{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["8(1)"],"submitter":["Scholz A"],"pubmed_abstract":["Glioblastoma multiforme (GBM) is treated by surgical resection followed by radiochemotherapy. Bevacizumab is commonly deployed for anti-angiogenic therapy of recurrent GBM; however, innate immune cells have been identified as instigators of resistance to bevacizumab treatment. We identified angiopoietin-2 (Ang-2) as a potential target in both naive and bevacizumab-treated glioblastoma. Ang-2 expression was absent in normal human brain endothelium, while the highest Ang-2 levels were observed in bevacizumab-treated GBM. In a murine GBM model, VEGF blockade resulted in endothelial upregulation of Ang-2, whereas the combined inhibition of VEGF and Ang-2 leads to extended survival, decreased vascular permeability, depletion of tumor-associated macrophages, improved pericyte coverage, and incre"],"journal":["EMBO molecular medicine"],"pagination":["39-57"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4718155"],"repository":["biostudies-literature"],"pubmed_title":["Endothelial cell-derived angiopoietin-2 is a therapeutic target in treatment-naive and bevacizumab-resistant glioblastoma."],"pmcid":["PMC4718155"],"pubmed_authors":["Meinhardt M","Frueh JT","Ullrich E","Deckert M","Yalcin BH","Trojan J","Timmer M","Plate KH","Schittenhelm J","Reiss Y","Harter PN","Braun C","Glas M","Yamaji M","Di Tacchio M","Steinbach JP","Cremer S","Herrlinger U","Goldbrunner R","Gurnik S","Mittelbronn M","Krex D","Sommer K","Baumgarten P","Scholz A","Weyerbrock A","Bahr O"],"additional_accession":[]},"is_claimable":false,"name":"Endothelial cell-derived angiopoietin-2 is a therapeutic target in treatment-naive and bevacizumab-resistant glioblastoma.","description":"Glioblastoma multiforme (GBM) is treated by surgical resection followed by radiochemotherapy. Bevacizumab is commonly deployed for anti-angiogenic therapy of recurrent GBM; however, innate immune cells have been identified as instigators of resistance to bevacizumab treatment. We identified angiopoietin-2 (Ang-2) as a potential target in both naive and bevacizumab-treated glioblastoma. Ang-2 expression was absent in normal human brain endothelium, while the highest Ang-2 levels were observed in bevacizumab-treated GBM. In a murine GBM model, VEGF blockade resulted in endothelial upregulation of Ang-2, whereas the combined inhibition of VEGF and Ang-2 leads to extended survival, decreased vascular permeability, depletion of tumor-associated macrophages, improved pericyte coverage, and incre","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Jan","modification":"2025-04-18T16:28:36.82Z","creation":"2019-03-27T02:07:07Z"},"accession":"S-EPMC4718155","cross_references":{"pubmed":["26666269"],"doi":["10.15252/emmm.201505505"]}}