor." Journal of Theoretical Medicine 4, no. 2 (2002): 133–45. http://dx.doi.org/10.1080/1027366021000003270.

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Tumour angiogenesis is the process whereby a capillary network is formed from a pre-existing vasculature in response to tumour secreted growth factors (TAF). The capillary network is largely composed of migrating endothelial cells which organise themselves into dendritic structures. In this paper we model angiogenesis via the theory of reinforced random walks, whereby the chemotactic response of the endothelial cells to TAF and their haptotactic response to the matrix macromolecule fibronectin is accomplished through transition probability rate functions. Tumour secreted growth and inhibitory factors are modelled on the basis of Michaelis–Menten kinetics. Particular attention is focussed on the action of anti-angiogenic agents (i.e. angiostatins). That is as a mechanism whereby angiostatin acts as a protease inhibitor. Numerical simulations yield results, which are in good agreement with the experimental observations obtained by Folkman and his co-workers in their classical rabbit eye cornea experiments. The model offers a theoretical understanding of how some angiostatins work to inhibit tumour growth.
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Warejcka, Debra J., and Sally S. Twining. "Specific conformational changes of plasminogen induced by chloride ions, 6-aminohexanoic acid and benzamidine, but not the overall openness of plasminogen regulate, production of biologically active angiostatins." Biochemical Journal 392, no. 3 (December 6, 2005): 703–12. http://dx.doi.org/10.1042/bj20050907.

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The overall conformation of plasminogen depends upon the presence of anions and molecules such as AHA (6-aminohexanoic acid) and BZ (benzamidine). The purpose of the present study was to determine the effect of conformation on the initial and secondary cleavages of plasminogen to generate active angiostatins. Plasminogen was digested with the physiologically relevant neutrophil elastase in one of the four Tris/acetate buffers: buffer alone or buffer plus NaCl, AHA or BZ. The initial cleavage of Glu1-plasminogen was much slower in the tight NaCl-induced α-conformation, fastest in the intermediate BZ-induced β-conformation and intermediate both in the control and in the AHA-induced open γ-conformation. Although the buffer system determined the relative amounts of the initial cleavage products, the same four cleavage sites were utilized under all conditions. A fifth major initial cleavage within the protease domain was observed in the presence of BZ. N-terminal peptide cleavage required for angiostatin formation occurred as either the initial or the secondary cleavage. Angiostatins were generated fastest in the presence of BZ and slowest in the presence of NaCl. Both the initial and secondary cleavages were affected by the modifying agents, indicating that they influence the conformation of both Glu-plasminogen and the initial cleavage products. The angiostatins produced under the different conditions inhibited proliferation of human umbilical-vein endothelial cells. These results suggest that plasminogen conversion into active angiostatins is dependent more on the specific conformation changes induced by the various modifying reagents rather than on the overall openness of the molecule.
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Dorrell, Michael I., Heidi R. Kast-Woelbern, Ryan T. Botts, Stephen A. Bravo, Jacob R. Tremblay, Sarah Giles, Jessica F. Wada, et al. "A novel method of screening combinations of angiostatics identifies bevacizumab and temsirolimus as synergistic inhibitors of glioma-induced angiogenesis." PLOS ONE 16, no. 6 (June 2, 2021): e0252233. http://dx.doi.org/10.1371/journal.pone.0252233.

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Tumor angiogenesis is critical for the growth and progression of cancer. As such, angiostasis is a treatment modality for cancer with potential utility for multiple types of cancer and fewer side effects. However, clinical success of angiostatic monotherapies has been moderate, at best, causing angiostatic treatments to lose their early luster. Previous studies demonstrated compensatory mechanisms that drive tumor vascularization despite the use of angiostatic monotherapies, as well as the potential for combination angiostatic therapies to overcome these compensatory mechanisms. We screened clinically approved angiostatics to identify specific combinations that confer potent inhibition of tumor-induced angiogenesis. We used a novel modification of the ex ovo chick chorioallantoic membrane (CAM) model that combined confocal and automated analyses to quantify tumor angiogenesis induced by glioblastoma tumor onplants. This model is advantageous due to its low cost and moderate throughput capabilities, while maintaining complex in vivo cellular interactions that are difficult to replicate in vitro. After screening multiple combinations, we determined that glioblastoma-induced angiogenesis was significantly reduced using a combination of bevacizumab (Avastin®) and temsirolimus (Torisel®) at doses below those where neither monotherapy demonstrated activity. These preliminary results were verified extensively, with this combination therapy effective even at concentrations further reduced 10-fold with a CI value of 2.42E-5, demonstrating high levels of synergy. Thus, combining bevacizumab and temsirolimus has great potential to increase the efficacy of angiostatic therapy and lower required dosing for improved clinical success and reduced side effects in glioblastoma patients.
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Schmitz, Volker, Wang Lin, Miguel Barajas, Peng Dacheng, Jésus Prieto, and Qian Cheng. "Encymatic release of angiostatin like molecule and characterization of its angiostatic and antitumoral effects." Journal of Hepatology 36 (April 2002): 161. http://dx.doi.org/10.1016/s0168-8278(02)80581-5.

