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Series GSE12246 Query DataSets for GSE12246
Status Public on Dec 24, 2009
Title Identification of COX-2 as a major actor of transcriptomic adaptation of endothelial and tumor cells to cyclic hypoxia
Organism Homo sapiens
Experiment type Expression profiling by array
Summary Tumor hypoxia is not a stable phenomenon but cycles between periods of deep hypoxia and reoxygenation. Cyclic hypoxia originates from heterogeneities in red blood cell flux and from the permanent remodelling of the angiogenic vascular network. Endothelial cells lining tumor blood vessels are therefore also influenced by cyclic hypoxia. The gene expression pattern promoted by cyclic hypoxia differs from those observed under normoxia and even continuous hypoxia. PTGS2 is one gene exquisitely up-regulated in endothelial cells (and tumor cells) in response to cyclic hypoxia. Elevated COX-2 (the PTGS2 gene product) expression and activity account for cyclic hypoxia-driven increase in endothelial cell survival and angiogenesis.
Overall design In vitro culture of HUVEC submitted to hypoxia (oxygen rate less than 0.5%)
Contributor(s) Daneau G, Boidot R, Martinive P, Feron O
Citation(s) 20068092
Submission date Jul 25, 2008
Last update date Jul 10, 2019
Contact name Olivier Feron
Phone +32-2-7645264
Fax +32-2-7645269
Organization name UCL
Department IREC
Street address Avenue E. Mounier, 52 - FATH5349
City Brussels
ZIP/Postal code 1200
Country Belgium
Platforms (1)
GPL571 [HG-U133A_2] Affymetrix Human Genome U133A 2.0 Array
Samples (6)
GSM307678 Normoxia
GSM307679 Normoxia +1h
GSM307680 Chronic hypoxia
BioProject PRJNA113713

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE12246_RAW.tar 11.7 Mb (http)(custom) TAR (of CEL, CHP, EXP)
Processed data included within Sample table
Processed data provided as supplementary file

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