Linking tumor hypoxia with VEGFR2 signaling and compensatory angiogenesis: Glycans make the difference

Although blocking vascular endothelial growth factor (VEGF) signaling is clinically beneficial in certain cancers, tumor regrowth in treated patients suggests that compensatory angiogenic programs may limit the efficacy of anti-VEGF treatment. We found that association of galectin-1 with complex N-g...

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Detalles Bibliográficos
Autores principales: Croci, D.O., Rabinovich, G.A.
Formato: JOUR
Materias:
Angiogenesis
anti-VEGF
Cancer immunotherapy
Galectin
Glycans
Glycosylation
Inflammation
glycan
glycosyltransferase
immunoglobulin G3
immunoglobulin G4
vasculotropin receptor 2
article
carcinogenesis
catalysis
cell adhesion
glycosylation
human
hypoxia
lymphocyte proliferation
melanoma
nonhuman
protein binding
protein domain
protein processing
protein protein interaction
protein structure
sialylation
signal transduction
tumor microenvironment
tumor vascularization
upregulation
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_21624011_v3_n6_p_Croci
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
Descripción
Sumario:Although blocking vascular endothelial growth factor (VEGF) signaling is clinically beneficial in certain cancers, tumor regrowth in treated patients suggests that compensatory angiogenic programs may limit the efficacy of anti-VEGF treatment. We found that association of galectin-1 with complex N-glycans on VEGFR2 links tumor hypoxia to VEGFR2 signaling and preserves angiogenesis in response to VEGF blockade.

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