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Erschienen in: Child's Nervous System 12/2016

09.09.2016 | Review Paper

Glucocorticoids in the management of peritumoral brain edema: a review of molecular mechanisms

verfasst von: Roger Murayi, Prashant Chittiboina

Erschienen in: Child's Nervous System | Ausgabe 12/2016

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Abstract

Peritumoral brain edema (PTBE) is mediated by blood-brain barrier breakdown. PTBE results from interstitial vasogenic brain edema due to vascular endothelial growth factor and other inflammatory products of brain tumors. Glucocorticoids (GCs) are the mainstay for treatment of PTBE despite significant systemic side effects. GCs are thought to affect multiple cell types in the edematous brain. Here, we review preclinical studies of GC effects on edematous brain and review mechanisms underlying GC action on tumor cells, endothelial cells, and astrocytes. GCs may reduce tumor cell viability and suppress vascular endothelial growth factor (VEGF) production in tumor cells. Modulation of expression and distribution of tight junction proteins occludin, claudin-5, and ZO-1 in endothelial cells likely plays a central role in GC action on endothelial cells. GCs may also have an effect on astrocyte angiopoietin production and limited effect on astrocyte aquaporin. A better understanding of these molecular mechanisms may lead to the development of novel therapeutics for management of PTBE with a better side effect profile.
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Metadaten
Titel
Glucocorticoids in the management of peritumoral brain edema: a review of molecular mechanisms
verfasst von
Roger Murayi
Prashant Chittiboina
Publikationsdatum
09.09.2016
Verlag
Springer Berlin Heidelberg
Erschienen in
Child's Nervous System / Ausgabe 12/2016
Print ISSN: 0256-7040
Elektronische ISSN: 1433-0350
DOI
https://doi.org/10.1007/s00381-016-3240-x

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