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Wajih, Nadeem, and David C. Sane. "Angiostatin selectively inhibits signaling by hepatocyte growth factor in endothelial and smooth muscle cells." Blood 101, no. 5 (March 1, 2003): 1857–63. http://dx.doi.org/10.1182/blood-2002-02-0582.

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Angiostatin, an inhibitor of angiogenesis, contains 3 to 4 kringle domains that are derived from proteolytic cleavage of plasminogen. The antiangiogenic effects of angiostatin occur, in part, from its inhibition of endothelial cell surface adenosine triphosphate synthase, integrin functions, and pericellular proteolysis. Angiostatin has structural similarities to hepatocyte growth factor (HGF; “scatter factor”), a promoter of angiogenesis, that induces proliferation and migration of both endothelial and smooth muscle cells via its cell surface receptor, c-met. We hypothesized that angiostatin might block HGF-induced signaling in endothelial and smooth muscle cells. Angiostatin inhibited HGF-induced phosphorylation of c-met, Akt, and ERK1/2. Angiostatin also significantly inhibited proliferation of human umbilical vein endothelial cells (HUVECs) induced by HGF. In contrast, angiostatin did not inhibit vascular endothelial growth factor (VEGF)–or basic fibroblast growth factor (bFGF)–induced signaling events or HUVEC proliferation. Angiostatin bound to immobilized truncated c-met produced by A431 cells and could be immunoprecipitated as a complex with soluble c-met. HGF inhibited the binding of 125I-angiostatin to HUVECs. Soluble c-met, produced by several tumor cell lines, could inhibit the antiangiogenic effect of angiostatin. The disruption of HGF/c-met signaling is a novel mechanism for the antiangiogenic effect of angiostatin.
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STACK, M. Sharon, Stephen GATELY, Lisa M. BAFETTI, Jan J. ENGHILD, and Gerald A. SOFF. "Angiostatin inhibits endothelial and melanoma cellular invasion by blocking matrix-enhanced plasminogen activation." Biochemical Journal 340, no. 1 (May 10, 1999): 77–84. http://dx.doi.org/10.1042/bj3400077.

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Angiostatin, a kringle-containing fragment of plasminogen, is a potent inhibitor of angiogenesis. The mechanism(s) responsible for the anti-angiogenic properties of angiostatin are unknown. We now report that human angiostatin blocks plasmin(ogen)-enhanced in vitro invasion of tissue plasminogen activator (t-PA)-producing endothelial and melanoma cells. Kinetic analyses demonstrated that angiostatin functions as a non-competitive inhibitor of extracellular-matrix (ECM)-enhanced, t-PA-catalysed plasminogen activation, with a Ki of 0.9±0.03 μM. This mechanism suggests that t-PA has a binding site for the inhibitor angiostatin, as well as for its substrate plasminogen that, when occupied, prevents ternary complex formation between t-PA, plasminogen and matrix protein. Direct binding experiments confirmed that angiostatin bound to t-PA with an apparent Kd [Kd(app)] of 6.7±0.7 nM, but did not bind with high affinity to ECM proteins. Together, these data suggest that angiostatin in the cellular micro-environment can inhibit matrix-enhanced plasminogen activation, resulting in reduced invasive activity, and suggest a biochemical mechanism whereby angiostatin-mediated regulation of plasmin formation could influence cellular migration and invasion.
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Dudani, A. K., M. Ben-Tchavtchavadze, S. Porter, and E. Tackaberry. "Angiostatin and plasminogen share binding to endothelial cell surface actin." Biochemistry and Cell Biology 83, no. 1 (February 1, 2005): 28–35. http://dx.doi.org/10.1139/o04-109.

