Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia.
Details
State: Public
Version: author
Serval ID
serval:BIB_7B8DA1DF886B
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia.
Journal
PloS One
ISSN
1932-6203
Publication state
Published
Issued date
2009
Peer-reviewed
Oui
Volume
4
Number
6
Pages
e5947
Language
english
Abstract
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
Yes
Create date
19/06/2009 10:58
Last modification date
20/08/2019 15:37