Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapy

Autores
Zhou, Zhichao; Bolontrade, Marcela Fabiana; Reddy, Krishna; Duan, Xiaoping; Guan, Hui; Yu, Ling; Hicklin, Daniel J.; Kleinerman, Eugenie S.
Año de publicación
2007
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
PURPOSE: We previously showed that bone marrow cells participate in new tumor vessel formation in Ewing's sarcoma, and that vascular endothelial growth factor 165 (VEGF(165)) is critical to this process. The purpose of this study was to determine whether blocking VEGF receptor 2 (VEGFR-2) with DC101 antibody suppresses tumor growth, reduces tumor vessel formation, and inhibits the migration of bone marrow cells into the tumor. EXPERIMENTAL DESIGN: An H-2 MHC-mismatched bone marrow transplant Ewing's sarcoma mouse model was used. Bone marrow cells from CB6F1 (MHC H-2(b/d)) mice were injected into irradiated BALB/cAnN mice (MHC H-2(d)). TC71 Ewing's sarcoma cells were s.c. injected 4 weeks after the bone marrow transplantation. Mice were then treated i.p. with DC101 antibody or immunoglobulin G (control) twice a week for 3 weeks starting 3 days after tumor cell injection. RESULTS: DC101 antibody therapy significantly reduced tumor growth and tumor mean vessel density (P < 0.05) and increased tumor cell apoptosis. Decreased bone marrow cell migration into the tumor was also shown after DC101 therapy as assessed by the colocalization of H-2K(b) and CD31 using immunohistochemistry. DC101 inhibited the migration of both human and mouse vessel endothelial cells in vitro. CONCLUSION: These results indicated that blocking VEGFR-2 with DC101 antibodies may be a useful therapeutic approach for treating patients with Ewing's sarcoma
Fil: Zhou, Zhichao. University of Texas; Estados Unidos
Fil: Bolontrade, Marcela Fabiana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina. University of Texas; Estados Unidos
Fil: Reddy, Krishna. University of Texas; Estados Unidos
Fil: Duan, Xiaoping. University of Texas; Estados Unidos
Fil: Guan, Hui. University of Texas; Estados Unidos
Fil: Yu, Ling. University of Texas; Estados Unidos
Fil: Hicklin, Daniel J.. ImClone Systems, Inc; Estados Unidos
Fil: Kleinerman, Eugenie S.. University of Texas; Estados Unidos
Materia
Ewing´S Sarcoma
Vegf
Progenitor Cell
Vasculogenesis
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/31578
Acceder
id CONICETDig_bc64534967d70aea45cdb07fda5a6189
oai_identifier_str oai:ri.conicet.gov.ar:11336/31578
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapyZhou, ZhichaoBolontrade, Marcela FabianaReddy, KrishnaDuan, XiaopingGuan, HuiYu, LingHicklin, Daniel J.Kleinerman, Eugenie S.Ewing´S SarcomaVegfProgenitor CellVasculogenesisPURPOSE: We previously showed that bone marrow cells participate in new tumor vessel formation in Ewing's sarcoma, and that vascular endothelial growth factor 165 (VEGF(165)) is critical to this process. The purpose of this study was to determine whether blocking VEGF receptor 2 (VEGFR-2) with DC101 antibody suppresses tumor growth, reduces tumor vessel formation, and inhibits the migration of bone marrow cells into the tumor. EXPERIMENTAL DESIGN: An H-2 MHC-mismatched bone marrow transplant Ewing's sarcoma mouse model was