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Previous studies from this laboratory have demonstrated that plasminogen binds to endothelial cell surface-associated actin via its kringles in a dose-dependent and specific manner. The purpose of this study was to determine whether angiostatin, a proteolytic fragment of plasminogen, shares binding properties with plasminogen. Our results indicated that like plasminogen, angiostatin bound to actin in a time-, concentration-, and kringle-dependent manner. Furthermore, this binding was significantly inhibited by excess plasminogen, suggesting that both proteins shared binding motifs on the actin molecule. Fluorescence studies demonstrated that angiostatin bound to intact endothelial cells through its kringles, and this binding was also inhibited by plasminogen but not by unrelated proteins. Ligand blot analyses on endothelial cell lysates indicated that angiostatin interacted with a 42 kDa protein, which was identified as actin. Furthermore, an anti-actin antibody inhibited binding of angiostatin to endothelial cells by approximately 25%. These results suggest that angiostatin and plasminogen share binding to endothelial cell surface actin and, therefore, that angiostatin has the potential to inhibit plasmin-dependent processes such as cell migration–movement.Key words: plasminogen, angiostatin, endothelial cells, actin.
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Dissertations / Theses on the topic "Angiostatine"

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Gogat, Karïn. "L'angiogenèse Oculaire : approche Fondamentale lors du Développement et Approche Thérapeutique." Paris 7, 2003. http://www.theses.fr/2003PA077215.

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Galaup, Ariane. "Inhibition de l'angiogénèse tumorale par transfert de gènes angiostatiques associés ou non à une chimiothérapie." Paris 7, 2003. http://www.theses.fr/2003PA077213.

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Drenberg, Christina Diane. "Angiostatic Regulators in Ovarian Cancer." Scholar Commons, 2010. http://scholarcommons.usf.edu/etd/3557.

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Angiogenesis by either normal or neoplastic cells involves a delicate balance of both angiogenic and angiostatic regulators. In the ovary, normal physiological angiogenesis occurs around the developing follicle and corpus luteum in response to hormonal shifts. Interestingly, carcinomas arising from the ovary are usually highly vascularized and are commonly clinically observed to produce cyst fluids or ascites which contain both angiostatic and/or angiogenic regulators. However, in contrast to normal angiogenesis, angiogenesis associated with epithelial ovarian cancer usually produces aberrant vasculature that may promote neoplastic progression. Therefore, the ovary and ovarian cancers provide models to study the mechanisms governing the strict balance of angioregulators in both normal and tumor angiogenesis. While most studies to date have focused on angiogenic regulators for normal and aberrant angiogenesis, we investigated the potential for dysregulation of angiostatic regulators to contribute to the etiology of epithelial ovarian cancer. Therefore, in this study, we examined two angiostatic regulators, angiostatin and semaphorin 3F, in epithelial ovarian cancer. Angiostatin, a cleavage product of the circulating zymogen plasminogen, was isolated from serum and urine of mice bearing a Lewis lung carcinoma and in vivo studies have demonstrated its potent angiostatic properties. Thus, we investigated the potential prognostic/diagnostic advantage of aberrant angiostatin expression with epithelial ovarian cancer. We found that urinary angiostatin, compared to other angioregulators in plasma or urine, could serve as an effective biomarker for early detection of epithelial ovarian cancer, especially when used in combination with cancer antigen 125. Additionally, urinary angiostatin correlated with both recurrent disease as well as successful tumor ablation further supporting its potential as a disease biomarker. Alternative biological functions for the axon guidance molecule, semaphorin 3F, have been reported particularly in regard to angiogenesis, tumor progression and metastasis. However, the underlying mechanisms governing semaphorin 3F regulation and dysregulation remain unclear. Therefore, we first investigated the clinical relationship between semaphorin 3F expression and epithelial ovarian cancer progression. These immunohistological studies revealed that, similar to lung cancer, semaphorin 3F expression decreased with progression supporting a tumor suppressor-like role for semaphorin 3F. Additionally, we found that calcium, an essential cellular signaling molecule, could mediate transcriptional suppression of semaphorin 3F expression in a CREB-dependent manner. Lastly, given the antagonistic relationship between semaphorin 3F and vascular endothelial growth factor, we sought to determine whether semaphorin 3F and vascular endothelial growth factor promoted opposing effects on a common downstream target. In the course of these studies we determined that telomerase is a novel molecular target of semaphorin 3F in ovarian cancer cells such that semaphorin 3F suppresses telomerase activity while vascular endothelial growth factor promotes telomerase activity. In addition, we found that the inverse relationship between semaphorin 3F and telomerase was mediated through transcriptional inhibition of the hTERT promoter by semaphorin 3F. In conclusion, this research shows that dysregulation of the angiostatic regulators, angiostatin and semaphorin 3F, may contribute to the etiology of epithelial ovarian cancer. In the future, dysregulation of these and other angiostatic regulators may be exploited for therapeutic intervention or as biomarkers for early detection which would allow women more treatment choices and hopefully, reduce the mortality associated with this insidious disease.
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Veitonmäki, Niina. "Angiostatic mechanisms of endogenous angiogenesis inhibitors /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-555-7/.

