| Literature DB >> 28718447 |
Jianxiong Jiang1, Jiange Qiu2, Qianqian Li3, Zhi Shi4.
Abstract
Elevated cyclooxygenase-2 (COX-2) and the associated inflammation within the brain contribute to glioblastoma development. However, medical use of COX inhibitors in glioblastoma treatment has been limited due to their well-documented vascular toxicity and inconsistent outcomes from recent human studies. Prostaglandin E2 (PGE2) has emerged as a principal mediator for COX-2 cascade-driven gliomagenesis. Are PGE2 terminal synthases and receptors feasible therapeutic targets for glioblastoma?Entities:
Keywords: EP receptors; PGE(2); glioblastoma; gliomagenesis; mPGES-1; neuroinflammation
Mesh:
Substances:
Year: 2017 PMID: 28718447 PMCID: PMC5518646 DOI: 10.1016/j.trecan.2016.12.002
Source DB: PubMed Journal: Trends Cancer ISSN: 2405-8025