dc.creator | Villeneuve, Jérôme | |
dc.creator | Galarneau, Hugo | |
dc.creator | Beaudet, Marie Josée | |
dc.creator | Tremblay, Pierrot | |
dc.creator | Chernomoretz, Ariel | |
dc.creator | Vallières, Luc | |
dc.date.accessioned | 2018-10-11T14:28:40Z | |
dc.date.available | 2018-10-11T14:28:40Z | |
dc.date.created | 2018-10-11T14:28:40Z | |
dc.date.issued | 2008-07 | |
dc.identifier | Villeneuve, Jérôme; Galarneau, Hugo; Beaudet, Marie Josée; Tremblay, Pierrot; Chernomoretz, Ariel; et al.; Reduced glioma growth following dexamethasone or anti-angiopoietin 2 treatment; Wiley Blackwell Publishing, Inc; Brain Pathology; 18; 3; 7-2008; 401-414 | |
dc.identifier | 1015-6305 | |
dc.identifier | http://hdl.handle.net/11336/62173 | |
dc.identifier | CONICET Digital | |
dc.identifier | CONICET | |
dc.description.abstract | All patients with glioblastoma, the most aggressive and common form of brain cancer, develop cerebral edema. This complication is routinely treated with dexamethasone, a steroidal anti-inflammatory drug whose effects on brain tumors are not fully understood. Here we show that dexamethasone can reduce glioma growth in mice, even though it depletes infiltrating T cells with potential antitumor activity. More precisely, T cells with helper or cytotoxic function were sensitive to dexamethasone, but not those that were negative for the CD4 and CD8 molecules, including gammadelta and natural killer (NK) T cells. The antineoplastic effect of dexamethasone was indirect, as it did not meaningfully affect the growth and gene expression profile of glioma cells in vitro. In contrast, hundreds of dexamethasone-modulated genes, notably angiopoietin 2 (Angpt2), were identified in cultured cerebral endothelial cells by microarray analysis. The ability of dexamethasone to attenuate Angpt2 expression was confirmed in vitro and in vivo. Selective neutralization of Angpt2 using a peptide-Fc fusion protein reduced glioma growth and vascular enlargement to a greater extent than dexamethasone, without affecting T cell infiltration. In conclusion, this study suggests a mechanism by which dexamethasone can slow glioma growth, providing a new therapeutic target for malignant brain tumors. © 2008 The Authors. | |
dc.language | eng | |
dc.publisher | Wiley Blackwell Publishing, Inc | |
dc.relation | info:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1111/j.1750-3639.2008.00139.x | |
dc.relation | info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1750-3639.2008.00139.x | |
dc.rights | https://creativecommons.org/licenses/by-nc-nd/2.5/ar/ | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | Angiopoietin-2 | |
dc.subject | Antitumor Immunity | |
dc.subject | Gene Profiling | |
dc.subject | Glioblastoma | |
dc.subject | Glucocorticoid | |
dc.subject | Tumor Endothelium | |
dc.title | Reduced glioma growth following dexamethasone or anti-angiopoietin 2 treatment | |
dc.type | info:eu-repo/semantics/article | |
dc.type | info:ar-repo/semantics/artículo | |
dc.type | info:eu-repo/semantics/publishedVersion | |