Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia.
Détails
Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_7B8DA1DF886B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia.
Périodique
PloS One
ISSN
1932-6203
Statut éditorial
Publié
Date de publication
2009
Peer-reviewed
Oui
Volume
4
Numéro
6
Pages
e5947
Langue
anglais
Résumé
Glioblastoma are rapidly proliferating brain tumors in which hypoxia is readily recognizable, as indicated by focal or extensive necrosis and vascular proliferation, two independent diagnostic criteria for glioblastoma. Gene expression profiling of glioblastoma revealed a gene expression signature associated with hypoxia-regulated genes. The correlated gene set emerging from unsupervised analysis comprised known hypoxia-inducible genes involved in angiogenesis and inflammation such as VEGF and BIRC3, respectively. The relationship between hypoxia-modulated angiogenic genes and inflammatory genes was associated with outcome in our cohort of glioblastoma patients treated within prospective clinical trials of combined chemoradiotherapy. The hypoxia regulation of several new genes comprised in this cluster including ZNF395, TNFAIP3, and TREM1 was experimentally confirmed in glioma cell lines and primary monocytes exposed to hypoxia in vitro. Interestingly, the cluster seems to characterize differential response of tumor cells, stromal cells and the macrophage/microglia compartment to hypoxic conditions. Most genes classically associated with the inflammatory compartment are part of the NF-kappaB signaling pathway including TNFAIP3 and BIRC3 that have been shown to be involved in resistance to chemotherapy.Our results associate hypoxia-driven tumor response with inflammation in glioblastoma, hence underlining the importance of tumor-host interaction involving the inflammatory compartment.
Pubmed
Web of science
Open Access
Oui
Création de la notice
19/06/2009 10:58
Dernière modification de la notice
20/08/2019 15:37