Blocking FGF2 with a new specific monoclonal antibody impairs angiogenesis and experimental metastatic melanoma, suggesting a potential role in adjuvant settings

Aguiar, Rodrigo Barbosa de; Parise, Carolina Bellini; Souza, Carolina Rosal Teixeira de; Braggion, Camila; Quintilio, Wagner; Moro, Ana Maria; Marques, Fábio Luiz Navarro; Buchpiguel, Carlos Alberto; Chammas, Roger; Moraes, Jane Zveiter de

doi:10.1016/j.canlet.2015.11.030

Cited by 30 publications

(25 citation statements)

References 25 publications

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“…Hybridoma, HUVEC and B16‐F10 melanoma cells were cultured as described previously . Antibody generation was obtained by hybridoma technology and VEGF‐binding antibody detection by ELISA .…”

Section: Methodsmentioning

confidence: 99%

Anti‐bevacizumab idiotype antibody vaccination is effective in inducing vascular endothelial growth factor‐binding response, impairing tumor outgrowth

et al. 2016

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Tumors require blood supply and, to overcome this restriction, induce angiogenesis. Vascular endothelial growth factor (VEGF) plays an important role in this process, which explains the great number of antiangiogenic therapies targeting VEGF. The research and development of targeted therapy has led to the approval of bevacizumab, a humanized anti‐VEGF monoclonal antibody (mAb), in clinical settings. However, side effects have been reported, usually as a consequence of bolus‐dose administration of the antibody. This limitation could be circumvented through the use of anti‐idiotype (Id) antibodies. In the present study, we evaluated the efficacy of an active VEGF‐binding immune response generated by an anti‐bevacizumab idiotype mAb, 10.D7. The 10.D7 anti‐Id mAb vaccination led to detectable levels of VEGF‐binding anti‐anti‐Id antibodies. In order to examine whether this humoral immune response could have implications for tumor development, 10.D7‐immunized mice were challenged with B16‐F10 tumor cells. Mice immunized with 10.D7 anti‐Id mAb revealed reduced tumor growth when compared to control groups. Histological analyses of tumor sections from 10.D7‐immunized mice showed increased necrotic areas, decreased CD31‐positive vascular density and reduced CD68‐positive cell infiltration. Our results encourage further therapeutic studies, particularly if one considers that the anti‐Id therapeutic vaccination maintains stable levels of VEGF‐binding antibodies, which might be useful in the control of tumor relapse.

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Section: Methodsmentioning

confidence: 99%

Anti‐bevacizumab idiotype antibody vaccination is effective in inducing vascular endothelial growth factor‐binding response, impairing tumor outgrowth

et al. 2016

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“…FGF is involved in angiogenesis by suppressing VEGF-C expression and stimulating expression of pro-lymphangiogenic factors including integrin α9, VEGFR-3, prox1 and netrin-1 [75]. In fact, blocking of FGF2 with anti-FGF2 monoclonal antibody results in impaired angiogenesis of B16-F10 cell induced melanoma in mice [89]. In addition, TNF-α binding to TNFR1/p55 and TNFR2/p57 receptors has been implicated in the secretion of cytokines and pro-angiogenic factors [72].…”

Section: Da Dr1 and Dr2mentioning

confidence: 99%

Role of the Nervous System in Tumor Angiogenesis

Kuol

Stojanovska

Apostolopoulos

et al. 2018

Cancer Microenvironment

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The development of cancer involves an intricate process, wherein many identified and unidentified factors play a role. Tumor angiogenesis, growth of new blood vessels, is one of the major prerequisites for tumor growth as tumor cells rely on adequate oxygen and nutrient supply as well as the removal of waste products. Growth factors including VEGF orchestrate the development of angiogenesis. In addition, nervous system via the release of neurotransmitters contributes to tumor angiogenesis. The nervous system governs functional activities of many organs, and, as tumors are not independent organs within an organism, this system is integrally involved in tumor growth and progression via regulating tumor angiogenesis. Various neurotransmitters have been reported to play an important role in tumor angiogenesis.

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“…At the extracellular level, blocking antibodies can be employed to block anti‐chondrogenic growth factors and cytokines, as well as growth factor inhibitors. This strategy is already at a clinical stage for a variety of diseases, including chemotherapy for cancer and rheumatoid arthritis . In the case of cytokines, modified soluble receptors are also available, such as etanercept for the treatment of arthritis .…”

Section: Targeted Modulation Of Anti‐chondrogenic Regulatorsmentioning

confidence: 99%

“…This strategy is already at a clinical stage for a variety of diseases, including chemotherapy for cancer and rheumatoid arthritis. 92,93 In the case of cytokines, modified soluble receptors are also available, such as etanercept for the treatment of arthritis. 92 Interestingly, the possibility of using these inhibitors to target antichondrogenic extracellular factors and direct cartilage repair is relatively unexplored.…”

Section: T a R G E T E D M O D U L A T I O N O F A N T I -Chondrogenimentioning

confidence: 99%

Targeting anti‐chondrogenic factors for the stimulation of chondrogenesis: A new paradigm in cartilage repair

Lolli

Colella

Bari

et al. 2018

Journal Orthopaedic Research

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Trauma and age-related cartilage disorders represent a major global cause of morbidity, resulting in chronic pain and disability in patients. A lack of effective therapies, together with a rapidly aging population, creates an impressive clinical and economic burden on healthcare systems. In this scenario, experimental therapies based on transplantation or in situ stimulation of skeletal Mesenchymal Stem/progenitor Cells (MSCs) have raised great interest for cartilage repair. Nevertheless, the challenge of guiding MSC differentiation and preventing cartilage hypertrophy and calcification still needs to be overcome. While research has mostly focused on the stimulation of cartilage anabolism using growth factors, several issues remain unresolved prompting the field to search for novel solutions. Recently, inhibition of anti-chondrogenic regulators has emerged as an intriguing opportunity. Anti-chondrogenic regulators include extracellular proteins as well as intracellular transcription factors and microRNAs that act as potent inhibitors of pro-chondrogenic signals. Suppression of these inhibitors can enhance MSC chondrogenesis and production of cartilage matrix. We here review the current knowledge concerning different types of anti-chondrogenic regulators. We aim to highlight novel therapeutic targets for cartilage repair and discuss suitable tools for suppressing their anti-chondrogenic functions. Further effort is needed to unveil the therapeutic perspectives of this approach and pave the way for effective treatment of cartilage injuries in patients. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res.

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Blocking FGF2 with a new specific monoclonal antibody impairs angiogenesis and experimental metastatic melanoma, suggesting a potential role in adjuvant settings

Cited by 30 publications

References 25 publications

Anti‐bevacizumab idiotype antibody vaccination is effective in inducing vascular endothelial growth factor‐binding response, impairing tumor outgrowth

Anti‐bevacizumab idiotype antibody vaccination is effective in inducing vascular endothelial growth factor‐binding response, impairing tumor outgrowth

Role of the Nervous System in Tumor Angiogenesis

Targeting anti‐chondrogenic factors for the stimulation of chondrogenesis: A new paradigm in cartilage repair

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