Blocking fgf2 with a new specific monoclonal antibody impairs angiogenesis and experimental metastatic melanoma, suggesting a potential role in adjuvant settings
dc.contributor.author | de Aguiar, Rodrigo Barbosa [UNIFESP] | |
dc.contributor.author | Parise, Carolina Bellini [UNIFESP] | |
dc.contributor.author | Teixeira Souza, Carolina Rosal | |
dc.contributor.author | Braggion, Camila [UNIFESP] | |
dc.contributor.author | Quintilio, Wagner | |
dc.contributor.author | Moro, Ana Maria | |
dc.contributor.author | Navarro Marques, Fabio Luiz | |
dc.contributor.author | Buchpiguel, Carlos Alberto | |
dc.contributor.author | Chammas, Roger | |
dc.contributor.author | de Moraes, Jane Zveiter [UNIFESP] | |
dc.date.accessioned | 2019-01-21T10:30:08Z | |
dc.date.available | 2019-01-21T10:30:08Z | |
dc.date.issued | 2016 | |
dc.description.abstract | Compelling evidence suggests that fibroblast growth factor 2 (FGF2), overexpressed in melanomas, plays an important role in tumor growth, angiogenesis and metastasis. In this study, we evaluated the therapeutic use of a new anti-FGF2 monoclonal antibody (mAb), 3F12E7, using for that the B16-F10 melanoma model. The FGF2 neutralizing effect of this antibody was certified by in vitro assays, which allowed the further track of its possible in vivo application. 3F12E7 mAb could be retained in B16-F10 tumors, as shown by antibody low-pH elution and nuclear medicine studies, and also led to reduction in number and size of metastatic foci in lungs, when treatment starts one day after intravenous injection of B16-F10 cells. Such data were accompanied by decreased CD34(+) tumor vascular density and impaired subcutaneous tumor outgrowth. Treatments starting one week after melanoma cell intravenous injection did not reduce tumor burden, remaining the therapeutic effectiveness restricted to early-adopted regimens. Altogether, the presented anti-FGF2 3F12E7 mAb stands as a promising agent to treat metastatic melanoma tumors in adjuvant settings. (C) 2015 Elsevier Ireland Ltd. All rights reserved. | en |
dc.description.affiliation | Departamento de Radiologia e Oncologia, Faculdade de Medicina, Universidade de São Paulo, Avenida Dr Arnaldo 251, 01246-000 São Paulo, SP, Brazil | |
dc.description.affiliation | Departamento de Biofísica, Escola Paulista de Medicina, Universidade Federal de São Paulo, Rua Botucatu 862, 04023-062 São Paulo, SP, Brazil | |
dc.description.affiliation | Laboratório de Biofármacos em Células Animais, Instituto Butantan, Avenida Vital Brasil 1500, 05503-900 São Paulo, SP, Brazil | |
dc.description.affiliation | Centro de Medicina Nuclear, Faculdade de Medicina, Universidade de São Paulo, Trav. Rua Dr. Ovídio Pires de Campos s/n, 05403-010 São Paulo, SP, Brazil | |
dc.description.affiliationUnifesp | Departamento de Biofísica, Escola Paulista de Medicina, Universidade Federal de São Paulo, Rua Botucatu 862, 04023-062 São Paulo, SP, Brazil | |
dc.description.source | Web of Science | |
dc.description.sponsorship | FAPESP [98/14247-6, 09/18631-1, 13/06120-8] | |
dc.description.sponsorship | CAPES | |
dc.description.sponsorship | CNPq [11934/2013-7] | |
dc.description.sponsorship | CAPES-UDELAR research grants | |
dc.description.sponsorshipID | FAPESP: 98/14247-6 | |
dc.description.sponsorshipID | FAPESP: 09/18631-1 | |
dc.description.sponsorshipID | FAPESP: 13/06120-8 | |
dc.description.sponsorshipID | CAPES: RBA | |
dc.description.sponsorshipID | capes: CBP | |
dc.description.sponsorshipID | capes: CB | |
dc.description.sponsorshipID | CNPq: CRTS | |
dc.description.sponsorshipID | CNPq: AMM, 11934/2013-7 | |
dc.format.extent | 151-160 | |
dc.identifier | https://doi.org/10.1016/j.canlet.2015.11.030 | |
dc.identifier.citation | Cancer Letters. Clare, v. 371, n. 2, p. 151-160, 2016. | |
dc.identifier.doi | 10.1016/j.canlet.2015.11.030 | |
dc.identifier.issn | 0304-3835 | |
dc.identifier.uri | http://repositorio.unifesp.br/handle/11600/49604 | |
dc.identifier.wos | WOS:000370457300002 | |
dc.language.iso | eng | |
dc.publisher | Elsevier ireland ltd | |
dc.relation.ispartof | Cancer Letters | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | Fgf2 | en |
dc.subject | Melanoma | en |
dc.subject | Monoclonal Antibody | en |
dc.subject | Angiogenesis | en |
dc.subject | MetastasisEndothelial Growth-Factor | en |
dc.subject | Human-Malignant Melanoma | en |
dc.subject | Tumor-Growth | en |
dc.subject | Antigen Cea | en |
dc.subject | In-Vivo | en |
dc.subject | Bevacizumab | en |
dc.subject | Cells | en |
dc.subject | Progression | en |
dc.subject | Expression | en |
dc.subject | Therapy | en |
dc.title | Blocking fgf2 with a new specific monoclonal antibody impairs angiogenesis and experimental metastatic melanoma, suggesting a potential role in adjuvant settings | en |
dc.type | info:eu-repo/semantics/article |