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Chen, Chang-Hwa Mary 1971. "The effect of angiostatin on the endothelial cell cycle." Thesis, Massachusetts Institute of Technology, 1998. http://hdl.handle.net/1721.1/50431.

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Levchenko, Tetyana. "The role of angiomotin in angiogenesis /." Stockholm, 2003. http://diss.kib.ki.se/2004/91-7349-761-4/.

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Cnudde, Sara Elizabeth. "The x-ray crystallographic structures of the angiogenesis inhibitor angiostatin bound to a peptide from the group A streptococcal surface protein PAM and the metal-bound conantokins con-G and con-T[K7gamma]." Diss., Connect to online resource - MSU authorized users, 2007.

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Stefanutti, Erin. "ANGIOSTATIN LIKE PEPTIDES IN MILK: POTENTIAL DEVELOPMENT FOR DAIRY PRODUCTS CAPABLE OF CANCER PREVENTION." DigitalCommons@CalPoly, 2011. https://digitalcommons.calpoly.edu/theses/479.

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For the past 40 years, antiangiogenic approaches have been of major interest in the development of methods to cure and prevent cancer. Angiogenesis, the development of blood vessels from pre-existing vascularization, is essential for cancer growth and spread of metastasis through the delivery of nutrients and oxygen essential to sustain the metabolic activity of these malignant cells. Blocking access to blood will cause cancerous cells to assume a dormant state creating inactive micro-tumors innocuous to the host. Angiostatin, the internal fragment of the fibrinolytic zymogen plasminogen, has shown great potential in reducing cancer size and number of metastatic colonies in animal models. Owing to the success of these preliminary results angiostatin is currently on clinical trials. Plasminogen is known to be transferred from blood to milk during lactation. The objectives of this research were to: 1) investigate the ability of various proteases in cleaving plasminogen, both from human and bovine sources, and consequently release the angiostatin like fragment; 2) determine the anticancer activity of bovine angiostatin; 3) examine ability of the antiangiogenic fragment to survive digestion; 4) purify the fragment of interest through column chromatography. Production of angiostatin was tested through hydrolysis of plasminogen via Bacillus Polymyxa protease (or dispase I), elastase, lactic acid bacteria and Bacilli originated enzymes. Once proteases capable of angiostatin like peptide production were identified, and sequence analysis of the fragments obtained conducted to confirm that bovine angiostatin was indeed produced, ability of angiostatin, both human and bovine, in inhibiting malignant melanoma as well as colon cancer cells was evaluated in vitro. From the results obtained we can confirm that bovine angiostatin inhibitory activity on cancerous cells is similar to that observed for human angiostatin. Analysis of bovine angiostatin survival through in vitro human digestion model was also examined. Results show good possibility of angiostatin surviving digestion, even if confirmation of these results is required through further in vivo studies. Additionally, digestive enzymes such as trypsin and α-chymotrypsin showed ability in cleaving plasminogen directly to release a 25kDa fragment. Knowing that each kringle has some degree of anticancer activity it would be of interest to further study the possibility of angiostatin related fragments to be produced during milk digestion. Finally, affinity chromatography through L-lysine used to purify human angiostatin resulted to be an adequate method for bovine angiostatin purification. Preliminary results obtained from this study open a new area worth investigating to uncover the potential of using bovine angiostatin in the development of novel food products capable of cancer prevention.
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Griscelli, Frank. "Utilisation d'adénovirus recombinants pour le ciblage de l'expression de gènes thérapeutiques : application dans le domaine de la cardiologie et de la cancérologie." Paris 11, 1999. http://www.theses.fr/1999PA11T015.