used. Bone marrow cells from CB6F1 (MHC H-2(b/d)) mice were injected into irradiated BALB/cAnN mice (MHC H-2(d)). TC71 Ewing's sarcoma cells were s.c. injected 4 weeks after the bone marrow transplantation. Mice were then treated i.p. with DC101 antibody or immunoglobulin G (control) twice a week for 3 weeks starting 3 days after tumor cell injection. RESULTS: DC101 antibody therapy significantly reduced tumor growth and tumor mean vessel density (P < 0.05) and increased tumor cell apoptosis. Decreased bone marrow cell migration into the tumor was also shown after DC101 therapy as assessed by the colocalization of H-2K(b) and CD31 using immunohistochemistry. DC101 inhibited the migration of both human and mouse vessel endothelial cells in vitro. CONCLUSION: These results indicated that blocking VEGFR-2 with DC101 antibodies may be a useful therapeutic approach for treating patients with Ewing's sarcomaFil: Zhou, Zhichao. University of Texas; Estados UnidosFil: Bolontrade, Marcela Fabiana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina. University of Texas; Estados UnidosFil: Reddy, Krishna. University of Texas; Estados UnidosFil: Duan, Xiaoping. University of Texas; Estados UnidosFil: Guan, Hui. University of Texas; Estados UnidosFil: Yu, Ling. University of Texas; Estados UnidosFil: Hicklin, Daniel J.. ImClone Systems, Inc; Estados UnidosFil: Kleinerman, Eugenie S.. University of Texas; Estados UnidosAmerican Association for Cancer Research2007-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/31578Guan, Hui; Duan, Xiaoping; Reddy, Krishna; Bolontrade, Marcela Fabiana; Zhou, Zhichao; Kleinerman, Eugenie S.; et al.; Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapy; American Association for Cancer Research; Clinical Cancer Research; 13; 16; 8-2007; 4867-48731078-04321078-0432CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://clincancerres.aacrjournals.org/content/13/16/4867.longinfo:eu-repo/semantics/altIdentifier/doi/10.1158/1078-0432.CCR-07-0133info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:10:38Zoai:ri.conicet.gov.ar:11336/31578instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:10:38.395CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapy
title Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapy
spellingShingle Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapy
Zhou, Zhichao
Ewing´S Sarcoma
Vegf
Progenitor Cell
Vasculogenesis
title_short Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapy
title_full Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapy
title_fullStr Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapy
title_full_unstemmed Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapy
title_sort Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapy
dc.creator.none.fl_str_mv Zhou, Zhichao
Bolontrade, Marcela Fabiana
Reddy, Krishna
Duan, Xiaoping
Guan, Hui
Yu, Ling
Hicklin, Daniel J.
Kleinerman, Eugenie S.
author Zhou, Zhichao
author_facet Zhou, Zhichao
Bolontrade, Marcela Fabiana
Reddy, Krishna
Duan, Xiaoping
Guan, Hui
Yu, Ling
Hicklin, Daniel J.
Kleinerman, Eugenie S.
author_role author
author2 Bolontrade, Marcela Fabiana
Reddy, Krishna
Duan, Xiaoping
Guan, Hui
Yu, Ling
Hicklin, Daniel J.
Kleinerman, Eugenie S.
