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      Effect Of Bevacizumab On Growth Of Human Nasal Polyposis In Vitro; An Off-Label Use Of Anti-Angiogenic Agent For Nasal Polyposis Treatment

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          Nasal polyposis (NP) is a frequent problem during adulthood. Treatment of NP is primarily based on drugs, such as oral or topical steroids and in some types, by surgery. Despite of available therapeutic options for NP, recurrence after polypectomy is found. Vascular endothelial growth factor (VEGF) is a known factor involved in NP. Bevacizumab is a monoclonal antibody, which acts against VEGF.


          Regarding the availability of bevacizumab and its use in ophthalmic off-label application, in this study, we hypothesized that it could be a choice of non-invasive treatment. The researchers aimed at evaluating the use of bevacizumab in vitro on the growth of NP.

          Materials and methods

          In this experimental study, the researchers used eight non-allergic NP tissues from patients admitted for polypectomy clinic of Imam Reza Hospital, Mashhad. Tissues were cultured in DMEM medium based on standard protocols in the presence or absence of bevacizumab (10 to 250 μM) then incubated. The mean of the responses was reported. The level of VEGF and MTT test for NP epithelial cell viability were determined for each group. Data were analyzed using the SPSS software.


          The researchers demonstrated that bevacizumab leads to a decrease in the level of VEGF (the most common cause of angiogenesis in NP) in media culture of NP, dose-dependently (P<0.001). The highest mean was related to the 10-μM group and the least mean was related to the 250-μM group. In MTT test after 5 days, it was shown that the percentage of viable epithelial NP cells (due to apoptosis) was decreased dose-dependently and could lead to resolving NP tissue (P<0.001), significantly.


          This study showed that bevacizumab could help decrease the growth of NP tissue dose-dependently in organ culture in vitro by inhibiting VEGF. It seems that bevacizumab could be a good candidate for the treatment of non-allergic NP.

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          Most cited references 35

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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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            Biological activity of bevacizumab, a humanized anti-VEGF antibody in vitro.

            Bevacizumab (Avastin, Genentech) is a humanized monoclonal antibody targeting vascular endothelial growth factor (VEGF), a critical angiogenic factor involved in both physiological and pathological conditions. It has been recently approved by the US FDA as a first-line therapy for widespread metastatic colorectal cancer. This report is a detailed biological characterization of bevacizumab in a variety of in vitro models. It is shown that bevacizumab potently neutralizes VEGF and blocks its signal transduction through both the VEGFR-1 and VEGFR-2 receptors, as demonstrated by the inhibition of VEGF-induced cell proliferation, survival, permeability, nitric oxide production, as well as migration and tissue factor production. Although bevacizumab retains the ability to bind to human Fcgamma receptors and complement protein C1q, it does not demonstrate cell or complement-mediated cytotoxicity in either VEGF producing or targeting cells. Thus the mechanism of anti-tumor activity of bevacizumab is most likely due to its anti-angiogenesis effect through binding and neutralization of secreted VEGF.
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              • Abstract: not found
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              Regression of retinal and iris neovascularization after intravitreal bevacizumab (Avastin) treatment.


                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                24 September 2019
                : 13
                : 3383-3389
                [1 ]Rhino-sinus, Ear, and Skull Base Diseases Research Center, Guilan University of Medical Sciences , Rasht, Iran
                [2 ]Cardiology Department, Imam Reza & Ghaem Hospital, Faculty of Medicine, Mashhad University of Medical Sciences , Mashhad, Iran
                [3 ]Pharmaceutical Research Division, Booali Research Center, Mashhad University of Medical Sciences , Mashhad, Iran
                [4 ]Faculty of Medicine, Guilan University of Medical Sciences , Rasht, Iran
                [5 ]Pharmaceutical Research Division, Booali Research Center, Mashhad University of Medical Sciences , Mashhad, Iran
                [6 ]Faculty of Medicine, Ear, Nose and Throat Department, Mashhad University of Medical Sciences , Mashhad, Iran
                Author notes
                Correspondence: Amin Saeidinia Faculty of Medicine, Mashhad University Complex , Azadi Square, Mashhad9177948564, IranTel +98 511 9119451607 Email saeidiniaa971@mums.ac.ir
                © 2019 Nemati 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. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 3, Tables: 3, References: 38, Pages: 7
                Original Research


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