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La multiplication des protocoles cliniques laisse espérer que la thérapie génique fera partie dans l'avenir de l'arsenal thérapeutique pour le traitement des maladies acquises comme les cancers, même si un long chemin reste à parcourir pour mettre au point des vecteurs totalement sûrs et efficaces. Les adénovirus recombinants sont actuellement les vecteurs de choix très utilisés pour cette approche, car ils sont capables de délivrer l'information génétique dans un grand nombre de tissus. Afin d'éviter l'expression ubiquitaire du transgène dans tous ces tissus, nous montrons qu'il est possible de cibler l'expression du transgène à l'aide d'adénovirus recombinants, dans un seul type cellulaire, ce qui permettra d'utiliser ces vecteurs avec une plus grande sécurité. Nous montrons que l'utilisation de promoteurs spécifiques de tissus est une des approches possibles pour cibler l'expression d'un transgène. Nous avons pris l'exemple du promoteur de l'isoforme 2v de la chaîne légère de la myosine pour valider cette approche. Deux adénovirus recombinants ont été construits contenant le gène de la B-galactosidase mis sous contrôle de la version longue (2100 bp) ou courte (250 bp) du promoteur cardiaque. Nous montrons que ces deux promoteurs conservent leur spécificité d'origine in vivo après injection intracardiaque du virus et in ovo après injection systémique du virus dans des embryons de poulets, mais que leurs activités restent faibles par rapport à celles observées avec les promoteurs viraux. Cette voie semble être néanmoins intéressante pour le ciblage de l'expression de gènes. Notre position au sein du centre anticancéreux de Villejuif nous a fait nous intéresser au développement de la thérapie génique anti-angiogénique dans la lutte anticancéreuse. C'est une voie prometteuse car elle vise à inhiber le développement et la dissémination tumorale. De plus cette thérapeutique est adaptée à tous les cancers pour transformer une tumeur active, maligne en tumeur "dormante" et bénigne. Nous avons construit deux adénovirus recombinants qui codent pour l'angiostatine humaine, un fragment amine­terminal du plasminogène (résidu 1-333) ou pour l'ATF murin, un fragment amine-terminal de l'urokinase (résidu 1-135), qui ont in vivo et in vitro respectivement la propriété d'inhiber la prolifération de cellules endothéliales activées et les cellules endothéliales ayant acquis un phénotype migratoire. Nous montrons que le transfert du gène de l'angiostatine et de l'ATF dans plusieurs modèles de xénogreffes murins entraîne un arrêt significatif de la croissance tumorale qui est corrélé avec une importante inhibition de la vascularisation péri-tumorale et intra­ tumorale. Nous montrons également que le transfert du gène de l'ATF murin permet d'inhiber in vitro la migration des cellules tumorales et in vivo la formation de métastases dans deux modèles expérimentaux murins, un carcinome pulmonaire et un carcinome du côlon. Avec cette thérapie, seules lès cellules endothéliales angiogéniques sont affectées, alors que les cellules endothéliales vasculaires ne le sont pas, ce qui laisse présager de l'absence de toxicité vasculaire de cette approche.
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Raisler, Brian. "Adeno-associated virus type-2 mediated expression of pigmented epithelium derived factor or kringles 1-3 of angiostatin reduced neovascular retinopathies." [Gainesville, Fla.] : University of Florida, 2003. http://purl.fcla.edu/fcla/etd/UFE0002385.

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Book chapters on the topic "Angiostatine"

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Soriano, Jesus V., and B. Kim Lee Sim. "Angiostatin and Endostatin." In The New Angiotherapy, 573–95. Totowa, NJ: Humana Press, 2002. http://dx.doi.org/10.1007/978-1-59259-126-8_30.

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de Groot, Heink, Vera Schmit-Eilenberger, Janna Kirchhof, and Albert J. Augustin. "Angiostatic and Angiogenic Factors." In Anti-VEGF, 1–3. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320005.

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Sim, B. Kim Lee. "Angiostatin Protein and Other Plasminogen Fragments." In Antiangiogenic Agents in Cancer Therapy, 225–36. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-453-5_14.