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Ewing´S Sarcoma
Vegf
Progenitor Cell
Vasculogenesis
topic Ewing´S Sarcoma
Vegf
Progenitor Cell
Vasculogenesis
dc.description.none.fl_txt_mv PURPOSE: We previously showed that bone marrow cells participate in new tumor vessel formation in Ewing's sarcoma, and that vascular endothelial growth factor 165 (VEGF(165)) is critical to this process. The purpose of this study was to determine whether blocking VEGF receptor 2 (VEGFR-2) with DC101 antibody suppresses tumor growth, reduces tumor vessel formation, and inhibits the migration of bone marrow cells into the tumor. EXPERIMENTAL DESIGN: An H-2 MHC-mismatched bone marrow transplant Ewing's sarcoma mouse model was used. Bone marrow cells from CB6F1 (MHC H-2(b/d)) mice were injected into irradiated BALB/cAnN mice (MHC H-2(d)). TC71 Ewing's sarcoma cells were s.c. injected 4 weeks after the bone marrow transplantation. Mice were then treated i.p. with DC101 antibody or immunoglobulin G (control) twice a week for 3 weeks starting 3 days after tumor cell injection. RESULTS: DC101 antibody therapy significantly reduced tumor growth and tumor mean vessel density (P < 0.05) and increased tumor cell apoptosis. Decreased bone marrow cell migration into the tumor was also shown after DC101 therapy as assessed by the colocalization of H-2K(b) and CD31 using immunohistochemistry. DC101 inhibited the migration of both human and mouse vessel endothelial cells in vitro. CONCLUSION: These results indicated that blocking VEGFR-2 with DC101 antibodies may be a useful therapeutic approach for treating patients with Ewing's sarcoma
Fil: Zhou, Zhichao. University of Texas; Estados Unidos
Fil: Bolontrade, Marcela Fabiana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina. University of Texas; Estados Unidos
Fil: Reddy, Krishna. University of Texas; Estados Unidos
Fil: Duan, Xiaoping. University of Texas; Estados Unidos
Fil: Guan, Hui. University of Texas; Estados Unidos
Fil: Yu, Ling. University of Texas; Estados Unidos
Fil: Hicklin, Daniel J.. ImClone Systems, Inc; Estados Unidos
Fil: Kleinerman, Eugenie S.. University of Texas; Estados Unidos
description PURPOSE: We previously showed that bone marrow cells participate in new tumor vessel formation in Ewing's sarcoma, and that vascular endothelial growth factor 165 (VEGF(165)) is critical to this process. The purpose of this study was to determine whether blocking VEGF receptor 2 (VEGFR-2) with DC101 antibody suppresses tumor growth, reduces tumor vessel formation, and inhibits the migration of bone marrow cells into the tumor. EXPERIMENTAL DESIGN: An H-2 MHC-mismatched bone marrow transplant Ewing's sarcoma mouse model was used. Bone marrow cells from CB6F1 (MHC H-2(b/d)) mice were injected into irradiated BALB/cAnN mice (MHC H-2(d)). TC71 Ewing's sarcoma cells were s.c. injected 4 weeks after the bone marrow transplantation. Mice were then treated i.p. with DC101 antibody or immunoglobulin G (control) twice a week for 3 weeks starting 3 days after tumor cell injection. RESULTS: DC101 antibody therapy significantly reduced tumor growth and tumor mean vessel density (P < 0.05) and increased tumor cell apoptosis. Decreased bone marrow cell migration into the tumor was also shown after DC101 therapy as assessed by the colocalization of H-2K(b) and CD31 using immunohistochemistry. DC101 inhibited the migration of both human and mouse vessel endothelial cells in vitro. CONCLUSION: These results indicated that blocking VEGFR-2 with DC101 antibodies may be a useful therapeutic approach for treating patients with Ewing's sarcoma
publishDate 2007
dc.date.none.fl_str_mv 2007-08
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/31578
Guan, Hui; Duan, Xiaoping; Reddy, Krishna; Bolontrade, Marcela Fabiana; Zhou, Zhichao; Kleinerman, Eugenie S.; et al.; Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapy; American Association for Cancer Research; Clinical Cancer Research; 13; 16; 8-2007; 4867-4873
1078-0432
1078-0432
CONICET Digital
CONICET
url http://hdl.handle.net/11336/31578
identifier_str_mv Guan, Hui; Duan, Xiaoping; Reddy, Krishna; Bolontrade, Marcela Fabiana; Zhou, Zhichao; Kleinerman, Eugenie S.; et al.; Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapy; American Association for Cancer Research; Clinical Cancer Research; 13; 16; 8-2007; 4867-4873
1078-0432
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://clincancerres.aacrjournals.org/content/13/16/4867.long
info:eu-repo/semantics/altIdentifier/doi/10.1158/1078-0432.CCR-07-0133
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv American Association for Cancer Research
publisher.none.fl_str_mv American Association for Cancer Research
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1842270127860482048
score 13.13397

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