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      Monitoring antiangiogenesis of bevacizumab in zebrafish

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          Abstract

          Bevacizumab, which is a humanized anti-VEGF antibody, has been successfully applied in clinics since 2004. Bevacizumab in combination with chemotherapy showed high safety and has been applied to solid tumors. However, studies on the insight into the mechanism about the antiangiogenesis activity of bevacizumab were mostly done on mice models, and so there are no visual and intuitive models to observe the process of antiangiogenesis. Here, we first used a zebrafish model to investigate the angiogenesis suppressing behavior of bevacizumab. Our results showed that bevacizumab inhibited formation of zebrafish subintestinal veins, which mimics the process of tumor angiogenesis in vivo. Meanwhile, bevacizumab caused specific vasculature formation defects in subintestinal veins but not in the trunk. Our study also indicated that bevacizumab could inhibit zebrafish retinal angiogenesis with therapeutic potential.

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          Most cited references 28

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          Angiogenesis: an organizing principle for drug discovery?

           Judah Folkman (2007)
          Angiogenesis--the process of new blood-vessel growth--has an essential role in development, reproduction and repair. However, pathological angiogenesis occurs not only in tumour formation, but also in a range of non-neoplastic diseases that could be classed together as 'angiogenesis-dependent diseases'. By viewing the process of angiogenesis as an 'organizing principle' in biology, intriguing insights into the molecular mechanisms of seemingly unrelated phenomena might be gained. This has important consequences for the clinical use of angiogenesis inhibitors and for drug discovery, not only for optimizing the treatment of cancer, but possibly also for developing therapeutic approaches for various diseases that are otherwise unrelated to each other.
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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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              Bevacizumab (Avastin), a humanized anti-VEGF monoclonal antibody for cancer therapy.

              Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen in vitro and an angiogenic inducer in vivo. The tyrosine kinases Flt-1 (VEGFR-1) and Flk-1/KDR (VEGFR-2) are high affinity VEGF receptors. VEGF plays an essential role in developmental angiogenesis and is important also for reproductive and bone angiogenesis. Substantial evidence also implicates VEGF as a mediator of pathological angiogenesis. Anti-VEGF monoclonal antibodies and other VEGF inhibitors block the growth of several tumor cell lines in nude mice. Clinical trials with VEGF inhibitors in a variety of malignancies are ongoing. Recently, a humanized anti-VEGF monoclonal antibody (bevacizumab; Avastin) has been approved by the FDA as a first-line treatment for metastatic colorectal cancer in combination with chemotherapy. Furthermore, VEGF is implicated in intraocular neovascularization associated with diabetic retinopathy and age-related macular degeneration.
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                Author and article information

                Journal
                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                Drug Design, Development and Therapy
                Dove Medical Press
                1177-8881
                2018
                06 August 2018
                : 12
                : 2423-2430
                Affiliations
                [1 ]Department of Respiratory and Critical Care Medicine, Ruijin Hospital, Institute of Respiratory Diseases, School of Medicine, Shanghai Jiaotong University, Shanghai, People’s Republic of China, xiangyiht@ 123456163.com
                [2 ]Respiratory Department of Shanghai East Hospital Affiliated to Tongji University, Shanghai, People’s Republic of China
                Author notes
                Correspondence: Yi Xiang Department of Respiratory and Critical Care Medicine, Ruijin Hospital, Institute of Respiratory Diseases, School of Medicine, Shanghai Jiaotong University, No 197 Ruijin 2nd Road, Shanghai, People’s Republic of China, Email xiangyiht@ 123456163.com
                [*]

                These authors contributed equally to this work

                Article
                dddt-12-2423
                10.2147/DDDT.S166330
                6084084
                © 2018 Zhang et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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