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Kwon, Mijung, and David M. Waisman. "Mechanism of Angiostatin Formation from Plasminogen." In Plasminogen: Structure, Activation, and Regulation, 135–56. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0165-7_8.

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Folkman, Judah. "Angiostatin and Endostatin: Angiogenesis Inhibitors in Blood and Stroma." In Angiogenesis, 129–46. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71518-6_12.

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Cao, Yihai. "Endogenous Angiogenesis Inhibitors: Angiostatin, Endostatin, and Other Proteolytic Fragments." In Inhibitors of Cell Growth, 161–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72149-6_8.

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O’Reilly, M. S. "Angiostatin: An endogenous inhibitor of angiogenesis and of tumor growth." In Experientia Supplementum, 273–94. Basel: Birkhäuser Basel, 1997. http://dx.doi.org/10.1007/978-3-0348-9006-9_11.

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Schulkens, Iris A., Arjan W. Griffioen, and Victor L. Thijssen. "Angiostatic Cancer Therapy by Targeting Galectins in the Tumor Vasculature." In ACS Symposium Series, 233–47. Washington, DC: American Chemical Society, 2012. http://dx.doi.org/10.1021/bk-2012-1115.ch013.

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Tuong Nguyen, Josephine. "Adeno-Associated Virus and Other Potential Vectors for Angiostatin and Endostatin Gene Therapy." In Advances in Experimental Medicine and Biology, 457–66. New York, NY: Springer US, 2002. http://dx.doi.org/10.1007/0-306-46817-4_40.

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Steiner, Rudolf. "Angiostatic activity of anticancer agents in the chick embryo chorioallantoic membrane (CHE-CAM) assay." In Experientia Supplementum, 449–54. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7001-6_75.

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Conference papers on the topic "Angiostatine"

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Mok, CC, S. Soliman, LY Ho, F. Mohamed, FI Mohammed, and C. Mohan. "FRI0257 Urinary angiostatin, cxcl4 and vcam-1 as biomarkers for lupus nephritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3951.

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Algergawy, S. "245 High dose of vitamin d therapy and urinary angiostatin among egyptians juvenile lupus." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.245.

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van Zoggel, Hanneke, Yamina Hamma-Kourbali, Cécile Galanth, Ali Ladram, Pierre Nicolas, José Courty, Mohamed Amiche, and Jean Delbé. "Abstract B41: Antitumoral and angiostatic activities in skin secretion of frogPhyllomedusa bicolor." In Abstracts: AACR International Conference on Translational Cancer Medicine--; Mar 21–24, 2010; Amsterdam, The Netherlands. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcme10-b41.

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Zhang, Wei, Giulia Fulci, Samuel D. Rabkin, Xiang Zhang, and Robert L. Martuza. "Abstract 2568: Combination treatment of bevacizumab and oncolytic HSV armed with angiostatin show enhanced antitumoral and antiangiogenic effects." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2568.

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Sterclova, M., M. Vasakova, M. Metlicka, J. Pavlicek, L. Kolesar, and I. Striz. "Angiostatic Versus Angiogenic Chemokines in Idiopathic Pulmonary Fibrosis (IPF) and Chronic Extrinsic Alergic Alveolitis (EAA)." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3009.

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Long, Xiaoping, Ulrich Costabel, Xuan He, Thomas E. Wessendorf, Dirk Theegarten, Josune Guzman, and Francesco Bonella. "Effect of nintedanib on the release of angiogenic/angiostatic cytokines by alveolar macrophages (AMs) in interstitial lung diseases (ILD)." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3054.

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Cole, Shelby A., and Jian-Wei Gu. "Abstract 898: Exercise inhibits the growth of breast cancer and reduces fat mass in postmenopausal obese mice associated with a circulating angiostatic phenotype and the inhibition of angiogenesis in those tissues." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-898.

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Reports on the topic "Angiostatine"

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Weichselbaum, Ralph. Radiation and Angiostatin Target the Tumor Vasculature: A New Paradigm for Prostate Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada390509.

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Huwiler, Kristin G., and Deane F. Mosher. Biophysical Studies of the Type 1 Repeats of Human Thrormbospondin-1 to Characterize the Structural Basis of Its Angiostatic Effect. Fort Belvoir, VA: Defense Technical Information Center, August 1997. http://dx.doi.org/10.21236/ada333301.

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