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      In vitro Tumor Angiogenesis Assays: Plasminogen Lysine Binding Site 1 Inhibits in vitro Tumor-Induced Angiogenesis

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          Abstract

          It is generally accepted that tumors are angiogenesis-dependent. For research and clinical purposes it would be very attractive to have a simple in vitro model that allows a rapid screening of the angiogenic potential of tumors and to study the effect of angiogenic inhibitors. In vitro angiogenesis models were developed, based on endothelial sprouting/tube formation on a collagen gel, using both tumor cell lines and tumor biopsies. Best results were obtained using conditioned medium of tumor cell lines. In this model it was found that the plasminogen fragment lysine binding site 1 (LBS-1) inhibited in vitro endothelial cell sprouting. This is the first demonstration that LBS-1, which includes angiostatin, is inhibitory for new vessel formation in an in vitro angiogenesis model. We conclude that the assay system allows for rapid and reliable screening of angiogenesis inhibitors.

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          Most cited references 6

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          Angiostatin: a novel angiogenesis inhibitor that mediates the suppression of metastases by a Lewis lung carcinoma.

          The phenomenon of inhibition of tumor growth by tumor mass has been repeatedly studied, but without elucidation of a satisfactory mechanism. In our animal model, a primary tumor inhibits its remote metastases. After tumor removal, metastases neovascularize and grow. When the primary tumor is present, metastatic growth is suppressed by a circulating angiogenesis inhibitor. Serum and urine from tumor-bearing mice, but not from controls, specifically inhibit endothelial cell proliferation. The activity copurifies with a 38 kDa plasminogen fragment that we have sequenced and named angiostatin. A corresponding fragment of human plasminogen has similar activity. Systemic administration of angiostatin, but not intact plasminogen, potently blocks neovascularization and growth of metastases. We here show that the inhibition of metastases by a primary mouse tumor is mediated, at least in part, by angiostatin.
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            Angiostatin induces and sustains dormancy of human primary tumors in mice

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              Tumor infarction in mice by antibody-directed targeting of tissue factor to tumor vasculature.

              Selective occlusion of tumor vasculature was tested as a therapy for solid tumors in a mouse model. The formation of blood clots (thrombosis) within the tumor vessels was initiated by targeting the cell surface domain of human tissue factor, by means of a bispecific antibody, to an experimentally induced marker on tumor vascular endothelial cells. This truncated form of tissue factor (tTF) had limited ability to initiate thrombosis when free in the circulation, but became an effective and selective thrombogen when targeted to tumor endothelial cells. Intravenous administration of the antibody-tTF complex to mice with large neuroblastomas resulted in complete tumor regressions in 38 percent of the mice.
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                Author and article information

                Journal
                JVR
                J Vasc Res
                10.1159/issn.1018-1172
                Journal of Vascular Research
                S. Karger AG
                1018-1172
                1423-0135
                1998
                April 1998
                16 April 1998
                : 35
                : 2
                : 109-114
                Affiliations
                a Department of Internal Medicine, University Hospital Maastricht, and b Department of Natural Science, Open University of the Netherlands, Heerlen, The Netherlands
                Article
                25572 J Vasc Res 1998;35:109–114
                10.1159/000025572
                9588874
                © 1998 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 5, References: 27, Pages: 6
                Categories
                Research Paper

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